Week 9 Hypertension Flashcards Preview

Med 1 UBC Fall 2019 > Week 9 Hypertension > Flashcards

Flashcards in Week 9 Hypertension Deck (77)
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1

Different actions of angiotensin II at low versus high levels

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

2

Summarize the RAAS

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.

3

Effects of angiotensin II

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.

4

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

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.

5

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

- 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

6

where are cardiopulmonary baroreceptors located?

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.

7

Physiologic effects of ANP and BNP (4)

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.

8

Local regulation of blood flow

- acute local regulation mediated by tissue factors

9

tissue factors that cause vasodilation

- CO2, lactic acid, H+, K+, adenosine, ADP, histamine, bradykinin, prostacyclin, NO (or eNO)

10

tissue factors that cause vasodilation

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

11

Impact of chronic high BP on vasculature (2)

- 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.

12

Primary Hypertension

= 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.

13

Autoregulation of blood pressure

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

14

Causes of secondary hypertension

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)

15

The importance of fundoscopy in assessing BP

- 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

16

Hypertensive heart disease

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

17

Implications of autoregulation of BP in HTN

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.

18

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

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)

19

hypertensive emergencies - define - treatment

= 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.

20

Epidemiology of hypertension

- 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

21

Diagnosis of HTN

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

22

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

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

23

Lifestyle factors that contribute to HTN (5)

- Aging

- Obesity and insulin resistance

- High salt and low potassium diet

- Low physical activity

- Stress

24

How does aging relate to HTN

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).

25

What is the most common cause of adolescent hypertension?

obesity and insulin resistance

26

How do obesity and insulin resistance contribute to HTN?

Though activation of RAAS and sympathetic nervous system

27

How does sedentariness contribute to HTN? (3)

- 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

 

28

How does diet contribute to HTN?

- Variation in this association. 

- 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

29

Metabolic syndrome

- HTN - Dyslipidemia - Diabetes - Obesity

30

Role of K in HTN (2)

- 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