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CDL301 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Rationale for treatment and why?

A

Important preventable cause of premature morbidity and mortality
Why?
1. A symptomatic- people don’t know they have it
2. drug therapy- could cause side effects

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2
Q

people with hypertension are at major risk for?

A
  • stroke- block artery supplying brain
  • MI- atherosclerosis build up, thrombosis, Heart attack
  • HF- high HR, afterload increase
  • chronic renal failure- kidneys control this through renal output and blood flow
  • cognitive decline - dementia, small vessel changes in brain ischaemia
  • premature death
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3
Q

Hypertension facts

A

Increasing systolic BP by 2mmHg is associated with :

  • 7% increase mortality- IHD
  • 10% increased mortality from stroke
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4
Q

Risk factors for increased BP

A
  • height and age
  • normally distributed through population
  • top of normal range there is more risk to get high and would benefit from treatment
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5
Q

Diagnosing suspected hypertension- clinical

A

Clinical BP = 140/90 or higher

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6
Q

quality statement for hypertension

A

people with suspected hypertension are offered aambulatory blood pressure monitoring (ABPM) to confirm diagnosis of hypertension

  • time against BP
  • every half hour and hour at night
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7
Q

Stages of hypertension

A

Stage 1

  • clinic= 140/90
  • ABPM-135/85

Stage 2

  • clinic= 160/100
  • ABPM= 150/95
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8
Q

What are the primary treatments for hypertension

A
  1. lifestyle modification

2. antihypertensive drug therapy

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9
Q

Treatments for secondary hypertension

A

LOOK AT PATIENT

  • young person, resistant BP, signs and symptoms underlying
  • reflective of another problem
  • endocrine, hormonal, kidney disease
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10
Q

Who to offer antihypertensive treatment to stage 1 people under 80 with one of these problems:

A
  1. target organ damage- eye, heart, kidney
  2. established CVD
  3. renal disease
  4. diabetes
  5. 10+ year of cardiovascular risk over 20%

*or anyone with stage 2

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11
Q

goal BP to have

A

Under 80 - clinic <140/90, ABPM <135.85

over 80- clinic <150.90, ABPM < 145/85

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12
Q

Why are the elderly BP targets slightly higher?

A 
Blood vessels lose compliance (arteries_
arteries distend (stiffer) and contract back to form secondary pulse wave,
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13
Q

Mechanism of BP control

Targets for therapy

A
  1. CO and periphery resistance - co= SV x HR
  2. interplay between
    a) renin- angiotensin-aldosterone system
    b) sympathetic NS
  3. local vascular vasoconstrictor and vasodilator mediators
    - peripheral resistance
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14
Q

Angiotensin II vasoconstrictor effects

A
  1. vascular growth
    - hyperplasia
    - hypertrophy
  2. salt retention
    - aldosterone release
    - tubular Na reabsorption
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15
Q

Interfere

A 
ACE inhibitors 
ARB 
BB 
renin inhibitor 
centralling acting 
ca channel blocker 
alpha blocker 
aldosterone antagonist
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16
Q

What are the main clinical indications of ACE inhibitors?

A

Hypertension, HF, diabetic and nephropathy

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17
Q

What are ace drugs?

A

Ramipril, perindopril, enalapril, trandolapril

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18
Q

What are sartan drugs?

A

same mechanism of action as ACE inhibitors, vary due to duration and cost
ARB

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19
Q

What are the main clinical indications for ARB inhibitors?

A

hypertension, diabetic and nephropathy and HF

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20
Q

ARB drug names

A 
Candesartan 
valsartan 
Losartan 
IREsartan 
telmasartan
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21
Q

what are the main adverse effects of ARB inhibitors?

A 
Sympotomatic hypotension
hyperkalaemia 
potential for renal dysfunction 
rash 
angio-oedema 
* Contradicted in pregnancy, generally very well treated
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22
Q

How does ARB work?

A

it inhibits angiotension II to AT1 receptor
highly specific blocker
Block ACE reduce angiotensin II so substrate of enzyme increase so overcome drug effect as it competes

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23
Q

What are the main indications for calcium channel blockers? and the drugs you would use with each one

A

hypertension- amlodipine, felodipine, nifedipine, lacidipine
Ischaemic heart disease and arrhythmia- diltiazem and verapamil
attach the peripheral resistance with CCB

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24
Q

L type calcium channel blockers

A
  1. Dihydropyridines-: nifedipine, amlodipine, felodipine, lacidipine
  2. Phenylalkylamines: verapamil
  3. Benzothiazepines: diltiazem
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25
Q

Action of L type Ca channel blockers- dihydropyridines

A

Preferentially affect vascular smooth muscle
peripheral arterial vasodilators
Not used as much for hypertension as they are shorter acting

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26
Q

Phenylaklylamines action

A

Main effects on the heart
negatively chronotropic and ionotropic
Has the opposite effect, has major effect on heart (conducting tissue and muscle of heart)- used for arrhythmias and angina

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27
Q

Benzothiazepines Ca channel blocker action

A

Intermediate heart and peripheral vascular affects

halfway

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28
Q

4 main adverse effects of Ca channel blockers

A
  1. due to peripheral vasodilation= flushing, headache, oedema, palpatations
  2. due to negatively chronotropic effects= bradycardia (feel faint), atrioventricular block
  3. negative ionotropic effects= worsening of cardiac failure
  4. verapamil causes constipation
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29
Q

Name 3 other antihypertensives

A
  1. a-1 adrenoreceptor blocker
  2. centrally acting anti-hypertensives
  3. direct renin inhibitor
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30
Q

A-1 adrenoreceptor blockers drug names and how they work

A
  • doxazosin, indoramin, terazosin, nazosin
    peripheral vasculature in under sympathetic tone- A blocker relaxes that reduces BP
    Postural hypotension= problem
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31
Q

Centralling acting anti-hypertensives names and how they work

A
  1. Monoxidine- imizoline type 1 receptor agonist
  2. methyldopa- (old and used in pregnancy)- activates pre synaptic alpha 2 receptors to decrease noradrenaline release and competitive inhibitor of dopa decarboxylase
  3. Clonidine- activates pre synaptic alpha 2 receptors ti decrease noradrenaline
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32
Q

direct renin inhibitor names and and effect

A 
Aliskiren 
- hyperkalaemia= raised blood K 
- dizziness 
arrhythmia- joints, aches and pains 
- diarrhoea 
- caution with other RAA inhibitors, combination not recommended
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33
Q

treatment steps for hypertension

A

step 1
under 55- ACE or angiotensin blocker
over 55- Ca channel blocker

Step 2
- ACE/ARB + CCB

Step 3
- ACE/ARB+CCB+ thiazide- like diuretics

Step 4

  • resistant hypertension
  • spironolactone
  • high doze thiazide diuretic
  • alpha and beta blockers
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34
Q

What is our pulmonary circulation?

A

Highly dense network of arteries and veins
capillaries allow gas exchange
Right= Lung
Left= to body

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35
Q

What is pulmonary hypertension?

A

increase in blood pressure from lungs
gas exchange is much less efficient in the lungs
Less O2 around the body -double pressure that would happen normally

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36
Q

Pulmonary artery pressure in normal and PAH?

A

pulmonary artery
- normal= 15-30mmHg
- Pulmonary artery= 35->100
same for the right ventricles

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37
Q

What is pulmonary arterial hypertension?

A

cause by an increased mPAP in PH

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38
Q

consequences of pulmonary hypertension?

A
  • right ventricular hypertrophy
  • right heart failure
  • high morbidity and death ~2.8 years
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39
Q

What causes pulmonary hypertension?

A 
shunting of systemic blood pressure 
thrombus formation
sustained pulmonary vasoconstriction
pulmonary vascular remodelling 
* conditions or idiopathic
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40
Q

What is the most common form of pulmonary hypertension?

A

schistosomiasis
represents 1%
autoimmune disorders PH can occur in up to 15%

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41
Q

What happens if there is a hole in the heart?

A

lots of pressure build up on right side of the heart

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42
Q

If there is a blood clot>

A

Pulmonary embolism blocks blood flow and increases pressure of blood

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43
Q

Sustained pulmonary vasoconstriction?

A

vessels constricted so don’t relax and narrow areas of blood flow

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44
Q

Remodelling causing PAH?

A

cells not in normal state
constricted
can trigger number of things to happen

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45
Q

Clinical presentation of PAH?

A

24hour old female
progressive external breathlessness and chest pains
syncopal episode after excretion

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46
Q

How can you see if someone has PAH?

A

ECG= right heart strained, raised pulmonary artery systolic pressure and dilated right heart
CxR= Normal lungs, increased PA and heart size
lung function tests= normal lung function
+ CTPA/HRCT/MRI/Q scan

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47
Q

What is diastolic and systolic?

A 
Diastolic= between beats 
systolic= pressure ion contraction
48
Q

What is the mean pressure?

A

2/3 diastolic pressure + 1/3 systolic pressure

49
Q

Pulmonary vascular resistance

A

(mPAP- PAWP)/ cardiac output
PAWEP= pulmonary arterial wedge pressure
usually patients have low CO and pressure drop

50
Q

haemodynamic definition of PAH

A

mean artery pressure >25mmHg
PAWP/LVEDP < 15mmHg
PVR> 3
no evidence drugs work in any other groups

51
Q

What are the 5 groups of hypertension

A
  1. pulmonary arterial hypertension
  2. PH-left heart
  3. PH lung disease/hypoxia
  4. chronic thromboembolic pulmonary hypertension
  5. multifactorial/ unclear
52
Q

Pulmonary arterial hypertension (group 1) causes

A

idiopathic, heritable, drugs, HIV, portal hypertension, congenital heart disease, schistosomiasis haemodynamic anaemia

53
Q

PH-left heart (group 2) causes

A

Systolic dysfunction
diastolic dysfunction
Valvular disease

54
Q

PH lung disease/ hypoxia (group 3) causes

A

interstitial lung disease
sleep disorder
alveolar hypoventilation

55
Q

Chronic thromboembolic pulmonary hypertension (group 4) causes

A

operable
inoperable
- result of embolism
- happens when the blood clot goes, 1st/2nd branches easier to get to, remove with surgery - most distal is more difficult to treat

56
Q

Group 1 prevalence and incidence

A 
15-50% per million  population 
2-3 per million per year 
-40% IPAH- don't know why 
- 10% hentable disease- mutation in gene 
- 40% APAH- 4x more common in women
57
Q

What drug lead to an epidemic?

A 
Diet pills 
animal incidence of 25-50 
PH with LHD is common 
PH with lung disease is common 
CTEPH= 40% of people after PE
58
Q

PAH pathogenesis- compare what is seen in scans of a healthy lung compared to PAH?

A
  • contrast imagine and MRI show crescent shape, 200 micron size in a healthy lung
  • muscle stimulated to go from contractile state where they activate cell cycle and start proliferating

Whereas PAH lung

  • unchecked proliferation of cells on muscle cells, contractile to unregulated proliferation state
  • continually progressive
59
Q

mechanism of PAH

A
  1. vasoconstrictive mediators such as ET-1, thromboxane A2, Prostacylin and nitric oxide are dysregulated in PAH
  2. Fatcors drive constriction and stimulate the initial proliferative response as resident PASMC and myofibroblast
  3. increase turnover of ECM, endothelial remodelling- narrowing of lumen of artery
  4. ultimately the remodelling requires the development of vasa vascrum to fuel this process- occlusion of lumen and cessation of blood flow
60
Q

What drives remodelling?

A

Fatcors- BMPR2, Ion channels , endothelium, 5-HT, proteases. elastases. MMPs and TF

61
Q

How much of a patients pulmonary vasculature tree can be lost before they become symptomatic?

A

2/3 r

remodelling has consequences on heart

62
Q

What happens if there is an increase in resistance to blood flow and increase afterload?

A

causes the right ventricle to undergo hypertrophy, to where it impinges the LV causing cardiac output to fail

63
Q

Images of the different types of lung- SMC

A 
Concentric= onions, made up of layers- endothelial in middle and some outside, collateral formation to cope with blockage
plexiform= rarer, end stages, haemodynamic pressure is too much so get inflammatory and apoptotic cells- loss of SMC
64
Q

Elastin and ECM degradation

A

loss of elastin

  • increases vascular stiffness
  • promotes SMC proliferation and EC apoptosis
  • loss of vascular integrity/ vascular leak
65
Q

What happens if there is extensive neointimal PA lesion

A

Cells held in place by in and external lamina (rings of matrix)- if this lamina is burst it stimulates vessels/cells to grow and divide, breakdown elastin and increase proliferation

66
Q

pulmonary artery remodelling in PAH

A
  • elastin, EC and SMC
  • EC dysfunction/ apoptosis- ecm breakdown
  • Growth factors inflammation
  • proliferation/migration
67
Q

What happens in response to injury?

A
  1. break in endothelial layer that permits extravasation of serum factors in the subepithelium which stimulates VSMC to produce endogenous vascular elastase
  2. proteolytic action of elastase is enhanced by activation of MMPs - found at site of vascular remodelling
  3. results in liberation of matric bound GF-
  4. transcription and EC deposition of TN is associated with amplification of SMC proliferation
  5. elastase stimulates SMC migration through the degradation of elastin stimulating production of glycoprotein fibronectin
68
Q

Falling cost of whole gene sequencing

A

now around 1000 per patient

start using this to treat diseases- gene therapy

69
Q

What were the first identification of mutations in PAH

A

heterozygous germline mutation in BMPR2 encoding TGF-B receptors
cause familial primary pulmonary hypertension

70
Q

KLK1 GENE

A

Subgroup of serine proteases having diverse physiological function
potential in noval cancer bromance

71
Q

GGCX gene

A

codes enzymes that catalyses post transcriptional modification of Vit K (coagulation)- haemostasis mutations cause coagulation defect or Pxe disorders

72
Q

Identification transcriptional regulation in disease

A

BMP

73
Q

Vasodilatory drug treatment in PAH- got drug to target the 3 pathways

A
  1. endothelin pathway
    - signalling via G protein and PLC converts PIP2 into IP3
    - causes ca influx and vasoconstriction/ proliferation
  2. nitric oxide
    - endogenous vasodilator produced by endothelial cells
    - guanylate cyclase converts CTP- cGMP via PKG inhibits Ca influx
  3. prostaglandin pathway
    - endogenous vasodilator
    - acts on IP receptors via G protein, activates cAMP and PKC to promote SMC relaxation
74
Q

Vasodilator drugs

A

ERA- endothelium receptor antagonist- 2001, 2007, 2013
PDE-5i- Phosphodiesterase- 5 inhibitor- 2005, 2008
sGC stimulator- soluable guanylate cyclase- 2013
prostanoids- 1995- 2013
IP receptor agonists= 2015

75
Q

3 major pathways involved

A
  1. endothelium pathway
  2. nitric oxide
  3. prostacylin
76
Q

Calcium channel blockers approved therapy for PAH- response and side effects

A

diltiazem and nifedipine

  • evidence only in patients with acute vasodilator response= inhaled NO given during RHC, drop in mean PAP to 10mmHg
  • side effects= systemic hypotension, bradycardia, peripheral odema
77
Q

Phosphodiesterase type 5 inhibitors

A

sildenafil (Viagra) and tadalfil (adcira)
-PKG- multiple action
promoting vasodilation= activates MLCP, K channels and inhibits
K dependent Ca channel increasing

78
Q

PDE5 inhibitors

A

first line monotherapy

  • Viagra patient experied
  • avoid in patients on nitrates
  • useful combination with inhaled iloprost
79
Q

Side effects of PDE5 inhibitors

A 
headache 
flushing 
epistaxis
altered colour vision 
rarely- non ischaemic optic neuropathy and priapism
80
Q

Riocigulant

A

New class of agents
stimulate guanylyate cyclase
licensed for CTEPH
avoid combination with PDE5

81
Q

Side effects of riociguat

A

headaches
dizziness
diarrhoea
indegestion

82
Q

Endothelium receptor antagonists- names of drugs and what are they ?

A

Bosentan
ambrisentan
macitentan
endothelium converting enzyme (ECE) catalyzes conversion of ET to inactive precursor
ET binds ET and ETb - GPCR family ubiquitously distributed in the body

83
Q

Effects of ET

A

determined by the receptor type they bind
Binding ETa and ETb on VSMC= vasoconstriction
Binding ETb on endothelial cells= vasodilation
induce fibrous, contraction and proliferation depending on location

84
Q

ERA

A

often given in combination of oral therapy

added to PDE5 inhibitor

85
Q

Side effects ERAs

A 
abnormal liver function- bosentan 
headache 
nasopharyngitis 
peripheral odema 
anaemia
86
Q

What is macitentan called?

endothelian receptor agonist

A
  • slower receptor dissociation rate

- enhanced tissue penetration due to greater lipid solubility

87
Q

What is seraphin?

A

largest clinical trial
742 patients
delayed clinical worsening

88
Q

What can receptor inhibition help to do?

Problems with the drugs?

A

Can overcome with prolonged ET-1 stimulation

underlying system with increased expression of agonist (competition) so efficacy of drug decreases

89
Q

What are prostacyclin derivatives (4th approved therapy for PAH)

A

Epoprostenol- IV
Iloprost - inhaled
treprostinil- IV
Beraprost- oral

90
Q

Prostacyclin pathway mechanism?

A

Arachadonic acid goes to prostaglandin H2 which activates Prostacylin (PGI2)
this increase IP2 which stimulates cAMP
- vasodilation and antiproliferation

91
Q

What happens when there Is vasodilation of the pulmonary and systemic vascular beds?

A
  • lower PAP+ PVR
  • reduce ventricular afterload
  • inhibits proliferation of human pulmonary artery SMC in vitro
92
Q

Why was prostacyclin pathway therapy not used earlier ?

A

IV

cost

93
Q

What are stable prostacyclin analogues?

A

increased stability
longer half life
Only managed to get from 2 mins to a couple of hours - give often as not sustainable

94
Q

What are the problems of prostacyclin therapy?

A 
tolerance 
diarrhoea, flushing, headaches 
cost - £110k per person per year 
continuous delivery 
line related complications 
made up daily and has to be kept cold
95
Q

Problems with inhaled iloprost?

A

6-9 inhalations daily- compliance
side effects= diarrhoea, headache, cough
thereapy stopped overnight

96
Q

problems with treprostinal- delivered?

A

Erthymia- redmess of skin, skin injury and infection

induration- hard spot formed

97
Q

What is selexipag?

A

Noval new non- prostanoid IP receptor agonist
in phase 3 clinical trial
drug hydrolysed in body

98
Q

What is the max dose for patients taking selexipag?

A

Max dose is the best dose for the person to have- tolerance and efficacy
Personalise

99
Q

Prostacyclin selectivity?

A

Poor
usually select IP3 but can also bind and activate prostanol receptor- EP3
These receptors counteract the IP signalling by decreasing cAMP through GI - thus inhibiting relaxation

100
Q

Why can an IP receptor combat disease?

A

The Ip receptor is in PAH so down regulation can combat

least selective to receptors they bind to

101
Q

Binding to IP

A

IV forms bind slightly different receptors they bind the IP1 to cause vasoconstriction and cell proliferation
Least selective for receptors they bind

102
Q

Other treatments for PAH

A

Anticoagulation-recommend to patients on IV, mainstay of treatment for CTEPH
oxygen- based of COPD trial, los O2 administered at rest
diuretics- treat odema due to right HF

103
Q

What is the efficacy of current treatments?

A

5 year survival with 50%

still 12/13% drop for 3/4 years when combined treatment in comparison to mono

104
Q

What are disease triggers in pulmonary vascular remodelling?

A

Host factors
genetic mutation
sex hormones

Acquired

  • somatic mutation
  • inflammation
  • hypoxia
  • drug

injury

  • shear stress
  • pathogens
105
Q

Molecular consequences of pulmonar vascular remodelling?

A 
impaired BMP/TGF signalling 
dysregulated miRNA
release GF
DNA damage 
metabolic changes 
increased cytokine production
106
Q

Cell/ tissue phenotype in pulmonary vascular remodelling

A 
Endothelial dysfunction 
EC apoptosis 
SVC proliferation
fibroblast proliferation
Ecm remodelling- elastin, collagen and fibronectin
107
Q

Parr pathology in pulmonary vascular remodelling

A 
pulmonary vasocontriction 
hypertrophy 
intimal thickening 
plaxiform lesioning 
vascular stiffness 
perivascular inflammation
108
Q

Targeting BMP signalling with FK506/ Tacrolimus induced BMPR2 signalling

A

looked to see if drugs could stimulate downstream of receptors in the signalling pathway
take animal- give drug- reverse so of symptoms

109
Q

BMP9 as novel therapy

A

BMP9 effects on endothelial cells in PAH
inhibits endothelial cell proliferation induced by VEF-A
protects endothelial cells from apoptosis, stabilises endothelial network

110
Q

What does BMP9 do?

A
  • inhibits endothelial cell proliferation induced by VEF-A
  • protects endothelial cells from apoptosis, stabilises endothelial network
  • inhibits endothelial cell permeability induced by inflammation
  • increase expression of BMPR-2
111
Q

Sex hormones in PAH

A

gender bias
more women than men with PAH
acromatase- increase in lungs

112
Q

Anaztrazole in PAH

A

safe and efficacy with patients with PAH
double blind placebo test
phase 2 84 patients

113
Q

Oestrogen blockage for PAH

A

Tamoxifen therapy to treat pulmonary arterial hypertension
double blind, random
4 weeks

114
Q

Endpoints in oestrogen blockage trial

A

1- change in TAPSE

2- ECKLO metrics- oxidant stress sex hormones

115
Q

Elastase inhibitor in PAH

A

relative elastin deficiency despite HNE’ase-

  • breakdown of elastin lamina
  • elastin inhibited to treat PAH
116
Q

OPG/TRAIL axis

A

Pathway related to TNF
2 proteins upregulated with PAH patients
higher level= worse prognosis
anti-OPG therapeutic antibody- give with existing drugs

117
Q

Potential targets to modulate pulmonary vascular remodelling

A 
inflammation 
fibrosis 
DNA damage 
metabolism 
kinase inhibitors

CDL301 (7 decks)

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