Hypertension & Hypotension Flashcards

1
Q

Name the 5 main types of hypertensives

A
Angiotensin converting enzyme inhibitor (ACEi)
Angiotensin II Receptor Blocker (ARB)
Beta adrenoreceptor blockers (B Blocker)
Ca channel blocker (CCB)
Thiazides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What’s the treatment for hypertension in patients <55?

A
  1. ACEi/ARB/B Blocker
  2. Add CCB/thiazides
  3. CCB + thiazide
  4. High dose thiazide/spironolactone or alpha Blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What’s the treatment for patients >55 or of afro-Caribbean descent?

A
  1. CCB/ Thiazides

2. ACE/ARB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the effects of ACEi

A

Vasodilation
Reduce afterload
Reduced BP
Reduces aldosterone (increased Na+, H20 secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Side effects of ACEi

A

Persistent dry cough
Hypotension
Hyperkalaemia
NSAIDs used in conjunction with ACEi increase RF risk
Stop medication if patient is in renal failure, has an AKI or renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examples of ACEi

A

Ramipril. Max 10mg, initial 2.5mg OD

Lisinopril: Max 80mg, initial 2.5

Perindopril:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanism of action for B blockers

A

Blocks B1 adrenergic receptors:
In SAN has negative chronotrophic effect

In myocardium has negative ionotrophic effects (decreases force of contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Side effects of B Blocker

A
Bronchospasm
Fatigue
Cold extremities
Headaches
GI disturbance 
Sleep disturbance

Contraindication: Asthmatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of B Blockers

A

Atenolol: 25-50mg daily
Propanolol: 40mg OD to TD
Metoprolol: IVI max 15mg oral 50-200 mg
Bisoprolol: 10mg daily max. Long term

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of ARB

A

Blocks binding of angiotensin II to angiotensin I receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of ARB

A

Losartan (Cozaar)
Candesartan (Atacand)
Valsartan (Diovan)
Olmesartan (Olmetec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of Calcium channel blockers

A

Dihydropyridines (Nifedipine and Amlodipine)

Nondihydropyridines (Verapamil and diltiazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CCBs mechanisms of action

A

Prevent calcium entering the heart and blood vessels walls. Thereby preventing contraction and relaxing the heart and blood vessels to relieve BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Uses of CCB

A

HTN, Angina, Raynaud’s, AF (nondihydropyridines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Isolated systolic HTN

A

Elevated systolic reading (>160 mmHg, 140mmHg-159 bordeline,) with a normal diastolic reading (<90mmHg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common causes of secondary hypertension

A

Vascular
Renal artery stenosis
Coarctation of aorta
Pre-eclampsia

Renal
CKD
Glomerulonephritis
Nephrotic syndrome
Obstructive uropathy
Polycystic kidney disease
Endocrine
Phaeochromocytoma
Hyperaldosteronism
Cushings
Hyper/Hypothyroidism
Hyperparathyroidism
17
Q

Orthostatic/postural hypotension

A

Systolic BP drop off at least 20mmHg or diastolic BP drop of at least 10mmHg within 3 minutes of standing

18
Q

Pathophysiology of orthostatic hypotension

A

When an otherwise healthy person stands, about 700 mL of blood pools in the leg veins and the lower abdominal veins. Venous return to the heart decreases, resulting in a transient decline in cardiac output. This leads to baroreflex-mediated sympathetic activation with an increase in cardiac stroke volume and peripheral vasoconstriction, as well as parasympathetic withdrawal with an increase in heart rate. These rapid haemodynamic changes prevent blood pressure from falling.

Failure of these mechanisms causes orthostatic hypotension.

19
Q

Typical presentation of orthostatic patient

A

Light headed, dizzy, weak, faintness, dimming of vision usually doesn’t occur supine.

Parkinsonian features

Cerebellar ataxia from multisystem atrophy (MSA or Shy-Drager syndrome). Ataxia of gait and speech is the most common for MSA

Resting tachycardia-sign of diabetic loss of parasympathetic

Abnormal GI, erectile dysfunction-Autonomic neuropathy

20
Q

What may elicit orthostatic hypotension

A

Early in the morning (because of relative volume depletion after overnight fast and pressure diuresis)

In hot environments (because of cutaneous vasodilation)

After meals (because of splanchnic blood pooling)

After standing motionless (because of decreased venous return caused by loss of muscle pump action)

After exercise (because of metabolic vasodilation).

21
Q

Common causes of orthostatic hypotension

A
In elderly:
Anti-hypertensives
Alpha-blockers
Diuretics
TCA
Prolonged bed rest resulting in physical deconditioning

Diabetes and amyloidosis cause autonomic neuropathy

Parkinson’s disease with lewy body dementia
Multiple system atrophy (MSA) commonly have cerebellar ataxia resulting in ataxia of speech and gait

22
Q

Management of orthostatic hypotension

A

Lifestyle
Fludrocortisone and NaCl (volume expansion)
Midodrine (presser)
Droxidopa (noradrenaline)

23
Q

Causes of shock

A

Cardiogenic: after myocardial infarction, due to cardiomyopathy, valvular abnormalities, or arrhythmias. (pump dysfunction)

Hypovolemic: haemorrhages, burns, GI loss, heat stroke

Distributive (failure of vasoregulation)

Obstructive: PE, cardiac tamponade, tension pneumothorax