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CVS-Alaa > Hypertension > Flashcards

Hypertension Flashcards

1
Q

define the stages of hypertension

A

Stage 1>> 140/90mmHg

Stage 2>> 160/100mmHg

SEVERE>> 180/110mmHg

disbetics:130/80

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2
Q

explain the impact of hypertension on organs and tissues in the body

A

MAIN 5 ORGANS at RISK -heart -eye -kidney -brain -BV

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3
Q

investigations

A
  • 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.
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4
Q

what causes hypertension?

A

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

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5
Q

blood pressure urgency vs emergency

A

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).

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6
Q

explain how blood pressure is controlled in the short and longer term

A

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

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7
Q

Treatment of urgency vs emergency

aim of therapy? (timing)

A

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!

  1. Sodium nitroprusside
  2. Labetalol
  3. GTN (1 - 10 mg/hr)
  4. 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.

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8
Q

pheochromocytioma triad
?

A

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

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9
Q

what shpuld u be aware of in sodium nitroprusside?

A

cyanide toxicity!

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10
Q

What factors stimulates renin release? (3) Where is it released? What cells r resposible?

A

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.

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11
Q

What neurotransmitter is released by the sympathetic nervous system acting on the heart and what type of receptor does it act on?

A

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

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12
Q

What is the intracellular signalling mechanism of the neurotransmitter Na and how does by what mechanism does it effect the heart?

A

Adenlylyl cyclase > CAMP > Activates PKA

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13
Q

If a patient has a systolic BP of 120mmHg and a diastolic BP of 90mmHg calculate the mean arterial BP

A

Diastolic pressure + 1/3 (pulse pressure)= 90 + 1/3 x 30 = 100 mmHg

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14
Q

what r the neurohumoral pathways the control circulating BV and BP?

A

SARA

1) Sympathetic 2) ANP 3) RAAS 4) ADP

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15
Q

Why are baroreceptors not able to control longer term changes in BP?

A

bc they RE-SET Does not control sustained increases because the threshold for baroreceptor firing resets

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16
Q

What would be the typical symptoms of an individual with hypertension?

A

Chest pain

Headache

Confusion

Difficulty breathing

Vision problems

17
Q

What would be the effect on blood pressure if you gave the patient a drug which antagonises α1 adrenoreceptors?

A

A1 adrenoreceptor agonists will cause vasodilation

This decreases blood pressure

18
Q

List some modifiable risk factors for developing hypertension.

A

-obesity -high cholestrol -inactivity

19
Q

what is the most powerful arteriolar constrictor?

A

angiotensin 2!

20
Q

where r ur barorecpters located? which nerve? where do they feedback to?

A
  • carotid sinus (at bifurcation)>via glossopharangeal
  • aortic arch >vagus CVS centre in medulla in brain inhibits sympathetic! to heart and BV sensitive to stretch!
21
Q

what detects the decreases in renal perfusion id the kidneys?

A

Barorecepters in the AFFERENT ARTERIOLE!

22
Q

What r functions if angiotensin 2?

A

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
23
Q

what r the 2 types of Angiotensin 2 receptors? which receptor has the most action? what type of receptor is it?

A

AG1 & AG2 Main action via AT1 recepter GPCR

24
Q

why do ppl who take ACE inhibitors develop a dry cough?

A

bradykinin doesn’t break down bradykinin accumulates>>cry cough

25
Q

what r the roles of the ADH in regulating BP> what stimulates its release? what is its other name?

A

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
26
Q

roles of ANP? where is is made? what stimulates its release?

A
  • 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
27
Q

roles of Dopamine, when is it used? where r their receptor found?

A

-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!

28
Q

why do those with parkinsons disease who r taking Dopamine, have a drop in BP?

A

bc dompamine also cause VASODILATION

29
Q

how can renovascular disease cause hypertension (4)

A

renal artery stenosis> low perfusion to kidney>cause renin release> RAAS> VASOCONSTRICTION & Na retention in other kidney

30
Q

what can go wrong in the adrenal medulla that can cause HYPERTENSION? (3)

A
  • 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)
31
Q

how can hypertension lead to heart failure and MI etc?

A

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.

32
Q

what r some treatments for hypertension? 6

A
  • 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
33
Q

what r some non pharmacological approaches in treating Hypertension?

A

-excersize -Diet -Reduced Na intake -reduce alchohol intake -lifestyle change!

34
Q

what r specific pharmacolgical targets in RAAS when treating hypertension

A
  • ACE inhibitors
  • Angiotensin 2 recepter antagonist>>STRONG EFFECT! bc angiotensin 2 is a powerful vasoncontricotr -
35
Q

what could u give to treat hypertension by vasoldilating Bv?

A
  • L-type CA+ CHANNEL BLOCKERS smooth muscle relaxation and prevents ca+ from coming in
  • A1-BLOCKERS vasodilators- reduces sympathetic tone
36
Q

What are the major population of adrenoceptors that mediate vasoconstriction of the vasculature?

A

a1-adrenoceptor.

37
Q

What are the main unwanted side effects of using a- adrenoceptor antagonists to treat hypertension?

A

• postural hypotension • impotence • Diarrhoea (due to increased gastrointestinal motility) • Arrhythmias (very rare)

CVS-Alaa (21 decks)

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