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Flashcards in Hypertension Deck (38):
1

Examples of ACE inhibitor

Ends in pril
Captopril
Prindopril

2

Examples of ARB

Sartan
Olmesartan
Valsartan

3

Example of Ca channel blocker

Ends in pine
Amlodipine
Felodipine
Or
Verepamil

4

Example of thiazides

Chlorathiildone
Hydrochlorothiazide
Indapimide

5

Examples of Beta blocker

End in lol
Propranolol
Metoprolol

6

Side effects of ACE inhibitor

Cough
Hyperkalemia
Renal Impairment
Angiodema

7

Side effects of ARB

Hyperkalemia
Renal impairment
Rare- cough and angiodema

8

Side effect of Ca channel blocker (dihydropiradine)

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

9

Side effects of Ca channel blocker (non-dihydropyradine)

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

10

Side effects of Thiazides

Hypokalemia
Hyponatremia
Postural hypertension
Dizziness
Hyperuricalcemia
Hyperglycemia

11

Side effects of Beta blocker

Bradycardia
Postural hypertension
Worsening HF
Bronchospasm
Cold extremities

12

Contraindications of ACE/ARB

Pregnancy
Hyperkalemia
Bilateral renal artery stenosis

13

Contraindication for thiazides

Gout
Age

14

Contraindication for Beta blocker

Asthma
Bradycardia
AV block

15

Combination for hypertension and diabetes

ACE/ARB and Ca channel blocker

16

Combination for hypertension post stroke or HF

ACE/ARB + diuretic

17

Combination post MI or HF

ACE/ARB + Beta blocker

18

Combinations to avoid

ACE + ARB —> renal impairment
Verapamil + beta blocker —> risk of heart block

19

What is more dangerous, high systolic or high diastolic

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

20

End organ damage in HT

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

21

Prehypertensive range

120-139/80-89

22

Risk management in prehypertensive range

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

23

Types of HT

1. Essential/Idiopathic HT (Primary)
2. Secondary HT

24

What determines the systolic BP (CO or TRP)

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