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43 Cards in this Set
- Front
- Back
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Hypertension definition |
Blood pressure at rest which exceeds a normal 'cut off' usually 90mmhg diastolic pressure caused by narrowing of the arteries |
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Primary hypertension |
High bp which has proven risk factors but for which no medical condition is known |
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Secondary hypertension causes |
aortic coartation (narrowing) Renal disease Thyroid disease Eclampsia |
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Optimal blood pressure |
<120/80mmHg |
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Normal bp |
<130/85 mmHg |
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High blood pressure |
130-139/85-89mmHg |
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Grade 1 hypertension |
140-159/90-99mmHg |
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Grade 2 hypertension |
160-179/100-109mmHg |
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Grade 3 and SEVERE hypertension |
>180mmHg/>110mmHg |
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Non-medicinal intervention to reduce blood pressure |
weight reduction 5-10mmHg decrease per 10Kg diet modifications 8-14mmHg reduced sodium intake 2-8mmHg physical activity 4-9mmHg alcohol 2-4mmHg |
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Clinical guidance for medical treatment to patients under 55 (white) |
step 1: Ace inhibitor or Angiotensin receptor blocker Step 2: ACE inhibitor + ca2+ channel blocker step 3: step2 + thiazide diuretic Step 4: step 3 + B BLOCKER |
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Pathophysiology of hypertension |
Initially there is an increase in Cardiac output and Total peripheral resistance remains normal Overtime CO returns to normal and TPR increases |
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Why is there an increase in tpr during hypertension over time? |
blood pressure is related to the kidneys , in hypertension there is the inability of the kidneys to excrete Na resulting in an increase in ANF secretion to promote salt excretion Overactive ras = vasoconstriction |
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What is ANF |
Anti-nuclear factor which is an antibody created which increases the secretion of Na+ salts antibodies cause inflammatory response causing vasoconstriction of blood vessels INCREASING TPR |
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RAAS system |
Decreased renal blood flow (vasoconstriction of afferent neurons) results in the secretion of renin which ultimately produces AngII |
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What is AngII |
A potent vasoconstrictor produced by ACE enzyme catalysed conversion of AngI to AngII it increases blood pressure and secretion of aldosterone causing na+ retention and H20 THIS INCREASES BLOOD VOLUME also stimulates secretion of ADH= increases blood volume |
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regulation of rennin secretion from the kidney |
Sympathetic nerves (b1) low renal blood pressure - PGE released and inflammation causes increased bp Low Na- want to increase re-absorption |
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What receptors are activated to cause vasoconstriction ? |
AT1- greater affinity for angII gq- increasing calcium= contraction gi - decrease cAMP (turning off contraction) MAP kinase(increase production of growth hormones) |
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What does AT2 receptors do? |
Vasodilation when stimulated |
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Why target RAAS system to decrease blood pressure? |
by inhibiting the RAAS system we can prevent vasoconstriction of blood vessels and decrease blood volume by increasing water excretion, this would decrease tpr and therefore decrease the workload on heart |
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What is ADH |
an anti-diuretic hormone which increases the collecting duct permeability to H20 increasing re-absorption, this increases the blood volume. Stimulated by decrease blood pressure (in kidneys) |
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Aldosterone |
Release stimulated by angII from adrenal cortex stimulates Na+ reabsorption + K+ excretion by the renal tubule indirect negative feedback on RAAS (stops angII) |
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Atrial Natruiretic peptide (ANP) |
promotes loss of sodium and H20 secretion cause renal dilation increasing GFR INHIBITS RENIN! |
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autoregulation |
maintains blood supply and protects- prevents high pressures damaging the kidney |
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Tissue renin |
found in heart, blood vessels + cardiovascular centres |
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ACE INHIBITORS |
catopril (hypotension on first dose) enalapril (longer t1/2 as prodrug) lisinopril ramipril (tissue specific) fosinopril inhibit the formaton of AngII |
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What effect does inhibiting ace have? |
fall in circulating angII = decrease aldosterone secretion and a DECREASE IN BLOOD PRESSURE by decreasing TPR vasodilation, anti-proliferation + thrombic actions too increases formation of ang1-7 which opposes angII effect NO EFFECT ON CO OUTPUT |
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Adverse effects of ace inhibitors |
hypotension renal failure in patients cough angio-oedema RENAL FAILURE IN FETUS |
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Angiotensin receptor blockers |
losartan valsartan irbesartan candesartan all inhibit AngII binding, preventing vasoconstriction |
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problems with ARB |
do not decrease circulating level of angII remains to be estabilshed if more effective than ACE inhibitors |
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benefits of ARB over ACE inhibitors |
does not cause cough |
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Renin inhibitors |
zamkiren, aliskiren more specific decreasing levels of angI non peptides do not cause cough |
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Vasopeptidase inhibitors |
omapatrilat - duel inhibition of ACE + NEP NEP breaks down ANP Inhibiting this increases h20 excretion and reduces angII |
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Diuretic drugs |
the most important diuretic drugs act by decreasing NA+ reabsorption Na+ influences blood volume |
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Carbonic anhydrase inhibitors site of action? |
site: proximal convoluted tubule
enzyme action: HCO3- reabsorption which is coupled to 1/3 Na+ reabsored here (no longer used but developed new ones) |
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Carbonic anhysrase inhibitor example |
Acetazolamide anti-convulsant action + increase co2 to brain used to treat glaucoma |
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Loop diuretics |
site of action: ascending limb of loop of henle mech: inhibit Na/K/2Cl co-transporter bind to Cl- site most powerful class because of loop of henle importance in reabsorption |
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Example loop diuretic |
Furosemide treatment of choice in severe oedema useful vasodilation action which is not understood |
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Adverse effects of furosemide |
loss of K+ Ca2+ and Mg2+ hyperglycaemic (decrease glucose tolerance due to decrease K+ as this can decrease Insulin secretion) |
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Thiazides |
site: distal convoluted tubule mech: inhibit Na/Cl co-transporter vasodilate well tolerated used in oedema + heart failure but decrease glucose tolerance |
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Example of thiazides |
bendroflumethiazole milder than loop reduce max diluting of kidney |
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Potassium sparing duiretics |
act on the last part of the distal convulted tuule and collecting duct aldosterone sensitive part (psd inhibit this) inhibiting aldosterone inhibits Na+ reabsorption therefore increases exretion of H20 |
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K+ sparing duiretic example |
spirolactone- reduces expression of NA/K pump and antagonists the effects of aldosterone weak diuretics but produce K+ retention |
