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Med Year 3 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

what is hypertension

A

high blood pressure above 140/90 in clinic or 135/85 not in clinic

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2
Q

causes of hypertension

A

essential/primary
or
secondary:
R - renal disease; could be renal artery stenosis
O - obesity
P- pre-eclampsia
E - endocrine (conn’s syndrome which is hyperaldosteronism)

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3
Q

what is hypertension a major risk factor for?

A 
stroke 
IHD
heart failure
CKD
cognitive decline 
premature death

for every 2mm rise in BP, risk increases by 10%

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4
Q

how do you measure BP NICE guidance

A

measure BP in both arms, if difference in readings between both is 15mmHg and then take the highest

if pulse irregularity: measure manually

if BP in clinic is 140/90 or higher, take second then third and then lowest

if BP is between 140/90 and 180/120, offer ambulatory BP monitoring to confirm the diagnosis of HT

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5
Q

what is ABPM and HBPM

A

ambulatory - reflects patients BP, constantly measures it over 24 horus

HPMB - allows patients to measure their own BP, 2 consecutive measures, twice daily, for 4-7 days and discard measurements

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6
Q

what are the stages of HT

A

stage 1: 135/85 to 149/94
stage 2: 150/95 to 179/119
stage 3: >180/120 (can result in hypertensive emergency aka malignant hypertension)

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7
Q

what is hypertensive urgency

A

systolic >180 mmHg or diastolic >110

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8
Q

what are the symptoms of HU

A

headache
SOB
nose bleed
severe anxiety

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9
Q

management of HU

A

oral anti-hypertensives
treat as outpatient

no target organ damage

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10
Q

what is hypertensive emergency

A

malignant hypertension

  • high BP leads to target organ damage
  • systolic >180, or diastolic >120
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11
Q

what are the symptoms of hypertensive emergency

A 
chest pain 
SOB 
back pain 
numbness and weakness 
vision change 
difficulty

can have severe, permanent effects on brain, heart and kidneys

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12
Q

how do you manage hypertensive emergency

A

IV nitroglycerine on admission

then IV and oral hypertensive drugs:

  • peripheral vasodilators
  • adrenergic inhibitors - eg labetalol

reduce 25% of BP over first few hours, then slowly over the next 24-48 hours to normal:

rapid drop should be avoided bc may precipitate cerebral or cardiac ischaemia

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13
Q

what investigations would you do for end organ damage

A

bloods:

  • u&Es, GFR: renal function
  • HbA1c
  • lipid profile
  • urine albumin:creatinine ratio - for proteinuria and dispstick for microscopic haematuria to assess for kidney damage

ECG for cardiac abnormalities

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14
Q

what is eye damage in hypertension

A

hypertensive retinopathy

grade 1: arteriosclerosis with moderatue vascular wall changes, to more severe hyperplasia

grade 2: AV nipping; predisposes to branch retinal vein occlusion (painless temporary vision loss)

grade 3: flame haemorrhages and cotton wool spots

grade 4: papilledema (optic disc oedema and yellow, hard exudates

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15
Q

end organ damage - brain

A

hypertensive cerebrovascular disease

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16
Q

end organ damage - heart

A

left ventricular hypertrophy, IHD with or without heart failure

  • concentric hypertrophy or LV muscles, eventually decreasing stroke volume
  • cardiomegaly
  • dilated LV - displaced apex beat
  • hypertrophied LV - tapping, powerful, apex beat
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17
Q

end organ damage - kidney

A

hypertensive nephropathy
-decreased blood flow to the kidneys from arterioral vasoconstriction = renin release = resulting in worsening hypertension via angiotensin 2 and aldosterone

-damaged glomeruli and decreased eGFR

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18
Q

what is the qrisk score

A

an algorithm for predicting CV risk estimates the risk of a person developing CVD over the next 10 years

NICE

19
Q

what are the lifestyle factors involved in hypertension

A 
healthy diet
salt - reduce dietary sodium intake 
coffee - discourage excess
smoking
alcohol intake - reduce if in excess 
regular exercise
20
Q

what is first line treatment for hypertension

A

ACE-I or ARB’s: if patients have diabetes or if they are <55 or if they are not african caribbean

CCB: if >55, or black african or caribbean any age

21
Q

what is the second line treatment

A

ACE-I or ARB’s
+
CCB or thiazide-like diuretic

if black, >55 etc, then CCB + ACE-I or ARB or thiazide

22
Q

what is the third line treatment

A

ACE-I or ABR + CCB + thiazide

23
Q

what is step 4 in hypertension treatment

A

confirm resistant hypotension, give spironolactone if blood potassium level is <4.5 or alpha-blocker or beta-blocker if potassium >4.5

24
Q

what is pheochromocytoma

A

tumour of adrenal gland tissue

  • paroxysmal elevations in BP
  • triad of headache, palpitations and sweating
25
Q

what is primary aldosteronism

A

adrenal gland produces too much aldosterone which is responsible for balancing potassium levels

unexplained hypokalaemia with urinary potassium wasting; however, more than one-half of patients are normokalemic

26
Q

what is cushing’s syndrome

A

high levels of cortisol

cushingoid faces, central obesity, proximal muscle weaknes

may have a history of gcc use

this increase in gcc increases Na+ and H20 retention

27
Q

what is sleep apnoea syndrome

A

primarily seen in obese men who snore loudly while asleep

breathing starts and stop, leading to lower amounts of oxygen inhaled and hence heart pumps harder which increases BP

28
Q

what is coarctation of the aorta

A

congenital disease when aorta is unusually narrow

hypertension in arms wth diminshed or delayed femoral pulses and low or unobtainable BP in the legs

left brachial pulse is diminished and equal to the femoral pulse if origin of left subclavian artery is distal to coarctation

29
Q

what is primary hyperparathyroidism

A

elevated serum calcium

30
Q

what is the short term control of BP

A

short term: CNS response, baroreceptors and chemoreceptors

31
Q

what do the baroreceptors do

A
  • activated by stretch
  • carotid and aortic body

important in maintaining postural BP

32
Q

what are chemoreceptors

A

sensitive to low O2, high CO2 and acidosis
2 carotid bodies and 1-3 aortic bodies

reduction in blood flow causes metabolic stimulation excitatory effect on vasomotor centre

33
Q

long term control: RAAS

A

liver releases angiotensin

forms angiotensin 1 (by renin from the JGA) = angiotensin 2 by ACE from lungs and endothelium

34
Q

what does angiotensin 2 do

A

increases:

  • sympathetic activity of ANS
  • Na, Cl reabsorption and k, H+ excretion and H20 retention
  • aldosterone secretion from adrenal gland, which does the same
  • ADH secretion from the posterior pituitary gland, which increases H20 resoprtion
  • systemic arteriolar vasoconstriction
35
Q

what is JGA

A

juxtoglomerular apparatus
-macula densa: sense changes in NaCl delivery to the distal convuluted tubule and causes renin release and reduction of afferent arteriole resistance, increasing glomerular filtration

  • juxtaglomerular cells
  • mesangial cells
36
Q

basic summary: pathophys of hypertension

A
  • reduction in blood flow
  • kidneys release renin
  • leading to two pathways
    first: aldosterone = increase in sodium and water reabsorption = increase blood volume = increases CO = increase in BP and reduction in blood flow

second: angiotensin = ang 1 –> ang 2 –> vasoconstriction –>PR –> increase in BP

37
Q

in certain conditions you avoid ACE-I, why?

A

bc blocks ACE so no vasoconstricition of efferent arterioles which means less glomeruli filtration rate

38
Q

what receptor does adrenaline work on and what is its clinical use

A

works on beta > alpha

anaphylactic shock, cardiogenic shock, cardiac arrest

39
Q

what receptor does noradrenaline work on and what is its clinical use

A

B1 and alpha 1 more than the others

severe hypotension and septic sock

40
Q

what receptor does dopamine work on and what is its clinical use

A

B1 = B2 > alpha 1

acute heart failure, cardiogenic shock

41
Q

what receptor does dobutamine work on and what is its clinical use

A

b1>b2>a1

acute heart failure
cardiogenic shock
refractory heart failure

42
Q

how is the BP controlled by the ANS

A

sympathetic vasomotor nerve fibres leave cord through T and L spinal nerves to form sympathetic chain

sympathetic nerves innervate viscera eg heart and bowels

spinal innervate vasculature

vagus nerve - PNS

43
Q

what does the vasomotor centre consist of

A
  • vasoconstrictor area - origin of excitatory preganglionic vasoconstrictor neurones (pass to sympathetic chain)
  • vasodilator area - internal inhibition of vasoconstrictor area
  • sensory area - input from vagus and glossopharyngeal nerves modulate vasoconstrictor / dilator area activity
44
Q

how does the SNS raise arterial pressure

A

SNS release NA from nerve terminals

acts on the alpha-adrenergic receptors of the vascular smooth muscle

all arterioles remain in state of partial constriction in homeostasis

heart is directly stimulated

things not innervated: capillaries, pre-capillary sphincters)

Med Year 3 (25 decks)

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