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Medicine 1 (Year 1) > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Normal Blood pressure

A

120/80

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2
Q

Hypertension is worlds number 1 cause of preventable mortality/morbidity?

True

False

A

true

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3
Q

would a rise in 2mmHg cause an increase in mortality?

A

Yes

7% in mortality from ischaemic heart disease

10% in mortality from stroke

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4
Q

the graded relationship between BP and CVD

A

starts from 115/75

if the patient has sitting blood pressure 135/85 the risk of cardiovascular death is almost doubled regardless of age.

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5
Q

Blood pressure prevalence

A

>65

important risk for myocardial infarction, heart failure, stroke and cardiovascular disease.

accounts for 41% of all cardiovascular disease deaths.

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6
Q

organs hypertension affects on brain

A

Brain - cerebrovascular accident, stroke, haemorrhage

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7
Q

organs hypertension effects on heart

A

heart - lapidary hypertrophy. coronary heart disease, congestive heart failure, myocardial infarction

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8
Q

organs hypertension effects on eyes

A

eyes causing retinopathy

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9
Q

organs hypertension effects on blood vessels

A

peripheral vascular disease - blood supply to arms and legs, causing peripheral vascular disease.

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10
Q

organs hypertension effects on kidneys

A

renal failure, the requirement for transplantation, proteinuria.

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11
Q

risk factor for hypertension

A

smoking

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12
Q

can blood pressure vary throughout the day?

A

yes typically fluctuates during day likely due to:

stress physically

mental stress.

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13
Q

stage 1 hypertension

A
  • clinic bp 140/90

Ambulatory bp (home) 135/85

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14
Q

stage 2 hypertension

A
  • clinic bp 160/100

Ambulatory bp (home) 150/95

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15
Q

stage 3 or severe hypertension

A
  • clinic bp 180/120
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16
Q

what is ABPM

A

ambulatory bp measurement - takes average 30 measurements both day time and night time

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17
Q

in 80-80% of cases no cause can be found - what hypertention type is this?

A

primary hypertension

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18
Q

what type of hypertension has a cause?

A

secondary hypertenion. e.g. chronic renal disease, renal artery stenosis

endocrine disease e.g. Cushings, primary hyperaldosteronism (Conns syndrome) phaeochromocytoma, Glucocorticoid-remediable aldosteronism (GRA)

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19
Q

Cushing’s syndrome

A

occurs when your body makes too much of the hormone cortisol over a long period of time.

Cortisol also helps maintain blood pressure and regulate blood glucose,

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20
Q

Primary aldosteronism (PA), also known as primary hyperaldosteronism or Conn’s

A

a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension

ectopic expression of aldosterone synthase activity hyperaldosteronism and suppression of angiotensin II-stimulated aldosterone production in the zona glomerulosa. (kidney)

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21
Q

pheochromocytoma

A

a noncancerous (benign) tumour that develops in an adrenal gland.

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22
Q

what age is likely for secondary hypertension?

A

younger - 20s

all under the age of 40 should be referred to a specialist to investigate ? secondary

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23
Q

risks of hypertension

A

smoking

diabetes

renal disease

males over females

hyperlipidaemia

previous myocardial infarction or stroke

left ventricular hypertrophy

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24
Q

what are contributors to blood pressure?

A

cardiac output - stroke volume, (amount blood pumped with each stroke) and heart rate

Peripheral vascular resistance - resistance that vasculature provides to slow cardiac output or blood flow.

sympathetic nervous system

* each can be manipulated by drug therapy*

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25
Q

How is the sympathetic nervous system in blood pressure?

A

SNS produces venoconstruction = peripheral resistance
reflex for tachycardia = increase stroke volume + cardiac output

stimulated RAAS - angiotensin 2 and aldosterone

SNS are rapid and account for second to second blood pressure control

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26
Q

importance of RAAS for blood pressure

A

RAAS pivotal for long term bp control

raas responsible for: maintaining sodium balance, controlling blood volume, control of blood pressure

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27
Q

what stimulates RAAS to do with blood pressure?

A

fall in bp; fall in circulating vol; sodium depletion

  • stimulate renin release from juxtaglomerular apparatus

renin converts angiotensin to angiotensin 1

angiotensin 1 converts to angiotensin 2 by (ACE)

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28
Q

what factors would prompt us to think a patient has secondary hypertension?

A

severe/resistant hypertension (non-reactive to several medications given)

they are a child/adolescence

worsening of previous stable hypertension

malignant hypertension

no other risk factors identified and they are under age 30

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29
Q

investigations for secondary hypertension

A

renal function and urinalysis

renal imaging: ultrasound, MRA renal arteries

Aldosterone to renin ratio (ARR)

24-hour urine or catecholamines/metanephrines looking for pheochromocytoma or paraganglioma (only if clinical suspicion)

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30
Q

causes for secondary hypertension : renal

A

renal disease 20%) - chronic pyelonephritis (Kidney infection )
fibromuscular dysplasia
renal artery stenosis - common atherosclerotic disease; polycystic kidneys

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31
Q

causes for secondary hypertension - drug induced

A

drug-induced - NSAIDs, combined oral contraceptive
corticosteroids cocaine and other stimulants

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32
Q

causes for secondary hypertension - pregnancy

A

gestational hypertension

pre-eclampsia

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33
Q

causes for secondary hypertension - endocrine

A
  • primary hyperaldosteronism (conns)

Cushings

pheochromocytoma

vascular - coarctation aorta

sleep apnoea

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34
Q

what age would you not expect to see coarctation of the aorta (cause secondary hypertension)

A

rarely over 35 as often died by then

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35
Q

focal fibromuscular dysplasia

A
  • often young woman. no atherosclerotic disease

stenosis

treat single stent to affected kidney = normalise bp

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36
Q

what symptom/indigation on inspection would you expect of focal fubromuscular dysplasia?

A

bruit ofer the affected kidney

**bruit a sound, especially an abnormal one, heard through a stethoscope; a murmur. described as blowing sounds*

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37
Q

multifocal fibromuscular dysplasia

A

significant hypertension beaded appearance

requires triple therapy: angioplasty

bilateral 30% cases

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38
Q

polycystic kidney disease

A

often genetic

cysts form - necessary for remove kidneys and have transplant or dialysis

this is spontaneous (mutation)

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39
Q

pheochromocytoma

A

tumour adrenal gland (often benign)

may present accelerated hypertension, resistant hypertension, headaches, flushing, sweating, palpitations. Genetic predisposition.

essential to involve a multidisciplinary team with endocrinologists and surgeons

long term follow-up and monitoring essential

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40
Q

Cushings disease

A

malignant tumour on the left adrenal gland

treat chemotherapy and regular antihypertensive therapy.

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41
Q

what does differing blood pressures on either arm potential indicate?

e.g. 225/124 mmHg R 175/100 L

A

aortic coarctation

*rarely hear a murmur

not obvious on ECG

best to have MRI

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42
Q

nocturnal dip with prolonged hypertesnion

A

the problem if prolonged hypertension throughout the day will cause damage they will lose the nocturnal dip

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43
Q

Loss of nocturnal dip

A

persistently high even sleeping or higher.

cause = night worker? or person who had lost it.

high nocturnal poor prognostic

need night medications

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44
Q

masked hypertension

A

normal blood pressure leaves medical staff and rises.

carries significant cv event risk

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45
Q

first assessments for hypertensive patients

A
  • History - previous MI, stroke - ischaemic heart disease
  • smoker? - diabetic hypercholestraimia
  • Family history - physical examination
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46
Q

hypertension - assessment for end-organ damage

A

ECH - for left ventricular hypertrophy

echocardiogram - for left ventricular hypertrophy

proteinuria - urine analysis

renal ultrasound

renal function test - creatinine, EGFR,

47
Q

hypertension - what are the treatable causes (secondary)

A

common in young patients

  • obesity - renal artery stenosis/FMD (Fibromuscular dysplasia)
  • conns, cushings, pheochromocytoma
  • coarction - drug-induced - sleep apnea
48
Q

how to quantify risk hypertension

A

assign risk calculator/q risk

once assessed - set a target blood pressure

BHS suggest < 135/80-80mmHg

Treatment should be started at an overall CVD risk of 10%/10 years

49
Q

treating hypertension

reasons

how?

A

reasons - reduced cerebrovascular disease by 40-50%

reduced MI by 16-30

treat - stepped approach

a low dose of several drugs

the approach minimises adverse events and maximises the patient outcome

50
Q

What are NHS/BHS guidelines to reatment for hypertension?

A

Yong patients (high renin) A

Elderly (low renin) C D

A - ACE inhibitor/ARB

C - Calcium channel blocker

D- a diuretic - thiazide.

51
Q

for stage 1 hypertension (135/85 abpm)

who do we offer hypertensive drug treatment to and what factors

A

under 80s with 135/85 and with:

target organ damage

  • established cardiovascular disease
  • renal disease
  • diabetes
  • 10 year vascular risk equivalent to or above 10%
52
Q

for stage 2 hypertension (150/95)

who do we offer hypertensive drug treatment to and what factors

A

ABPM > 150/95

offer antihypertensive to any age with stage 2 hypertension

53
Q

for elderly patients >80 with stage 1 hypertension and no other factors/comorbitities what do we do?

A

offer age 80 and over the same antihypertensive at age 55-80 taking into account comorbidities

but blood pressure target different in patients >80 years

target = 145/95

elderly more susceptible to side effects be pragmatic.

54
Q

step 1 treatment hypertension in over 55 years and people of black/African or Caribbean family origin at any age

treatment =

A

calcium channel blocker

or a thiazide - like diuretic

55
Q

step 1 treatment for patients under 55 years

(not African or Caribbean)

not child bearing age

A

offer ACE inhibitor or ARB

56
Q

why would we avoid ACE1 /ARB treatment to under 55s who are:

African or Caribbean

childbearing age

A

African or Caribbean - less effective and significant risk angioedema (glottis, epiglottis, mouth face swelling of the area beneath the skin or mucosa) can be fatal

childbearing - teratogenic initial stages pregnancy and fetotoxic in later stages of pregnancy

57
Q

step 2 treatment hypertension

A

add thiazide type diuretic such as (indapamide to CCD or ACE1/ARB)

58
Q

pregnancy hypertension treatment?

A

Hydralazine

Methyldopa

Labetalol

Nifedipine

**Hypertensive Mums Love Nifedipine**

59
Q

treat stage 3 hypertension (meds)

A

Add Calcium channel blocker, Ace1, diuretic together

60
Q

treating resistant hypertension what treatment/considerations?

A

are there compliance issues (common)

higher dose thiazide-like diuretic if potassium level is higher than 4.5mmol

further diuretic therapy with low dose spironolactone (25mg once daily) if potassium is <4.5mmol

61
Q

medications ACE inhibitors

A

ramipril

perindopril

competitively inhibit the action of angiotensin-converting enzyme

62
Q

contraindications to ACE inhibitors

A

renal artery stenosis (renal failure or infarction)

impaired renal function

hyperkalaemia

hypotension

teratogenic in pregnancy

63
Q

drug to drug interaction of ace inhibitors

A

NSAIDs - precipitate acute renal failure

potassium supplements - hyperkalaemia

potassium-sparing diuretic - hyperkalaemia

64
Q

Angiotensin 2 antagonists (ARBS)

A

losartan, valsartan, candesartanm irbesartan

anhiotensin 2 antagonist competitively block action of angiotensin 2 at angiotensin 1 receptor.

advantage - fewer side effects e.g. cough.

65
Q

Calcium channel blocker medications

adverse reactions + contraindications

A

Amlodipine felodipine - vasodilator - reduce peripheral resistance

verapamil diltiazem - reduce heart rate (rate-limiting) produces some vasodilation

block the l-type calcium channel in monocytes of vasculature and heart

drug reactions: flushing, headache, ankle oedema, indigestion reflux

contraindications - acute MI, Heart failure, bradycardia

  • rate-limiting agents also cause - bradycardia - constipation
66
Q

medication treatment thiazide type diuretics

reactions risk

A

indapamide, chlorthalidone

commonly first-line treatment in mild-moderate hypertension in people of African origin.
can be used in combination with any other antihypertensive agents
proven beneficial in reducing the risk of stroke and myocardial infarction

low dose not common side effects = gout and erectile dysfunction

low sodium

67
Q

what are other less commonly used agents for hypertension (medications)

A

alpha-adrenoceptor antagonist - doxazosin

centrally acting agents - methyl dopa, moxonidine

vasodilator - hydralazine, minoxidil

68
Q

best order treating hypertension ? 55 years

A

start calcium channel blocker

then thiazide-type diuretic

then add ace inhibitor

then add beta-blocker

then if not working add less common drug

69
Q

first-generation beta blocker

A

beta 1 and 2 blockers

  • timolol - propanolol (also treat migraines)
  • nadolol - pindolol -sotalol (also blocks potassium)

side effect - increase intraoccular pressure = glaucoma

bronchoconstriction - asthma problem

70
Q

2nd generation beta-blocker

A

beta 1 receptor

esmolol atenolol metopralol bisoprolol acebutalol

less likely to cause hypoglycaemia

ok for asthma COPD

71
Q

what conditions can generation 1 and 2 beta-blockers also treat?

A

anxiety and thyroid storm

72
Q

generation 3 beta-blockers

A

beta 1 and alpha 1 blocker

labetalol carvedilol

cause vasodilation

can be used for peripheral vascular disease and given in pregnancy

and hypertensive crisis

73
Q

treatment of hypertension for young patients

A

start ACE1

(if childbearing age woman start calcium channel blocker or beta-blocker

then thiazide-type diuretic

then calcium channel blocker

then beta-blocker

74
Q

signs of gestational hypertension

A

hypertension

no proteinuria

75
Q

signs preeclampsia

A

bp rises severely from 20 weeks gestation

bp>40/90

and proteinuria >300mg/24hours

76
Q

meds for chronic hypertension pre-pregnancy

A

hypertensive Mums love nifedipine

nifedipine methyl dopa labetalol atenolol

77
Q

treating gestational hypertension

A

depends on the trimester of pregnancy

nifedipine modified release, methyl dopa, labetalol

78
Q

treatment for preeclampsia

A

treatment for gestational methyl dopa, labetalol, nifedipine

plus iv labetalol or hydralazine or esmolol

79
Q

acute severe hypertension types

A

hypertensive urgency

hypertensive emergency

80
Q

acute severe hypertension types hypertensive emergency:

A

hypertensive urgency

hypertensive emergency - severely elevated bp >180/120 with evidence of acute target organ damage. require admission for bp reduction

called malignant hypertension

cardiac failure, retinopathy e.g.

81
Q

acute severe hypertension types hypertensive urgency :

A

hypertensive urgency

severely elevated bp with NO evidence of acute target organ damage.

patients do not need admission and can be started on dual oral therapy and assessed after 24 hours

also called accelerated hypertension

(amlodipine 5 mg and atenolol 25 mg daily)

*pic below calcium channel blocker - dipine*

82
Q

treatment of hypertensive emergency

A

lower systolic bp by 10-20% within the first hour and then to 160/100mmHg over subsequent 6 hours

more aggressive lowering associated with increased morbidity and mortality.

change to oral meds once target bo achieved wean off iv meds over next 12-24 hours

dont give ARB ACE either

83
Q

what is indicator for rapid BP loweing?

A

normally you do NOT do this

you only do for ischaemic stroke whos bp > 195/110mmHg who are eligible for/who received thrombolysis within previous 24 hours OR bp 220/120mmHg and not ELIGIBLE FOR THROMBOLYSIS

aortic dissection - systolic bo should be rapidly lowered to target between 100-120mmHg systolic

84
Q

what is orthostatic hypotension?

A

bp dro when shifting to a standing

decrease of 20mmGm systolic and/or a diastolic pressure of 10mmHg within 3 minutes of standing,.

85
Q

what is constitutional hypotension

A

young people normally have

permanently low bp

86
Q

causes of orthostatic hypotension

A
  • age

diabetes

antihypertensive drugs

auto-immune systemic disease

neurological syndromes: pure autonomic failure, multiple systems atrophy, Parkinson’s disease

87
Q

if you see ST elevation - what is the best move?

A

primary

reestablish blood flow - go to cath lab for stent PCI (percutaneous coronary intervention)

give thrombolysis blood thinner if you cannot get to cath lab.

88
Q

risk of thrombolysis

A

bleeding

avoid when had recent stroke haemorrhage or intracranial bleed. recent surgery, on a blood thinner. outweigh the risks

89
Q

investigations got MI

A

repeated ECg

check biomarkers - troponin renal function, cholesterol, harmoglobin

90
Q

treatment for pain in MI

A

nitrates (GTN) - dilates or relaxes coronary artery (wont help complete blockage artery)

morphine for pain

91
Q

treatments for MI (initial)

A

platelets

asprin + 2nd antiplatelet clopidogrel tecagrrlor presugel

anticoagulant - heparin or low molecular weight heparin or fondaparinux

92
Q

other treatments to get patients started on for MI

A

beta-blockers - reduce work on heart, reduce risk of another event

statin - helps lower cholesterol

ace inhibitor - helps heart recover

93
Q

normal blood flow is __

A

laminar

94
Q

in blood cells where does the plasma flow and where do cells flow?

A

plasma on outer of lumen, cells central

95
Q

is regard to blood flow, what is stasis?

A

stagnant blood flow

96
Q

in regard to blood flow, what is turbulent flow?

A

abnormal, forceful and unpredictable flow

97
Q

what is a thrombus

A

formation of solid mass from the constituents of blood within vascular system during life

98
Q

normal artery

A

big lumen nothing wrong with intima, media or adventitia

99
Q

atheromatous coronary artery

A

lumen is smaller at rest, reducesin size. lumen taken up by atheromatous plawue

part calcification causing destruction

100
Q

what is the pathogenesis of thrombosis

A

endothelial injury

stasis or turbulent blood flow

hypercoagulability of blood

101
Q

pathogenesis of thrombosis

A

atheromatous coronary artery turbulent blood flow loss of intimal cells, denuded plaque collagen exposed, platelets adhere fibrin meshwork RBCs trapped alternating bands (lines of Zahn) further turbulence and platelet deposition propagation consequences

102
Q

the biggest risk for atherosclerosis

A

hypocholestraemia

histology fibrin buildup

103
Q

what is ischaemia

A

lack of blood supply to tissuea leading to inadequate o2 supply (hypoxia)

104
Q

types of hypoxia

A

hypoxic hypoxia

anaemic hypoxia

cytotoxic hypoxia

stagnant hypoxia

105
Q

factors affecting 02 supply

A

1 inspired o2 2 pulmonary function 3 blood constituents 4 blood flow 5 integrity of vasculature 6 tissue mechanism

106
Q

what is the cause of ischaemic heart disease in relation to blood flow

A

supply issues: coronary artery atheroma, cardiac failure (flow) pulmonary function - other disease or pulmonary oedema (left ventricular failure) anaemia, previous MI

Demand issues: heart has high intrinsic demand, exertion/stress

107
Q

what is atheroma/atherosclerosis

A

localised accumulation of lipid and fibrous tissue in intima of arteries

108
Q

effects of ischaemia

A

cell - different tissue variable 02 requirement and variably susceptible to ischaemia

cells with a high metabolic rate

cells with low metabolic rate

109
Q

effects of ischaemia

A

dysfunction

pain

physical damage

specialised cells

infarction

110
Q

what is infarction

A

ischaemic necrosis with a tissue/organ in living body produced by occlusion of either arterial supply or venous drainage

111
Q

aetiological examples of infarction

A

thrombosis

embolism

strangulation e.g. guy

trauma - cut/ruptured vessel

112
Q

appearance of infarcts after 24-48 hours?

A

pale infarcts: myocardium, spleen, kidney solid tissues

red infarcts: e.g. lung, liver, loose tissue, previously congested tissue; second/continuing blood supply, venous occlusion

113
Q

immediate treatment for MI

A

Medicine 1 (Year 1) (15 decks)

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