Hypertension Flashcards

1
Q

Examples of ACE inhibitor

A

Ends in pril
Captopril
Prindopril

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2
Q

Examples of ARB

A

Sartan
Olmesartan
Valsartan

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3
Q

Example of Ca channel blocker

A
Ends in pine
Amlodipine
Felodipine
Or
Verepamil
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4
Q

Example of thiazides

A

Chlorathiildone
Hydrochlorothiazide
Indapimide

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5
Q

Examples of Beta blocker

A

End in lol
Propranolol
Metoprolol

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6
Q

Side effects of ACE inhibitor

A

Cough
Hyperkalemia
Renal Impairment
Angiodema

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7
Q

Side effects of ARB

A

Hyperkalemia
Renal impairment
Rare- cough and angiodema

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8
Q

Side effect of Ca channel blocker (dihydropiradine)

A
Peripheral vasodilation —> odema (don’t treat with diuretic)
Postural hypertension 
Tachycardia
Chest pain 
Palpitation 
Gingival hyperplasia
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9
Q

Side effects of Ca channel blocker (non-dihydropyradine)

A

Bradycardia - because reduces HR and cardiac contractility
Constipation (severe with verapamil)
AV block
Heart fail

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10
Q

Side effects of Thiazides

A
Hypokalemia
Hyponatremia
Postural hypertension
Dizziness
Hyperuricalcemia 
Hyperglycemia
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11
Q

Side effects of Beta blocker

A
Bradycardia
Postural hypertension 
Worsening HF
Bronchospasm
Cold extremities
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12
Q

Contraindications of ACE/ARB

A

Pregnancy
Hyperkalemia
Bilateral renal artery stenosis

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13
Q

Contraindication for thiazides

A

Gout

Age

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14
Q

Contraindication for Beta blocker

A

Asthma
Bradycardia
AV block

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15
Q

Combination for hypertension and diabetes

A

ACE/ARB and Ca channel blocker

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16
Q

Combination for hypertension post stroke or HF

A

ACE/ARB + diuretic

17
Q

Combination post MI or HF

A

ACE/ARB + Beta blocker

18
Q

Combinations to avoid

A

ACE + ARB —> renal impairment

Verapamil + beta blocker —> risk of heart block

19
Q

What is more dangerous, high systolic or high diastolic

A

High systolic - indicates left ventricular hypertrophy esp if patient >50 years old

20
Q

End organ damage in HT

A
Heart - ischemic heart disease, congestive heart failure
CNS - TIA, stroke
Kidney- hypertensive nephropathy
Eyes - hypertensive retinopathy
Vessels - athrosclorosis
21
Q

Prehypertensive range

A

120-139/80-89

22
Q

Risk management in prehypertensive range

A
Change in lifestyle
Physical activity increase
smoking avoidance
hyperlipidemia mangement
stress mangement
weight mangement
salt reduction 
more fruits and veggies
relax
23
Q

Types of HT

A
  1. Essential/Idiopathic HT (Primary)

2. Secondary HT

24
Q

What determines the systolic BP (CO or TRP)

A

cardiac output

25
BP=
CO x TRP
26
Systolic BP relation to heart
ventricular squeeze in presence of open valves = systolic BP, because no resistance, the BP can be read in arteries
27
Diastolic BP relation to the heart
no relationship, because valve closed. related to TRP and the amount of blood left
28
Changes in systolic indicate
changes in CO
29
Changes in diastolic indicate
changes in TRP or vessel dilation/contriction
30
What influences CO
1. Blood volume | 2. Cardiac factors
31
What influences BV
Na intake mineralocorticoid like aldosterone atriopeptides ANP = vasodilation
32
What cardiac factors influence CO
Heart rate contractility anxiety (increases symp = increase HR and contractility)
33
What influences TRP
Humoral factors - dilators | Neural factors
34
What causes the release of Renin
Reduced renal perfusion can be due to reduced BP or due to stenosis Overall - reduced Na in macular densa in DCT (because slowly flowing waste = increases Na retention)
35
Where is Renin released from
Juxtaglomerulo apparatus, which is modified afferent from arterioles and macular densa from DCT
36
What happens to Renin
converted to angiotensin 1 by angiotensinogen (from the liver)
37
What happens to Angiotensin I
converted to angiotensin 2 by ACE (angiotensin converting enzyme) from the lungs
38
What are the effects of Angiotensin II
Thirst - hypothalamus Vasoconstrictor - Arterial = increase TRP, venous increases CO Aldosterone release - from zonaglomulosa --> acts on principle cell to increase H2O and Na rentention thus increasing CO