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Med 1 UBC Fall 2019 > Week 9 Hypertension > Flashcards

Week 9 Hypertension Flashcards

1
Q

Different actions of angiotensin II at low versus high levels

A

At low levels, it induces vasoconstriction only in the efferent arteriole –> increased intraglomerular pressure –> increased glomerular filtration rate. At high levels, induces vasoconstriction in both afferent and efferent arteriole –> decrease renal blood flow –> decreased GFR

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2
Q

Summarize the RAAS

A

Low blood pressure is recognized by juxtaglomerular cells via three paths:

1) directly - they sense low blood pressure in the afferent arteriole
2) Sympathetic input via baroreceptors in the carotid sinus and aortic arch
3) Stimulation from macula densa cells in DCT, which sense low BP in the form of low levels of Na flowing past them.

JG cells secrete renin, which enters circulation and cleaves angiotensinogen to angiotensin I, which is then cleaved by ACE (mostly in the lung endothelium) to angiotensin II.

Angiotensin II exerts many effects:

1) at low levels - vasoconstriction of efferent arteriole to increase intraglomerular pressure, thereby increasing GFR 2) at high levels - vasoconstriction of afferent and efferent arterioles, thereby reducing renal blood flow and GFR
3) increased Na reabsorption in PCT
4) stimulation of hypothalamus, resulting in thirst and release of ADH, which promote insertion of aquaporins in the CD
5) stimulation of adrenal cortex to produce aldosterone, which promote upregulation of Na/K ATPase in the DCT and CD, to increase Na reabsorption.

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3
Q

Effects of angiotensin II

A

1) at low levels - vasoconstriction of efferent arteriole to increase intraglomerular pressure, thereby increasing GFR
2) at high levels - vasoconstriction of afferent and efferent arterioles, thereby reducing renal blood flow and GFR
3) increased Na reabsorption in PCT
4) stimulation of hypothalamus, resulting in thirst and release of ADH, which promote insertion of aquaporins in the CD
5) stimulation of adrenal cortex to produce aldosterone, which promote upregulation of Na/K ATPase in the DCT and CD, to increase Na reabsorption.

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4
Q

Preganglionic neurons of the parasympathetic nervous system related to the cardiovascular system are located in the…

A

dorsal motor nucleus of the vagus nerve (Xth cranial nerve) and the nucleus ambiguus. Their axons terminate on neurons within parasympathetic ganglia in and around the heart and great vessels.

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5
Q

Describe how the baroreceptor reflex would act in a case of extreme blood loss

A
  • baroreceptors in carotid sinus and aortic arch less stretched and send less frequent firing to medulla via glossopharyngeal and vagus nerves. - vasomotor centre increases sympathetic output: increase vasconstriction/venoconstriction, therefore increasing PVR and preload in heart.
  • cardiac control centre increases sympathetic output (cardiac accelerator) and decreases parasympathetic output (cardiac decelerator): increased HR and contractility
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6
Q

where are cardiopulmonary baroreceptors located?

A

in the RA, RV, pulmonary arteries and pulmonary veins. These are all relatively low-pressure systems, so increased stretch is usually just caused by increased blood volume.

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7
Q

Physiologic effects of ANP and BNP (4)

A
  1. Venodilation, resulting in decreased venous return and decreased cardiac output
  2. Vasodilation, resulting in decreased peripheral vascular resistance and therefore decreased BP
  3. Increased GFR, resulting in diuresis and natriuresis, bringing down BP
  4. Decreased renin release, which leads to decrease in Angiotensin II and Aldosterone as well.
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8
Q

Local regulation of blood flow

A
  • acute local regulation mediated by tissue factors
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9
Q

tissue factors that cause vasodilation

A
  • CO2, lactic acid, H+, K+, adenosine, ADP, histamine, bradykinin, prostacyclin, NO (or eNO)
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10
Q

tissue factors that cause vasodilation

A

decrease in O2, 5-HT (aka serotonin) and endothelin

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11
Q

Impact of chronic high BP on vasculature (2)

A
  • VASCULAR REMODELING: Hypertrophy of muscularis layer, decreasing the size of the lumen and the ability of blood to get to organs.
  • ATHEROSCLEROSIS: High BP, smoking, lipids, and genetics all contribute. Plaques form and activate a coagulation cascade. Clots form and can detach, leading to stroke or infarction elsewhere in the body.
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12
Q

Primary Hypertension

A

= idiopathic HTN - complicated interaction of many factors, namely genetics and exposures. - Lifestyle modification can greatly reduce cardiovascular risk (reduced salt, smoking, fats) - May be due to overactivity of sympathetic NS.

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13
Q

Autoregulation of blood pressure

A

We have mechanisms to raise and lower blood pressure, but it is generally kept at a relatively constant level.

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14
Q

Causes of secondary hypertension

A

A - Accuracy of technique

A - Sleep Apnea

A - Primary hyperAldosteronism (most common)

B - Bad kidneys/Bruits (renovascular HTN, stimulating RAAS)

C - Catecholamines - Pheochromocytoma (rare tumor of adrenal medulla)

C - Coarctation of the aorta

C - Cushing’s syndrome (tumor of pituitary gland or longterm corticosteroid use)

D - Diet (Na and fats)

D - Drugs (Prednison, NSAIDs, BCP, meth, cocaine, alcohol)

E - EPO

E - Endocrine (hyperthyroidism causes high BP and hypothyroidism causes compensatory mechanisms that elevate BP)

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15
Q

The importance of fundoscopy in assessing BP

A
  • Blood vessels of the retina are the only blood vessels that can be visualized directly without opening a person up
  • When people have high BP, vessels undergo vascular remodelling, possibly causing arterial venous nicking (looks like sausage links). When nicking occurs, HTN has been present for weeks or months
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16
Q

Hypertensive heart disease

A
  • HTN can cause left ventricular hypertrophy (concentric) - Can be visualized in CXR - Risk factor for sudden cardiac death
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17
Q

Implications of autoregulation of BP in HTN

A

People with chronic HTN have shifted autoregulation. If you try and normalize their BP too quickly, you may kill them because at low pressures, their body is set to reduce flow a lot more than a normal person.

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18
Q

Summarize the pathophysiologic mechanisms of hypertension and the various target end-organ effects

A

Hypertension affects target organs by stimulating vascular remodeling and accelerating atherosclerosis, both of which lead to increased peripheral vascular resistance and reduced flow to the tissues.

Leads to coronary artery disease (-> myocardial infarction), stroke, and/or peripheral vascular disease.

Can also lead to chronic kidney disease.

 eyes (retinopathy)

 brain (cerebrovascular disease)

 heart (hypertensive heart and coronary artery disease)

 kidneys (hypertensive nephrosclerosis)

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19
Q

hypertensive emergencies - define - treatment

A

= Severely elevated BP with target organ damage. Target to lower BP by 10-20% in first hour and another 15% over the next 24 hr. Exceptions are stroke and dissection - need to lower more rapidly.

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20
Q

Epidemiology of hypertension

A
  • about 1 in 4 canadians aged 20-79 have HTN
  • higher in men
  • After age 60, more than 50% will have HTN
  • Prevalence of HTN worldwide is increasing
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21
Q

Diagnosis of HTN

A

When systolic BP>160 or diastolic BP>100 mmHg averaged across three separate visits at lead one week apart. The target values for treatment are lowered in patient with pre-existing diabetes or chronic renal failure. HTN can be diagnosed at one visit if BP>180/110 mmHg

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22
Q

How much variation in blood pressure is thought to be due to genetics?

A

30% (based on twin studies); HTN is polygenic

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23
Q

Lifestyle factors that contribute to HTN (5)

A
  • Aging
  • Obesity and insulin resistance
  • High salt and low potassium diet
  • Low physical activity
  • Stress
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24
Q

How does aging relate to HTN

A

Elastin in intima-medial wall of arteries is replaced by collagen, leading to arterial stiffness, which manifests in a widened pulse pressure (difference bt systolic and diastolic pressure).

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25
Q

What is the most common cause of adolescent hypertension?

A

obesity and insulin resistance

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26
Q

How do obesity and insulin resistance contribute to HTN?

A

Though activation of RAAS and sympathetic nervous system

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27
Q

How does sedentariness contribute to HTN? (3)

A
  • taking breaks from sedentariness positively associated with decreased size, BMI, and plasma glucose.
  • increased screen time correlated with increased levels of insulin
  • Chronic unbroken periods of muscular unloading causes suppression of skeletal muscle lipoprotein lipase activity (necessary for HDL production) and reduced glucose uptake
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28
Q

How does diet contribute to HTN?

  • Variation in this association.
A
  • High Na and low K related to development of HTN
  • Sensitivity to salt intake varies between people and higher in older adults, african american individuals, obese individuals, and patients with metabolic syndrome or chronic kidney disease
  • Impaired renal excretion of Na can lead to volume retention –> HTN
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29
Q

Metabolic syndrome

A
  • HTN - Dyslipidemia - Diabetes - Obesity
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30
Q

Role of K in HTN (2)

A
  • Increased K intake can decrease blood pressure significantly (2-3.3 mmHg on either end) and reduce risk of stroke
  • Na excretion is diminished in states of hypokalemia, so increasing K may increase excretion of Na
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31
Q

Masked hypertension - Definition

A

Office BP readings are in normal range, but out of office readings are higher. May occur in 10-30% of pt who appear to be ‘normotensive’ in office; Often work hypertension; People who have good BP at the doctor’s office but high BP at work because work is so stressful.

32
Q

Association bt alcohol intake and HTN (how?) (2)

A
  • Dose-related increase in HTN risk, especially with >5 drinks per day
  • Effect achieved by stimulation of sympathetic NS, RAAS, raised cortisol levels, and inhibition of NO
33
Q

Drugs that can cause hypertension

A
  • cocaine, amphetamines
  • decongestants: pseudophedrine
  • OCP (birth control)
  • Some anti-depressants: TCA, SSRI - NSAIDs -

Supplements: St. John’s Wort, Ephedra, Ginko, Ginseng, ginger, black liquorice

34
Q

When to suggest non-pharmacological/health behaviour change interventions to patients

A

Everyone w HTN and those at risk of HTN

35
Q

What lifestyle modifications may have a large impact on HTN? (6)

A
  • Exercise 30-60 mins/day, 4-7 days per week
  • Weight reduction to <25 kg/m^2 and waist circumference <102 cm (men) or < 88cm (women)
  • Less alcohol
  • Smoking cessation
  • Diet (DASH, less Na, more K)
  • Stress management (CBT and stress management)
36
Q

How can exercise reduce HTN and related end-organ damage? (2)

A

Exercise training increases endothelial production of NO synthase, decreases aortic stiffness, and increase whole-body insulin sensitivity; Reduces NE; Reduces hyperinsulinemia;

37
Q

What does the DASH diet consist of?

A
  • high in Ca, Mg, and K
  • fruit and veg
  • low intake of red meat
  • low fat dairy products
  • Plant protein
  • high fibre
38
Q

White Coat Hypertension - When to suspect - Prognosis

A

Suspect if patients do not have target organ damage, report lower readings out of office, and/or feel lightheaded/dizzy whens tarted in antihypertensive therapy - Lower CV risk than pt with sustained HTN, but not zero risk because they likely experience elevations in BP in other scenarios that cause them stress

39
Q

Concerns for pt with masked HTN

A
  • high er CVD risk than pt with sustained HTN
40
Q

When to suspect masked hypertension?

A

When target organ damage or left ventricle hypertrophy are observed, but the pt has normal office BP readings.

41
Q

Threshold for a hypertensive emergency and presenting symptoms. How to respond?

A

Very high BP: >180/>120 mmHg; Often symptomatic or mild headache; Urgency of response depends on presence of progressive/acute target organ damage;

42
Q

Hypertensive emergency vs hypertensive urgency

A

Hypertensive urgency does not present with target organ damage;

43
Q

How to respond to hypertensive urgency

A

Urgency can usually be managed in the ER ; Aim to bring down BP over several hours or over the day with medications they normally use of short-acting medications.

44
Q

Target organ damage in hypertensive emergencies (6)

A

from most to least common:

  • acute pulmonary edema
  • stroke
  • MI
  • acute aortic dissection
  • acute renal failure
  • hypertensive encephalopathy (acute confusion; rare)
45
Q

Investigations for target organ damage related to HTN

A
  • Poor kidney fxn: eGFR - Cardiac ischemia: signs & symptoms, ECG, cardiac enzymes - Brain ischemia: signs and symptoms of encephalopathy or stroke, CT or MR - Congestive heart failure: signs/symptoms, CXR, BNP - Acute aortic dissection: signs/symptoms, CT chest or echo - Papilledema on fundoscopy (optic disc swelling that is caused by increased intracranial pressure due to any cause)
46
Q

Target Organ Damage in hypertension

A
  • Stroke (thromboembolic and hemorrhagic stroke) - Hypertensive Heart Disease (LVH, heart failure, MI) - Hypertensive retinopathy
47
Q

Findings of mild vs moderate retinopathy of fundoscopy

A

Mild:

  • Arterial-venous nicking
  • arteriolar narrowing

Moderate:

  • hard exudates
  • flame-shaped hemorrhages
  • dot & blot hemorrhages
  • Papilledema (optic disk swelling)
48
Q

Investigations important for everyone who is diagnosed with hypertension:

A
  • history and physical, BMI, waist circumference
  • ECG
  • eGFR & urinalysis, electrolytes (Na, K, bicarb), Ca, TSH - Lipid profile, AIC/fasting glucose, ACR (if diabetes)
49
Q

Who should be screened for secondary hypertension?

A

HTN pt that is..

  • young
  • not controlled despite being on >3 medications
  • signs/symptoms/investigations indicative of secondary cause
50
Q

How many HTN patients have a secondary cause? What is the most common secondary cause?

A

5-10%, most commonly caused by primary hyperaldosteronism

51
Q

Obstructive sleep apnea - contribution to HTN - screening

A
  • sympathetic activity during periods of hypoxia result in aldosterone and sympathetic stimulation, which can contribute to hypertension
  • signs and symptoms (choking, obesity, gasping for air at night), polysomnography.
52
Q

Renal causes of hypertension

A
  • Chronic kidney disease
  • renal artery stenosis/renovascular disease
53
Q

How does chronic kidney disease cause hypertension? (2) Screening? (1)

A

Sodium and fluid retention as well as increased sympathetic nervous system and RAAS activation. Screen with eGFR and urinalysis

54
Q

Presentation of renal artery stenosis/renovascular disease in the context of HTN

A
  • These include atherosclerotic renal artery stenosis (most due to atherosclerosis) and fibromusclar dysplasia - May have abdominal bruits (renal artery), other vascular risk factors, rise in creatinine with ACEI/ARB, recurrent flash pulmonary edema
55
Q

Screening tests for atherosclerotic renal artery stenosis (3)

A

CT angiogram or MR angiogram (less radiation so use for younger people);

Renal captopril scan

56
Q

Screening tests for fibromuscular dysplasia (2)

A

CT angiogram Digital Subtraction Angiography

57
Q

What is fibromusclar dysplasia?

A

Heaping of collagen in renal arteries (and sometimes carotid arteries), causing sclerotic areas and eventually HTN.

58
Q

Types of hyperaldosteronism and how they are treated.

A
  • Idiopathic (bilateral adrenal hyperplasia). Treat with mineralocorticoid receptor antagonist. - Aldosterone producing adenoma. Can be cured surgically.
59
Q

How do pt with primary HTN present in terms of aldosterone and renin levels?

A

Aldosterone is high and renin is low. Overproduction of aldosterone leads to renal Na and water retention, thus increasing blood volume and CO, which in turn increase arterial pressure that is sensed in the kidney leading to suppression of renin.

60
Q

When to suspect primary hyperaldosteronism in HTN pt

A
  • ~6% of pt with HTN have aldosterone-producing tumors arising from adrenal gland
  • Suspect pt with resistant HTN, and those with hypokalemia or diuretic-induced hypokalemia
61
Q

Screening for primary hyperaldosteronism as an underlying cause of HTN

A

Upright plasma aldosterone concentration and renin activity

62
Q

What is Cushing’s Syndrome?

A

Hypercortisolism usually from an adrenal tumour but can include exogenous glucocorticoid use. Leads to increased Na and water retention.

63
Q

Screening for Cushing’s Syndrome

A

Based on signs and symptoms (i.e., moon face, striae, etc); 1 mg overnight dexamethason suppression test or 24 hr urine cortisol or late night salivary cortisol test (2 out of 3 abnormal for diagnosis)

64
Q

Signs and symptoms of Cushing’s syndrom

A
  • proximal muscle weakness
  • facial plethora (moon face)
  • fat deposition scapular area or face (‘buffalo hump’)
  • central obesity
  • thin, fragile skin with easy bruising
  • colourful stretch marks (>1cm wide)
  • hirsutism (male pattern hair growth), loss of libido
65
Q

Signs and symptoms of pheochromocytoma

A
  • headaches
  • palpitations
  • diaphoresis
  • panic attacks
  • pallor (not flushed)
  • hypertension or occurring with surgery, hard physical activity, or injury
66
Q

A patient presents with headaches, diaphoresis, and palpitations. You take their BP and observe that it is elevated. The most likely secondary cause of HTN in this setting would be…

A

pheochromocytoma - a tumour of the adrenal gland that produces excess Epi and NE

67
Q

When to screen for pheochromocytoma

A

When a pt presents with the classic triad of signs and symptoms: headache, diaphoresis, palpitations

68
Q

Screening tests for pheochromocytoma

A

24 hour urine fractionated metanephrines and catecholamines

69
Q

How may coarctation of the aorta be presented as hypertension?

A

upper limb hypertension and lower limb hypotension. Check and compare strength of pulses.

70
Q

A 28 year old woman presents with a 6 month history of elevated blood pressures (146/104 mmHg). Her BMI is 30, she has normal electrolytes and kidney function, and is otherwise healthy. She works 3 jobs and eats on the run a lot. What would we screen her for?

A

Likely elevated Na diet is causing the HTN. But because she is a young woman, we would screen for fibromuscular dysplasia (MR angiogram), use of OCP, and check for primary hyperaldosteronism.

71
Q

Equation for BP

A

BP = CO x SVR

72
Q

Equation for CO

A

CO = SV x HR

73
Q

What three factors determine CO?

A
  1. Preload 2. Afterload 3. Contractility
74
Q

What to prescribe for patients with isolated primary moderate-to-severe hypertension (i.e., in the absence of other cardiovascular risk factors or diseases such as diabetes mellitus)

A

Low-dose thiazide diuretic. ACE inhibitors and CCBs may have similar benefit but the evidence is lower quality. No other drug class is better than low-dose thiazides and high- dose thiazides and beta-blockers were actually less beneficial..

75
Q

What is pheochromocytoma?

A

A tumor of the adrenal gland that produces excess epinephrine and NE

76
Q

classic triad of symptoms in pheochromocytoma

A

headache, diaphoresis, palpitations

77
Q
A

Med 1 UBC Fall 2019 (16 decks)

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