Unit 12 Week 1 Flashcards
Diqgnosis of hypertension
hypertension is often symptomless so screening is vital
all adults should have their BP tyaken at least once every 5 years and annually after 80
dor those w type 2 diabetes it should also be measured annually
140/90 taken twice
ambulatory blood pressure monitoring
emasured as you move around
stage 1 hypertension
BP >140/90
stage 2 hypertension
BP 160/100
stage 3 hypertension
180/ 120
white coat effect
discrepency of more than 20/10 between clinic and average daytime ABPM at the time of diagnosis
relevence of looking at plasma glucose and BP
high blood glucose is a risk factor for hypertension
blood vessels lose their ability to stretch- due tp atherosclerosis
fluid in the body increases
insulin resistance
most people with diabetes will develop hypetension
relevence of checking urea in hypertension
done to see if the kidneys are working
high urea may suggest:
congetsive heart failure
kidney disease acute/ chronic
recent heart attacks
cleeding from the GI tract
high protein diet
cancer
trauma leadinf to muscle breakdown
sodium when checking for hypertension
increased sodium retention is linked to increased BV
eGFr and hypertension
chronic kidney disease is both a cause and a result of hypertension
eGFR used to estimate kidney function
damaged kidneys and therefore lower eGFR shows that less is being filtered by the kidneys, less ions excreted, more ions retained, greater blood pressure
serum lipid profile
measrued for CV risk prediction and includes 4 basic parameters:
total cholesterol
HDLcholesterol- absorbs cholsertol and tales it to liver
LDL cholesterol- collects on walls of arteries, hardening them
triglycerides
what position does the lead 2 in an ECG sit
at the apex of the heart
gives the clearest ecg
what is sinus tachycardia
the heartbeat is a sinus rhythm (regular controlled by the SAN) but is faster
Risk factors for hypertension
Elevated Blood Pressure
· Diabetes increases the risk for heart disease
· Unhealthy diet, eating too much sodium or not eating enough potassium increases the risk of hypertension
· Physical Inactivity: regular exercise keeps your heart and blood vessels strong and healthy
· Obesity: the heart must work harder to pump blood around the body
· Can lead to diabetes
· And high cholesterol
· Too much alcohol
· Tobacco use can damage the heart and blood vessels
· Nicotine raises blood pressure
· Breathing in carbon monoxide reduces the amount of oxygen that your blood can carry
· Genetics and Family History
· Age, race or ethnicity: Hypertension occurs more in Africans
factors affecting blood pressure
peripheral vascualr resistance is controlled by what in the short term
myogenic mechanism
neural and hormonal inputs
Vasoconstriction (angiotensin II, catecholamines, endothelin)
Vasodilation (kinins, prostaglandins and nitric oxide)
Renin-angiotensin-aldosterone system
- Regulation of blood volume long-term
- Low BP/High levels of catecholamines/Low sodium levels -> renin released by renal juxtaglomerular cells in afferent glomerular arterioles
- Na levels could fall when CO decreases and GFR is low as a result
- Renin cleaves plasma angiotensinogen to angiotensin I
- Angiotensin I is cleaved into angiotensin II by ACE which is present in vascular endothelium
- Angiotensin II raises BP by inducing vascular contraction, stimulating aldosterone secretion by the adrenal gland and increasing tubular sodium resorption in the kidneys
- Aldosterone increases BP by increasing sodium resorption (sodium thirst) and thus increasing water resorption in the DCT (ultimately increasing stroke volume and thus BP)
atrial natriuretic peptide
- Released by cardiac myocytes in the atria in response to stretch of the walls due to a high stroke volume/high blood pressure.
- important anti-hypertensive
- acts on the kidney and ultimately increases elimination of water and sodium through urine:
- stimulates vasodilation of afferent arteriole of glomerulus: results in increased renal blood flow and an increase in glomerular filtration rate. Increased glomerular filtration, coupled with inhibition of reabsorption, results in increases in excretion of water and urine volume - diuresis!
- stimulates vasoconstriction in efferent arteriole which also increases glomerular filtrate rate
- acts on several segments of the nephron- most notably the inner medullary collecting duct reducing sodium reabsorption- natriuresis
- ANP also inhibits Na+/H+ exchange in the proximal tubule and Na+/Cl- reabsorption in the distal tubule, both of which enhance sodium excretion.
renovascualr hypertension
innapropraite renin secretion is induced by renal artery stenosis, resulting in decreased glomerular flow
pressure natriuresis
intra-renal mechanism responsible for BP that leads to a change in renal sodium reabsorption
what usually prevents hypertension in normotensive people- hypertension occurs if it doesnt work!
can become dysfuntional with- CKD, diabetes or genetic predisposition
how does hypertension lead to disease
vasues vascular changes, remodelling and hypertrophy of the arteries leading to end organ damage.
takes years to become clinically relevent
causes degeneration in the walls of large and medium arteries that can lead to aortic dissection and cerebrovascsular haemorrhage
associated with hyaline arteruisclerosis and hyperplastic arteriosclerosis (thickens due to hyaline collagen deposition)
effect of hypertension on the heart
increase in vascular resistance means that there is a greater load imposed on the heart.
leads to left ventricular hypertrophy, left ventricular diastolic dysfunction and coronary artery disease
hypertension and kidneyu finction
peristent hypertension causes stenosis, weakening and sclerosing of the afferent arterial blood vessels.
these damaged vessels are elss elasticated and have a smaller cross-sectional area for turbulent blood flow
damaged kidneys fail to regulate blood pressure (less filtrate, less Na detected, detected as fallen BP by macula densa cells of juxtaglomerular apparatus in afferent arteriole, RAAS activation, increased sodium reabsorption, increased blood volume and pressure, damages kidney further)
Fundoscopy
AKA opthalmoscopy
allows you to inspect the fundus (back) of the eye. This consists of the:
- retina
- optic disc
- blood vessels
Amlodipine
anti-hypertensive
dihydropine L-type clacium channel antagonist
inhibits the influx of calcium into both vascular and cardiac muscle
peripheral vascular vasodilator that exerts its effect on vascular smooth muscle
name 8 kinds of antihypertensive groups of medication
diuretics
angiotensin converting enzyme inhibitors
ang II receptor blockers
direct renin inhibitors
beta-blockers
calcium channel blockers
central agonists
diuretics
lower blood pressure by increasing urinary sodium excretion, reducing plasma volume, ECF volume and cardiac output
ACE inhibitors
cause only a small fall in arterial blood pressure
stop the body producing as much angiotensin (responsible for narrowing arteries)
ANG II receptor blockers
selectively bind to AT1 receptors found in smooth muscle cells of vessels
blockage of these receptors directly causes vasodilation, reduces secretion of aldosterone and vasopressin
direct renin inhibitors
An analogue of the natural substrate of renin: angiotensinogen: aliskiren
competes with nagiotensinogen for access to the active site of the renin enzyme
beta-blockers
bind to beta-adrenoreceptors which block the binding of norepinephrine and epinephrine to these receptors.
Inhibits the sympathetic effects. decreases arterial BP by reducing cardiac output
calcium channel blockers
bind to L-type calcium channels located on vascular smooth muscle, cardiac myocytes and cardaic nodal tissue.
no influx of calcium, sm muscle relaxation, decreased HR and decreased conduction velocity
alpha blockers
bind to alpha adrenoreceptors located on the vascular smooth msucle.
most act as competitive antagonists to the binding of norepinephrine.
vasodilation by blocking the binding pf norepinephrine to sm. muscle receptors
central agonists
block sympathetic activity by binding to alpha2 adrenorecptors which causes symp outflow to the heart, decreasing cardiac output and contractility. reduced sympathetic output tp the vasculature
phentolamine
1* target= A1 receptor (GPCR)
Activity= antagonist (partial)
2* target= B1 receptor (GPCR)
Activity= Antagonist
smooth muscle relaxation— vasodilation.
partial blockage of alpha 1 receptors increases cardiac output through positive inotropic effects
Cocaine
alkaloid ester
local anaesthetic not used for its psychostimulatory properties in practice
inhinits NET (norepinephrine transporter) DAT (dopamine transporter) nad SERT (serotonine transporters) via competitive inhibition— binding to receptor sites inhibits catecholamin uptake at nerve terminals
why do some patients not attend helath checks?
lack of awareness or knowledge
misundertsanding the purpose of the check
time constraints
difficulty with travel
etc.
