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Flashcards in Hypertension Deck (38)
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1
Q

Examples of ACE inhibitor

A

Ends in pril
Captopril
Prindopril

2
Q

Examples of ARB

A

Sartan
Olmesartan
Valsartan

3
Q

Example of Ca channel blocker

A
Ends in pine
Amlodipine
Felodipine
Or
Verepamil
4
Q

Example of thiazides

A

Chlorathiildone
Hydrochlorothiazide
Indapimide

5
Q

Examples of Beta blocker

A

End in lol
Propranolol
Metoprolol

6
Q

Side effects of ACE inhibitor

A

Cough
Hyperkalemia
Renal Impairment
Angiodema

7
Q

Side effects of ARB

A

Hyperkalemia
Renal impairment
Rare- cough and angiodema

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
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

10
Q

Side effects of Thiazides

A
Hypokalemia
Hyponatremia
Postural hypertension
Dizziness
Hyperuricalcemia 
Hyperglycemia
11
Q

Side effects of Beta blocker

A
Bradycardia
Postural hypertension 
Worsening HF
Bronchospasm
Cold extremities
12
Q

Contraindications of ACE/ARB

A

Pregnancy
Hyperkalemia
Bilateral renal artery stenosis

13
Q

Contraindication for thiazides

A

Gout

Age

14
Q

Contraindication for Beta blocker

A

Asthma
Bradycardia
AV block

15
Q

Combination for hypertension and diabetes

A

ACE/ARB and Ca channel blocker

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
Q

BP=

A

CO x TRP

26
Q

Systolic BP relation to heart

A

ventricular squeeze in presence of open valves = systolic BP, because no resistance, the BP can be read in arteries

27
Q

Diastolic BP relation to the heart

A

no relationship, because valve closed. related to TRP and the amount of blood left

28
Q

Changes in systolic indicate

A

changes in CO

29
Q

Changes in diastolic indicate

A

changes in TRP or vessel dilation/contriction

30
Q

What influences CO

A
  1. Blood volume

2. Cardiac factors

31
Q

What influences BV

A

Na intake
mineralocorticoid like aldosterone
atriopeptides ANP = vasodilation

32
Q

What cardiac factors influence CO

A

Heart rate
contractility
anxiety (increases symp = increase HR and contractility)

33
Q

What influences TRP

A

Humoral factors - dilators

Neural factors

34
Q

What causes the release of Renin

A

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
Q

Where is Renin released from

A

Juxtaglomerulo apparatus, which is modified afferent from arterioles and macular densa from DCT

36
Q

What happens to Renin

A

converted to angiotensin 1 by angiotensinogen (from the liver)

37
Q

What happens to Angiotensin I

A

converted to angiotensin 2 by ACE (angiotensin converting enzyme) from the lungs

38
Q

What are the effects of Angiotensin II

A

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