Unit 12 Week 1

Question 1

Diqgnosis of hypertension

Answer 1

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

Question 2

ambulatory blood pressure monitoring

Answer 2

emasured as you move around

Question 3

stage 1 hypertension

Answer 3

BP >140/90

Question 4

stage 2 hypertension

Answer 4

BP 160/100

Question 5

stage 3 hypertension

Answer 5

180/ 120

Question 6

white coat effect

Answer 6

discrepency of more than 20/10 between clinic and average daytime ABPM at the time of diagnosis

Question 7

relevence of looking at plasma glucose and BP

Answer 7

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

Question 8

relevence of checking urea in hypertension

Answer 8

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

Question 9

sodium when checking for hypertension

Answer 9

increased sodium retention is linked to increased BV

Question 10

eGFr and hypertension

Answer 10

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

Question 11

serum lipid profile

Answer 11

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

Question 12

what position does the lead 2 in an ECG sit

Answer 12

at the apex of the heart

gives the clearest ecg

Question 13

what is sinus tachycardia

Answer 13

the heartbeat is a sinus rhythm (regular controlled by the SAN) but is faster

Question 14

Risk factors for hypertension

Answer 14

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

Question 15

factors affecting blood pressure

Answer 15

Question 16

peripheral vascualr resistance is controlled by what in the short term

Answer 16

myogenic mechanism

neural and hormonal inputs

Vasoconstriction (angiotensin II, catecholamines, endothelin)

Vasodilation (kinins, prostaglandins and nitric oxide)

Question 17

Renin-angiotensin-aldosterone system

Answer 17

• 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)

Question 18

atrial natriuretic peptide

Answer 18

• 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.

Question 19

renovascualr hypertension

Answer 19

innapropraite renin secretion is induced by renal artery stenosis, resulting in decreased glomerular flow

Question 20

pressure natriuresis

Answer 20

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

Question 21

how does hypertension lead to disease

Answer 21

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)

Question 22

effect of hypertension on the heart

Answer 22

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

Question 23

hypertension and kidneyu finction

Answer 23

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)

Question 24

Fundoscopy

Answer 24

AKA opthalmoscopy

allows you to inspect the fundus (back) of the eye. This consists of the:

• retina
• optic disc
• blood vessels

Question 25

Amlodipine

Answer 25

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

Question 26

name 8 kinds of antihypertensive groups of medication

Answer 26

diuretics

angiotensin converting enzyme inhibitors

ang II receptor blockers

direct renin inhibitors

beta-blockers

calcium channel blockers

central agonists

Question 27

diuretics

Answer 27

lower blood pressure by increasing urinary sodium excretion, reducing plasma volume, ECF volume and cardiac output

Question 28

ACE inhibitors

Answer 28

cause only a small fall in arterial blood pressure

stop the body producing as much angiotensin (responsible for narrowing arteries)

Question 29

ANG II receptor blockers

Answer 29

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

Question 30

direct renin inhibitors

Answer 30

An analogue of the natural substrate of renin: angiotensinogen: aliskiren

competes with nagiotensinogen for access to the active site of the renin enzyme

Question 31

beta-blockers

Answer 31

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

Question 32

calcium channel blockers

Answer 32

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

Question 33

alpha blockers

Answer 33

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

Question 34

central agonists

Answer 34

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

Question 35

phentolamine

Answer 35

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

Question 36

Cocaine

Answer 36

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

Question 37

why do some patients not attend helath checks?

Answer 37

lack of awareness or knowledge

misundertsanding the purpose of the check

time constraints

difficulty with travel

etc.