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411 > W10 Hypertension > Flashcards

W10 Hypertension Flashcards

1
Q

In what 2 ways does ANS control BP in the arteries and arterioles over the short term ?

A
  • by vasoconstriction or vasodilation

- by altering cardiac output

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2
Q

How is BP regulated over the long term ?

A

Modulation of solute and volume through feedback loops that involve the hypothalamus, pit gland, adrenal cortex and the kidneys

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3
Q

Where is SNS mediated vasoconstriction most powerful ?

A

Kidneys, intestine, spleen and skin

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4
Q

What is the effect of vasoconstriction on blood flow?

A

Shifts blood from pelvis and lower extremities to the right heart —> increased end diastolic volume —> increased force of contraction —> increased SV —> increased CO —> increased BP

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5
Q

What are chronotropic effects mediated by ?

A

B1- adrenergic receptors

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6
Q

Afferent sensory fibres from the carotid sinus and aortic arch baroreceptors travel via _______

A

The glossopharyngeal (CN IX) and vagus nerve to postolateral medulla and Lower pons

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7
Q

Increased carotid artery and aortic pressure response

A

Decrease sympathetic output, increased parasympathetic output —> decrease BP
Negative feedback loop = baroreceptor reflex

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8
Q

Response to increased afferent arteriole pressure

A

Inhibits release of renin from JG cells —> decreased BP

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9
Q

What is the effect of NPs on the kidney ?

A

Increase GFR —> natiuresis and diuresis
Decrease renin release —> further renal Na+ and water excretion, reduced vascular resistance
—> decrease BP

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10
Q

What does accumulation of CO2 and H+ in the Brain cause ?

A

Vasodilation

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11
Q

What does depletion of O2 and CO2 in the brain lead to ?

A

Vasoconstriction

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12
Q

What is rarefaction of a vessel ?

A

When a vessel becomes functionally useless

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13
Q

What happens to small arteries in patients with hypertension ?

A

Inward hypertrophy

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14
Q

Causes of secondary hypertension (As)

A

Accuracy
(Sleep) Apnea
(Primary) Aldosteronism (commonest cause of secondary hypertension)
- decreased K+ is sign (but labs often come back normal)

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15
Q

Causes of secondary hypertension (Bs)

A 
Bruits (renovascular hypertension)
- poor renal blood flow 
- renal artery stenosis 
Bad kidneys 
- chronic kidney disease
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16
Q

Causes of secondary hypertension (Cs)

A 
Catecholamines (pheochromcytoma) 
- tumour of adrenal medulla 
- fluctuations in BP 
Coarctation of the aorta 
- BP high in upper limbs, low in lower limbs 
Cushing’s syndrome 
- tumour of pituitary gland 
- increased aldosterone and cortisol
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17
Q

Causes of secondary hypertension (Ds)

A

Diet: DASH diet
(Prescription) Drugs
- prednisone, Motrin, Advil, naproxen
(Street) Drugs

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18
Q

Causes of secondary hypertension (Es)

A 
Erythropoietin 
Endocrine (thyroid and parathyroid) 
- compensatory mechanisms over correct —> high BP
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19
Q

Progression of fundoscopy findings with hypertension

A

Hypertensive retinopathy: AV nicking
MOderate hypertension: hard exudates, hemorhages
Pappiledema: blurring of the optic disc

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20
Q

Why is auto regulation important to consider when treating hypertension ?

A

Have to lower BP over weeks to months so that blood flow can adjust, otherwise the patient may become hypotensive

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21
Q

Hypertensive emergencies

A 
Hypertensive encephalopathy 
Aortic dissection 
MI 
Left heart failure 
Intracranial hemorrhage 
Post-transplantation (of kidney) 
Post op
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22
Q

Complications of hypertension

A 
Stroke 
Coronary artery disease 
Peripheral vascular disease 
Kidney disease 
Sudden death
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23
Q

Five key trends in healthcare

A
  1. Innovation in consumer technology market
  2. Advancement in electronic health records
  3. Shortage in health professional workforce
  4. Health system reorganization and financing
  5. Growth of consumerism of health care
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24
Q

Lifestyle factors for uncomplicated hypertension

A 
Aging
Obesity and insulin resistance 
High salt diet 
Low potassium diet 
Sedentariness
Stress
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25
Q

How does aging contribute to hypertension ?

A

Elastin replaced by collagen —> arterial stiffness —> widened pulse pressure —> isolated systolic hypertension
After ~ mid 50s

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26
Q

Why does arterial stiffness cause increased pulse pressure ?

A

Reflected systolic wave rebounds quicker and then contributes to systolic pressure instead of diastolic pressure like it should

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27
Q

What is the increased SBP with every 10% increase in weight ?

A

6.5mmHg

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28
Q

What % of hypertension fo weight gain and obesity account for ?

A

~25%

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29
Q

Mechanism of action for hypertension in obese and insulin resistant patients ?

A

Increase plasma volume and CO —> RAAS activation —> shifting of natriuresis to higher BP threshold in obesity —> SNS activation

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30
Q

What is Hypertension Canada recommended daily sodium limit ?

A

2g/day ~ 1 tsp salt ~ 5 g salt

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31
Q

What populations tend to be more sensitive to salt intake ?

A

Older
African Americans
Obese
Patients with metabolic syndrome or chronic kidney disease

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32
Q

What is the relation between potassium intake and BP

A

Inversely related

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33
Q

Why do diets rich in potassium help lower BP ?

A

Sodium excretion is diminished bu hypokalemia through increases in sodium reabsorption in proximal tubule and/or loop of Henle —> increased BP

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34
Q

What is work hypertension called ?

A

Masked hypertension: going to doctors office may be least stressful part of your day

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35
Q

What effect can >2 drinks per day have on hypertension

A

1.5 - 2 times more likely to develop hypertension than non-drinkers

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36
Q

How does excess alcohol consumption lead to hypertension ?

A

Stimulation of SNS, RAAS, raised cortisol levels, inhibition of nitric oxide

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37
Q

What are some other factors that can raise BP ?

A 
Stimulants: cocaine 
Decongestants: pseudoephedrine 
Prednisone 
Oral contraceptives 
Some anti-depressants 
NSAIDs
Supplements: St. John’s Wort, Ephedra, Ginko, Ginseng
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38
Q

Health behaviour changes to control hypertension:

A

Physical exercise (30-60 min moderate intensity, 4-7 days/week)
Weight reduction (BMI 18.5-24.9 optimal, waist circumfrance <102cm men, <88cm women)
Limit alcohol consumption: (<2/day, men <14/week, women <9/week)
DASH diet
Sodium reduction
Stress management via CBT and relaxation techniques

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39
Q

How does exercise help in management or prevention of hypertension ?

A 
Increase endothelial production of NO synthase
Decrease aortic stiffness 
Increase whole body insulin sensitivity 
Reduce circulation noradrenaline 
Decrease vascular resistance
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40
Q

What is the DASH diet ?

A 
High in calcium, potassium and magnesium 
Fruit and veggies 
Low intake of red meat 
Low fat dairy products 
Plant protein 
High fibre
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41
Q

What lifestyle change tends to have the greatest impact on BP ?

A

DASH diet
Normotensive: -3.6/-1.8
Hypertensive: -11.4/-5.5

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42
Q

What is criteria for hypertension in adults without diabetes ?

A

> 140/90 mm Hg

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43
Q

What is threshold for hypertension in adults with diabetes ?

A

> 130/80 mmHg

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44
Q

What is hypertension criteria for children and adolescents ?

A

S/DBP > 95th percentile for sex, age, BMI

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45
Q

When to suspect white coat hypertension

A

No TOD
Report lower out of office readings
Lightheaded or dizzy when started on antihypertensive therapy

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46
Q

What is normal BP for home/24 hour ABPM ?

A

24 hour average: <130/80
Daytime average: <135/85
Night time average: < 120/80

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47
Q

When to suspect masked hypertension ?

A

TOD present or LVH but normal office BP readings

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48
Q

Which type of hypertension puts a patient most at risk for CV events ?

A

Masked

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49
Q

When might someone be considered to be having a hypertensive emergency ?

A

BP >180/>120

Depends on presence of progressive/acute TOD

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50
Q

What constitutes hypertensive urgency ?

A

Severely elevated BP without TOD the

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51
Q

Management of hypertensive urgency

A

Done in ER
Lower BP by 25% or <160/<100 over hours or over the day
Use normal BP meds or short acting meds (oral captopril, oral lasix or oral clonidine)

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52
Q

Common causes of hypertensive emergencies

A 
Acute pulmonary edema 
Stroke
MI 
Acute aortic dissection 
Acute renal failure 
Hypertensive encephalopathy
53
Q

What TOD can be seen with hypertension ?

A 
Acute worsening of kidney function 
Cardiac ischemia
 Brain ischemia 
Acute CHF 
Acute aortic dissection 
Papilledema 
Stroke 
Hypertensive heart disease 
Hypertensive retinopathy
54
Q

Investigations for acute worsening of kidney function

A

GFR

55
Q

Investigations for cardiac ischemia

A

Signs and symptoms
ECG
Cardiac enzymes

56
Q

Investigations for brain ischemia

A

Signs and symptoms (encephalopathy, acute stroke)

CT or MRI

57
Q

Investigations for acute congestive heart failure

A

Signs and symptoms
CXR
BNP

58
Q

Investigations for acute aortic dissection

A

Signs and symptoms

CT chest or echo

59
Q

What % of strokes are attributable to hypertension ?

A

35%

60
Q

What % of patients with heart failure have hypertension ?

A

80-90%

61
Q

What does Hypertensive heart disease encompass ?

A

LVH
Heart failure
MI

62
Q

What can be seen on fundoscopy in patients with mild hypertensive retinopathy ?

A

A-V nicking

63
Q

What can be seen on fundoscopy in patients with moderate hypertensive retinopathy

A

Hard exudates
Flame shaped haemorrhages
Dot and blot hemorrhages

64
Q

What can be seen on fundoscopy in patients with papilledema ?

A

Blurring of the optic disc

65
Q

When is something considered a hypertensive emergency ?

A

Severely elevated BP with TOD

66
Q

Treatment of hypertensive emergency

A

Aim to lower BP by 10-20% in first hour than further 15% over next 24 hours
Acute stroke: Lower to less than 185/110 mmHg if getting tPA otherwise only Lower if BP> 220/120
Acute dissection: rapidly decrease SBP to <120 mmHg in 20 minutes

67
Q

What are standard investigations for patients diagnosed with hypertension ?

A

TOD: history and physical, ECG, GFR, urinalysis
Cardiac risk factors: history and physical, fasting lipid profile, ECG, weight, waist circumference, A1C or fasting blood glucose, UACR (if diabetic)
Secondary screen: history and physical, GFR, electrolytes, calcium, TSH

68
Q

Who should be screened for secondary hypertension ?

A

Young patients
Patients with resistant hypertension
Patients that have clinical features of secondary hypertension

69
Q

Cause of secondary hypertension

A 
Obstructive sleep apnea 
Chronic kidney disease 
Renal artery stenosis/ Reno vascular disease 
Fibro muscular dysplasia (FMD) 
Primary hyperaldosteronism 
Cushing’s syndrome 
Pheochromocytoma 
Thyroid disorders
Hyper parathyroidism 
Acromegaly 
Coarctation of aorta
70
Q

How can Obstructive sleep apnea lead to hypertension ?

A

Sympathetic activity during periods of hypoxia —> excess aldosterone —> SNS activation

71
Q

Screening tests for atherosclerotic RAS

A

CT angiogram
MR angiogram
Renal captopril scan

72
Q

Screen tests for FMD

A

CT angiogram

Digital subtraction angiography

73
Q

Treatment of hyperaldosteronism

A

Idiopathic: mineralcorticoid receptor agonist

Secondary to Adenoma or unilateral micro adenoma: may be cured with surgical adrenalectomy

74
Q

How does the ratio of aldosterone to renin present in patients with hyperaldosteronism ?

A

High

75
Q

Who should be screened for primary hyperaldosteronism ?

A

Resistant hypertension
Hypokalemia (although ~50% have Normal K)
Diuretic induced hypokalemia

76
Q

Screening tests for hyperaldosteronism

A

Upright plasma aldosterone concentration and renin activity

77
Q

What is Cushing’s Syndrome ?

A

Hypercortisolism usually from an adrenal tumour

78
Q

Screening test for Cushing’s syndrome

A

1 mg overnight dexamethasone suppression test or 24 hour urine cortisol or late night salivary cortisol test (2/3 abnormal)

79
Q

Clinical manifestations of Cushing’s syndrome

A 
Proximal muscle weakness
Facial plethora 
Fat deposition in scapular area or face
Central obesity 
Thing fragile skin with easy bruising 
Colourful stretch marks
Hirsutism, loss of libido
80
Q

Signs and symptoms of pheochromocytoma

A 
Episodes of: 
Headaches 
Palpitations 
Diaphoresis 
Panic attacks
Pallor
Hypertension 
Or 
These symptoms occurring with surgery, hard physical activity or injury
81
Q

Screening for pheochromocytoma

A

24 hour urine fractioned metanephrines and catecholamines

82
Q

Sign of hyperparathyroidism

A

Hypercalcemia

83
Q

What are the classes of anti-hypertensive drugs ?

A 
Diuretic agents 
Inhibitors of RAAS 
Calcium channel blockers
Adrenergic receptor antagonists 
Direct vasodilators
Central acting agents
84
Q

Different types of inhibitors of RAAS

A

ACE inhibitors
Angiotensin receptor blockers (ARBs)
Renin inhibitors
Aldosterone receptor antagonists

85
Q

What suffix is used in ACE inhibitors ?

A

Pril (ramipril)

86
Q

What is the mechanism of action of ACE inhibitors ?

A

Block conversion of Ang I to Ang II in the RAAS and block break down of bradykinin into its inactive form
—> inhibition of vasoconstriction
- inhibition of aldosterone secretion
- inhibition of NaCl reabsorption
- increased vasodilation (via Bradykinin)
—> decreased SVR and decreased preload

87
Q

Adverse effects of ACE inhibitors

A 
Cough (attributed to Bradykinin) 
Hyperkalemia (due to reduced aldosterone ) 
Renal dysfunction 
Hypotension 
Angioedema (rare)
88
Q

When are ACE inhibitors contraindicated ?

A

Pregnancy

Renal artery stenosis

89
Q

What suffix is used for ARBs ?

A

Sartan

90
Q

Mechanism of action of ARBs

A 
Antagonists that block the actions of Ang II 
Inhibition of vasoconstriction 
Inhibition of aldosterone secretion 
Inhibition of NaCl reabsorption 
—> decreased SVR and preload
91
Q

Adverse effects of ARBs

A

Dizziness and hypotension
Hyperkalemia (due to reduced aldosterone)
Renal dysfunction

92
Q

When are ARBs contraindicated ?

A

In pregnancy

93
Q

Mechanism of action of renin inhibitors

A 
Block conversion of angiotensinogen to Ang I 
- inhibition of vasoconstriction 
- inhibition of aldosterone secretion 
- inhibition of NaCl reabsorption 
—> decreased SVR and preload
94
Q

Adverse effects of renin inhibitors

A

Diarrhea

95
Q

Where are renin inhibitors contraindicated ?

A

In pregnancy

96
Q

What is currently the only drug in the renin inhibitors class?

A

Aliskiren

97
Q

Actions of calcium channel blockers

A

Decrease vascular smooth muscle contraction —> decrease SVR
Decrease cardiac conduction and contractility —> decrease HR, CO
Blocks Ca-signal to adrenal cortical cells to release aldosterone

98
Q

Different classes of calcium channel blockers

A

Dihydropyridines

Non-dihydropiridines

99
Q

Mechanism of action of dihydropyridines

A

Act primarily on vasculature —> vasodilation
Week effect on cardiac Ca-channels
—> decrease SVR and contractility

100
Q

Suffix of dihydropyridines

A

Dipine (amlodipine)

101
Q

What are the two subclasses of non-dihydropyridines ?

A

Benzothiazepines

Phenylalkylamines

102
Q

Mechanism of action of non-hydropyridines

A

Affect cardiac and vascular Ca-channels

—> decrease HR, contractility and SVR

103
Q

Examples of non-hydropyridines

A

Az: diltiazem
Ami: verapamil

104
Q

Adverse effects of calcium channel blockers

A

Dizziness and headache
Flushing, peripheral edema, reflex tachycardia
Bradycardia, hypotension

105
Q

Contraindications of dihydropyridine calcium channel blockers

A

Conditions worsened by tachycardia

- severe aortic stenosis

106
Q

Contraindications of non-hydropyridine calcium channel blockers

A 
Conduction disorders (Wolff-Parkinson’s-white syndrome, AV block)
Acute CHF

Maybe pregnancy

107
Q

Effects of activation of B1 receptors

A

Increase contraction, HR, renin secretion, BP

108
Q

Effects of B2 receptor activation

A

Bronchodilation, vasodilation of skeletal muscle arterioles (smooth muscle relaxation)

109
Q

Effects of a2 receptor activation

A

Vasoconstriction and venoconstriction of non-skeletal muscle vessels (smooth muscle contraction)

110
Q

Suffix off beta blockers

A

Lol

111
Q

Mechanism of action of beta blockers

A

Reduce sympathetic activity —>

  • decreased HR, contractility, renin secretion —>
  • decreased HR and CO
112
Q

What are the different classes of beta blockers ?

A

Cardioselective B-blockers
Non-cardioselective B-blockers
Mixed a and B-blockers
Partial agonists

113
Q

Location of action of cardioselective B blockers and some examples

A

Blocks B1 receptors

Metoprolol, atenolol, bisoprolol

114
Q

Site of action of non-cardioselective B-blockers and examples

A

Blocks all B receptors

Propranolol (B1, B2)

115
Q

Examples of mixed a and B blockers

A

Carvedilol, labetalol (a1, B1, B2)

116
Q

Example of a partial agonist beta blocker

A

Acebutolol (partial B1 agonist)

117
Q

Adverse effects of Beta blockers

A

Fatigue (due to increased CO)
Bradycardia
Broncho constriction (B2 blockade)
Rebound hypertension (if abruptly discontinued)

118
Q

Contraindications for Beta blockers

A

Asthma
Bradycardia or 2nd or 3rd degree heart block
Acute CHF

119
Q

Suffix of alpha 1 blockers

A

Zosin

120
Q

Mechanism of action of alpha 1 blockers

A

Decrease vasoconstriction and decrease venoconstriction —>

Decreased SVR

121
Q

Adverse effect of alpha 1 blockers

A

Orthostatic hypotension

122
Q

Action of direct vasodilators

A

Arteriolar vasodilation
Uncertain mechanism
—> decrease SVR

123
Q

Adverse effects of direct vasodilators

A

Reflex tachycardia
Flushing
Hypotension
Immunological lupus like reaction

124
Q

Central acting a2 agonists suffix

A

Nidine

125
Q

Action of central acting agents

A

Inhibit presynaptic release of norepinephrine —>

Decrease HR, SV and SVR

126
Q

Adverse effects

A

Sedation (central inhibition of neurotransmitter release
Dry mouth
Orthostatic hypotension
Rebound hypotension

127
Q

What risks increase if hypertension goes untreated ?

A 
Morbidity 
Coronary artery disease
Heart failure 
Stroke 
Peripheral vascular resistance
Kidney injury 
Vision loss
128
Q

What drug shows best evidence as first line treatment of hypertension ?

A

Thiazides

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