Perfusion HTN Flashcards

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1
Q

Describe symptomatic HTN

A

low perfusion - enough to cause “lightheadedness”, dizziness, pre-syncope, syncope, or abnormal weakness with normal activity, particularly getting up from a lying or sitting position. High risk for falls and trauma

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2
Q

Orthostatic Hypotension (Postural Hypotension) how can we determine if a patient has this?

A

Lying-to-standing or if very weak, lying-sitting-standing BP Drop in systolic BP of more than 20 mmHg

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3
Q

Orthostatic Hypotension Symptoms may occur with?

A

Symptoms may occur with volume depletion, overtreatment with BP medication, prolonged bed rest, older patients.

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4
Q

How do we get the baseline BP for patients with Orthostatic HTN.

A

Supine 2-3 min: baseline

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5
Q

How do we calculate MAP?

A

s + d +d/3

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6
Q

Why does prolonged best rest cause hypotension

A

the muscles are not contracting enough to get blood up the veins.

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7
Q

How can we determine a patient has HTN?

A

Two visits if ≥180/ ≥110 mmHg, Two visits if 140-179/90-109 with target organ damage, diabetes, or chronic kidney disease

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8
Q

Generally considered SBP≥_____ and / or DBP≥___ mm

A

Generally considered SBP≥140 and / or DBP≥90 mm

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9
Q

What nations of descent have a higher risk of being diagnosed with HTN and what gender?

A

Black Canadians and people of South Asian descent have a higher prevalence of hypertension than East Asians and Whites; it develops at a younger age, First nations canadians. HTN is more prevalent in older women than in older me

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10
Q

Isolated systolic HTN Describe

A

Common in older adults related to loss of elasticity in large arteries.

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11
Q

how do we calculate pulse pressure

A

systolic-diastolic

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12
Q

Primary hypertension describe

A

unclear (Idiopathic) or definite causes but we have associated causes eg smoking, lifestyle. 90–95% of patients

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13
Q

Secondary hypertension describe

A

5–10% in adults; >80% in children•Many causes; treatment aimed at the underlying cause

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14
Q

What are some of the risk factors of Primary Hypertension

A
low Vit D
Excess dietary sodium
Elevated serum lipids
Diabetes mellitus
Ethnicity
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15
Q

Secondary Hypertension: Etiology

A

Coarctation or congenital narrowing of the aorta
Renal disease such as renal artery stenosis (↓ flow to kidney → RAAS
Endocrine disorders such as Cushing’s syndrome and hyperaldosteronism

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16
Q

_________ in BP is more important than the absolute value.

A

rate of increase in BP is more important than the absolute value

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17
Q

patients with hypertensive Crisis are at risk of what

A

heart and kidney failure, bursting of blood vessels.

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18
Q

Who is at risking of hypertensive crisis?

A

May occur in patients with a history of HTN who have failed to comply with medications or who have been under-medicated

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19
Q

What is hypertensive crisis?

A

evere, abrupt increase in DBP (defined as >120–130 mm Hg) e.g. BP 220/120 mmHg

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20
Q

In emergency cases of hypertensive crisis what do we treat patients with?

A

Emergency treatment with vasodilator such as IV Nitroprusside

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21
Q

What is the first approach to HTN treatment

A

Lifestyle Modification prior to (or along with) medication therapy

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22
Q

What are the 7 first line Antihypertensive Drugs?

A

Thiazide/thiazide-like Diuretics (first choice if uncomplicated)
•ACE-I: Angiotensin converting enzyme inhibitors (non-black pt)
•ARB: Angiotensin II receptor blockers
•CCB: Calcium channel blockers
•Beta Blockers (Beta adrenergic receptor antagonists) (<60 y)
•Alpha Blockers (doxazoxin) (less common)
•Vasodilators (less common

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23
Q

An example of a Diuretics

A

Hydrochlorothiazide (HCTZ; HCT)

24
Q

What is the MOA for the diuretics

A
Increases urine output, decrease plasma and extracellular fluid volumes
Results
•Decreased preload and cardiac output
•Decreased arterial blood volume
•Decreased total peripheral resistance
25
Q

Diuretics may result in?

A

ay result in hypokalemia (K-wasting), hypovolemia

26
Q

MOA of ACE-I

A

inhibit angiotensin-converting enzyme, which is responsible for converting angiotensin I (through the action of renin) to angiotensin I. cause potassium-sparing diuresis through inhibition of Aldosterone (monitor for hyperkalemia

27
Q

what is the best ACE-I to use and why

A

Captopril- very short half life and is better to start the patient on that to watch for side effects.

28
Q

_____ reduces effectiveness of ACE-I, ARBs and diuretics and what is the side effect of when used in combination with these drugs?

A

NSAIDS reduce the effectiveness of Ace-Inhibitors, ARBs and diuretics and when used in combination increase the risk of renal failure. If used, close monitoring is required.

29
Q

Inhibiting ACE reduces the breakdown of what inflammatory substance and what are the side effects

A

Bradykinin and the side effects are nagging or chronic cough and angioedema (rare and fatal)

30
Q

What are the two ACE-I that can be used if a patient has liver dysfunction unlike the other ACE-I that are prodrugs?

A

Captopril and lisinopril can be used if a patient has liver dysfunction, unlike other ACE inhibitors that are prodr

31
Q

What is the contradiction of using a ACE-I?

A

Contraindicated if K ≥5.0 mmol/L (may causes K retention)

32
Q

What are the four major side effects of using ACE-I and what will likely occur with the first dose?

A
Orthostatic (Postural) hypotension
Fatigue
Dizziness
Possible hyperkalemia (lose Na, keep K)
 First-dose hypotension effect may occur!
33
Q

What is the MOA of ARB: Angiotensin II Receptor Blockers

A

ARBs block the receptors that receive angiotensin II,Blocks vasoconstriction and release of aldosterone

34
Q

Does ARB inhibit Bradykinin breakdown?

A

Does not inhibit Bradykinin breakdown therefore does not normally cause a dry cough

35
Q

Is the use of ACE-I and ARB recommended?

A

use of ACE-I plus ARB (or other renin blocker) is not recommended (especially with diabetic nephropathy) unless absolutely necessary (some HF pts) and they must be monitored for renal function, fluid volume, Na, BP

36
Q

What are two examples of ARB: Angiotensin II Receptor Blockers drugs?

A

Examples: losartan (Cozaar), valsartan (Diovan),

37
Q

_______common combination of losartan and hydrochlorothiazide diuretic

A

Hyzaar

38
Q

Common Adverse Effects of ARB: Angiotensin II Receptor Blockers drugs?

A

Orthostatic hypotension, dizziness, fatigue
•Upper respiratory infections
•Headache

39
Q

What is the MOA of Calcium Channel Blockers CCB

A

Cause smooth muscle relaxation by blocking the binding of calcium to its receptors Prevents contraction of the smooth muscle

40
Q

example of vascular CCB drug

A

nifedipine (Adalat)

41
Q

Where does the vascular CCB function?

A

Goes to the blood vessels, blocks channels to get a weaker contraction of the smooth muscle.

42
Q

What are the two types of CCB?

A

here are specific “vascular” (dihydropyridine) CCB, and specific “cardiac” (Non-dihydropyridine) CCB

43
Q

Common Adverse Effects of CCB:

A

Reflex tachycardia

44
Q

What are the two types of Beta-blockers (Beta Adrenergic antagonist)?

A

Cardioselective (Beta1 blockade)

Non-Cardioselective (Beta1 and Beta2 blockade)

45
Q

What are the 2 functions of Cardioselective (Beta1 blockade)

A
Reduces HR (beta1-blockade)
Reduce Renin production (beta1-blockade)
46
Q

What does the Reduction of Renin production (beta1-blockade) do?

A

.Reduces Angiotensin II induced vasoconstriction
.Reduces Aldosterone mediated volume expansion
.Long-term use reduces peripheral vascular resistance

47
Q

What are the examples of beta blockers drugs?

A

metoprolol, atenolol

48
Q

Non-Cardioselective ( Beta2 blockade) function and example of a drug?

A

Beta2 blockade can block bronchodilation and exacerbate asthma,
propranolol

49
Q

Function of Dual-action alpha1- and beta-receptor blocker

A

Reduced heart rate (beta1 blockade)

Vasodilation (alpha1 blockade)

50
Q

Serious Adverse Effects of Beta-blockers (Beta Adrenergic antagonist)?

A

bradycardia (avoid in patients with existing low HR), postural and post-exercise hypotension (cannot compensate), dizziness, drowsiness

51
Q

Alpha Blockers (Alpha Adrenergic antagonist) MOA

A

Dilate both arterial and venous blood vessels

52
Q

Example of Alpha blockers drugs

A

doxazosin

53
Q

Alpha1 is the blocker where?

A

Alpha1-blocker in peripheral vasculature

54
Q

Vasodilators examples?

A

sodium nitroprusside, hydralazin

55
Q

When are vasodilators used?

A

Treatment of hypertensive emergencies – IV infusion

56
Q

What is the MOA of vasodialotors

A

Acts directly on arterial and venous smooth muscle causing vasodilation and reducing SV

57
Q

What is the MOA of vasodilators

A

Acts directly on arterial and venous smooth muscle causing vasodilation and reducing SV