Hypertension Flashcards
define the stages of hypertension
Stage 1>> 140/90mmHg
Stage 2>> 160/100mmHg
SEVERE>> 180/110mmHg
disbetics:130/80
explain the impact of hypertension on organs and tissues in the body
MAIN 5 ORGANS at RISK -heart -eye -kidney -brain -BV
investigations
- Test for the presence of protein in the urine by sending a urine sample for estimation of the albumin: creatinine ratio and test for haematuria using a reagent strip.
- Blood rate, serum total cholesterol and HDL cholesterol.
- Bloods may suggest secondary cause (low potassium, high Na: hyperaldosteronism).
- Examine the fundi for the presence of hypertensive retinopathy.
- Arrange for a 12-lead ECG to be performed.
- Consider ECHO if suggestion of LVH, valve disease or LVSD or diastolic dysfunction.
what causes hypertension?
in around 95% of the population it is unknown “primary hypertension”-family history? genetics?
Secondary hypertension >> due to underlying patholgy patient has!
- renovascular disease ?? GN, PCKD, RVS
- chronic renal disease
*CVS: coartication, AR
• endocrine> Cushing’s syndrome, conns, pheo, hyperthyroi
other: drugs>> COCP, steroids
blood pressure urgency vs emergency
encephalopathy, pulmonary oedema, acute kidney injury, myocardial ischaemia
urgency >> (high BP without a critical illness, but may include ‘malignant hypertension’: associated with grade 3/4 hypertensive retinopathy).
explain how blood pressure is controlled in the short and longer term
short term= barocrecepter reflex
1) adjust parasympathetic and sympathetic inputs to the heart to adjust CO
2) adjust sympathetic input to Peripheral vessels to alter TPR
Treatment of urgency vs emergency
aim of therapy? (timing)
The aim of therapy is to reduce the diastolic BP to 110 mmHg in 3 - 12 hours (emergency) or 24 hours (urgency). IV to start:
sabibabt loya gabl azma!-emergency!
- Sodium nitroprusside
- Labetalol
- GTN (1 - 10 mg/hr)
- Esmolol acts within 60 seconds, with a duration of action of 10 - 20 minutes. Typically, the drug is given as a 0·5 - 1 mg/kg loading dose over 1 minute, followed by an infusion starting at 50 µg/kg/min and increasing up to 300 µg/kg/min as necessary.
Hypertensive urgency
Severe blood pressure elevation that will cause damage within days. Diastolic is usually > 130 mmHg and retinal changes will be apparent. The aim should be to reduce BP gradually to a diastolic of 100 mmHg over 48 - 72 hours using an oral regime. For oral treatment, any of the following drugs may be used: amlodipine 5 - 10 mg OD, diltiazem 120 - 300 mg daily, lisinopril 5 mg OD, etc.
A combination of a ACEI and calcium antagonist is effective and well tolerated.
Local expertise advises that the safest and most effective treatment regimen for the majority of patients is nifedipine 20mg + amlodipine 10 mg OD for three days, continuing with Amlodipine 10 mg OD thereafter.
pheochromocytioma triad
?
headache, sweating,tachycardia
24 hr urine collection of catecholimines
APLHA and BETA blockers
start with alpha then after 2 to 3 days BETA!
NEVER USE BETA FIRST
what shpuld u be aware of in sodium nitroprusside?
cyanide toxicity!
What factors stimulates renin release? (3) Where is it released? What cells r resposible?
from granular cells of Juxtamedullary complex in kidneys
a) Reduced NaCl to distal tubule
b) Decrease is SBP>decreased renal perfusion> release of renin c) sympathetic stimultion to juxtamedu. apparatus RELEASE RENIN.
What neurotransmitter is released by the sympathetic nervous system acting on the heart and what type of receptor does it act on?
NA, acts mainly on B1 recepters -increases heart rate (+chronotrophic effect) CaMP > increases funny current in SA node> this increases rate -force of contraction (+inotrophic effect) via Pka and ca release
What is the intracellular signalling mechanism of the neurotransmitter Na and how does by what mechanism does it effect the heart?
Adenlylyl cyclase > CAMP > Activates PKA
If a patient has a systolic BP of 120mmHg and a diastolic BP of 90mmHg calculate the mean arterial BP
Diastolic pressure + 1/3 (pulse pressure)= 90 + 1/3 x 30 = 100 mmHg
what r the neurohumoral pathways the control circulating BV and BP?
SARA
1) Sympathetic 2) ANP 3) RAAS 4) ADP
Why are baroreceptors not able to control longer term changes in BP?
bc they RE-SET Does not control sustained increases because the threshold for baroreceptor firing resets
What would be the typical symptoms of an individual with hypertension?
Chest pain
Headache
Confusion
Difficulty breathing
Vision problems
What would be the effect on blood pressure if you gave the patient a drug which antagonises α1 adrenoreceptors?
A1 adrenoreceptor agonists will cause vasodilation
This decreases blood pressure
List some modifiable risk factors for developing hypertension.
-obesity -high cholestrol -inactivity
what is the most powerful arteriolar constrictor?
angiotensin 2!
where r ur barorecpters located? which nerve? where do they feedback to?
- carotid sinus (at bifurcation)>via glossopharangeal
- aortic arch >vagus CVS centre in medulla in brain inhibits sympathetic! to heart and BV sensitive to stretch!
what detects the decreases in renal perfusion id the kidneys?
Barorecepters in the AFFERENT ARTERIOLE!
What r functions if angiotensin 2?
angioTENSIN 2 (gam yisabib tension alaa)
- vasoconstriction
- Stimulates Na reapsorption in kdney>>increase BV
- Stimulates ALDOsterone from arenal cortex
- increases release of ADH from posterior pituatry (translocates aquarporins to allow water retention
what r the 2 types of Angiotensin 2 receptors? which receptor has the most action? what type of receptor is it?
AG1 & AG2 Main action via AT1 recepter GPCR
why do ppl who take ACE inhibitors develop a dry cough?
bradykinin doesn’t break down bradykinin accumulates>>cry cough
what r the roles of the ADH in regulating BP> what stimulates its release? what is its other name?
Increases water reabsorption in detail nephron! therefore making urine more concentrated. stimulated by increases in:
- plasma osmolarity
- HYPOvolemia stimulates Na reabsorption as well
- acts in apical Na,cl,K contransporter Vasopressin -vasoconstriction
roles of ANP? where is is made? what stimulates its release?
- synthesised and stored in atrial myocytes
- released in response to STRETCH -promotes Na+ excretion & inhibits its reabsorption –> reduced filling of the heart – less stretch – less ANP released
roles of Dopamine, when is it used? where r their receptor found?
-formed locally in kidney from circulating L-dopa -dopamine recepters r on renal bv and PCT & ascendinf loop -VASODILATION IT IS NOT USED AS AN ANTIHYPERTENSIVE!
why do those with parkinsons disease who r taking Dopamine, have a drop in BP?
bc dompamine also cause VASODILATION
how can renovascular disease cause hypertension (4)
renal artery stenosis> low perfusion to kidney>cause renin release> RAAS> VASOCONSTRICTION & Na retention in other kidney
what can go wrong in the adrenal medulla that can cause HYPERTENSION? (3)
- Conn’s syndrome – ALDOSTERONE secreting adenoma – hypertension and hypokalaemia (fatty rich)
- Cushing’s syndrome –excess secretion of glucocorticoid CORTISOL – at HIGH concentrations acts on aldosterone receptors - Na+ and water reabsorbtion
- Tumour of the adrenal medulla – phaeochromocytoma – secretes catacholamines (noradrenaline and adrenaline)
how can hypertension lead to heart failure and MI etc?
Heart is pumping against a higher RESISTENCE>> this increases the Afterload on the heart, which will cause LV hypertrophy!, & increases oxygen demand on the myocardium.
what r some treatments for hypertension? 6
- ANGIOTENSIN CONVERTING ENZYME INHIBITORS (ACEi) inhibit the production of AII
- ANGIOTENSIN II INHIBITORS (ARBs) inhibit the action of ALL
- CA+ CHANNEL BLOCKERS smooth muscle vasodilators • A1-BLOCKERS vasodilators
- DIURETICS increase Na and water loss from the kidneys
- B-BLOCKERS reduce CO (by reducing force and rate of heart) and decrease renin production-we don’t use em alone tho
what r some non pharmacological approaches in treating Hypertension?
-excersize -Diet -Reduced Na intake -reduce alchohol intake -lifestyle change!
what r specific pharmacolgical targets in RAAS when treating hypertension
- ACE inhibitors
- Angiotensin 2 recepter antagonist>>STRONG EFFECT! bc angiotensin 2 is a powerful vasoncontricotr -
what could u give to treat hypertension by vasoldilating Bv?
- L-type CA+ CHANNEL BLOCKERS smooth muscle relaxation and prevents ca+ from coming in
- A1-BLOCKERS vasodilators- reduces sympathetic tone
What are the major population of adrenoceptors that mediate vasoconstriction of the vasculature?
a1-adrenoceptor.
What are the main unwanted side effects of using a- adrenoceptor antagonists to treat hypertension?
• postural hypotension • impotence • Diarrhoea (due to increased gastrointestinal motility) • Arrhythmias (very rare)
