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Cardio and Resp diseases > Secondary hypertension > Flashcards

Secondary hypertension Flashcards

1
Q

What are some causes of secondary hypertension?

A
  • renal disease (salt/H2O imbalance)
  • adrenal tumours (aldosterone)
  • aortic coarctation (narrowing of aorta)
  • Steroids, drugs, Rx
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2
Q

What are 6 determinants for secondary hypertension?

A
  • Renal diseases (e.g. Glomerulonephritis, diabetic nephropathy)
  • Vascular causes (e.g. Renal artery stenosis)
  • Hormonal abnormalities (e.g. Conn’s syndrome, Cushing’s syndrome, Pheochromocytoma)
  • Drugs (Contraceptive pill; liquorice)
  • Pregnancy (Pre-eclampsia)
  • Genetic disorders
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3
Q

What is glomerulonephritis?

A

Inflammation of glomeruli
• Can be acute or chronic
• Kidney becomes contracted and granular – due to cortical atrophy
• Some diseases induce this
• Causes fluid imbalance and swelling in the lower limbs

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4
Q

What are the causes of endocrine hypertension?

A

In the Adrenal cortex
• Adrenal adenoma producing aldosterone (Conn’s syndrome) – can be due to benign tumour
• Adrenal hyperplasia – can be due to benign tumour
• Cushing’s syndrome excess cortisol increasing adrenalin’s vasoconstrictive effect

Adrenal medulla
• Pheochromocytoma (adrenalin secreting tumour)

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5
Q

How can endocrine hypertension be treated?

A

Tumours can be removed and patients can be cured of secondary hypertension

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6
Q

What drugs can induce hypertension?

A
  • NSAIDs
  • Oral contraceptives
  • Alcohol
  • Cocaine
  • Erythropoietin
  • Glucocorticoids
  • Ginseng, yohimbin
  • Tyramine and MAO inhibitors (antidepressants)
  • Angiogenesis inhibitors
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7
Q

What does kidney cancer do (in terms of blood vessels) and what drugs are used for it?

A
  • It’s highly angiogenic and metastatic tumour – induce blood vessel growth
  • Antiangiogenic drugs inhibit growth of new vessels
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8
Q

How does angiogenesis take place in tumours?

A
  • Angiogenesis - formation of new blood vessels is essential for solid tumour growth and metastasis
  • Regulated by proangiogenic soluble mediators such as vascular endothelial growth factor (VEGF – vascular endothelial growth factor)
  • Tumours secret VEGF and they act on nearby capillaries causing them to grow and form new vessels
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9
Q

How do antiangiogenic drugs stop angiogenesis?

A

Antiangiogenic drugs that block the VEGF signalling pathway prolong progression free survival in several cancers and are now in broad clinical use

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10
Q

What is a side effect of antiangiogenic drugs?

A

Hypertension is the most common CVS toxicity of this therapeutic class affecting between 19%-67% of patients

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11
Q

What is the evidence that VEGF is involved in maintaining vascular tone?

A
  • Hypertension - Low VEGF/VEGF inhibited

* Hypotension - High VEGF

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12
Q

What are the primary receptors in the VEGF signalling pathway?

A
  • Primary receptors: VEGFr1, VEGFr2, VEGFr3

* Sit on endothelial cells with co-receptors

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13
Q

What is the most common VEGF?

A
  • VEGFA the most common VEGF but VEGFB/C/D also exist

* They bind to receptors and initiate blood vessel growth/formation from old vessels

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14
Q

What does VEGF-A binds to?

A

VEGF-A is the main component that binds to VEGFR-1 and VEGFR-2 with VEGFR-2 having predominant role in cell signalling

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15
Q

What are VEGF co-receptors?

A

Neuropilins (NRP1, NRP2) are VEGF co-receptors but can also signal independently

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16
Q

What are the functions of VEGF-B, VEGF-C and VEGF-D?

A
  • VEGF-B has restricted angiogenic activity e.g. in heart

* VEGF-C and VEGF-D involved in vasculogenesis and lymphangiogenesis

17
Q

What happens when VEGF binds to VEGF-2?

A

Through binding to its receptor there’s multiple pathways activated

  • Endothelial cell induces relaxation effect through NO – causes vasodilation
  • Angiogenesis induced through PIP2 calcium signalling
  • Protein Kinas B pathway activated – cell survive increased, apoptosis reduced
  • RAS/RAF/MEK/MAPKinaes pathway activated – increases gene expression, transcription and cell proliferation of endothelial cells, can induce angiogenesis
18
Q

What happens when VEGF is blocked?

A

Blocking VEGF binding blocks a lot of the processes – NO induction prevented, vascular tone increases

19
Q

What are different anti-angiogenic therapies?

A
  • Anti-VEGF
  • Receptor tyrosine kinase inhibitors
  • mTOR blocker
20
Q

Mechanism of anti-VEGF?

A
  • Binds to VEGF molecule

* Prevents from binding to receptor

21
Q

Mechanism of receptor tyrosine kinase inhibitors?

A

Small molecule inhibitors that target the receptors

22
Q

Mechanism of mTOR blocker?

A
  • mTOR is a protein in tumour cells that makes VEGF

* blocking it prevents VEGF synthesis

23
Q

Which drug causes the most/highest frequency of hypertension as a side effect?

A
  • VEGF inhibitors e.g. axitinib – 90% incidence of hypertension, cause the most hypertension
  • because they’re very potent
  • This side effect is known as an on-target effect (as opposed to off target side effect) – the drugs effects are specifically because of its target.
  • Also known as mechanism-dependent on-target toxicity – cause the effect is due to the mechanism of the drug
24
Q

How can hypertension induced by antiangiogenic drugs be treated?

A

Removal of anti-angiogenic leads to rapid decrease of blood pressure

25
Q

What are the mechanisms of antiangiogenic drug induced hypertension?

A

Not yet known!

Possibly:
• Downregulation of NOS/NO ↓ vasodilation
• Increase ET-1 ↑ vasoconstriction
• Increase bioavailability of ROS ↑ vasoconstriction, vascular remodelling
• EC dysfunction/apoptosis/rarefaction ↑ peripheral resistance

26
Q

What are the different pregnancy related hypertension?

A

Most common complication of pregnancy and leading cause of morbidity and maternal mortality

  • Chronic hypertension (already before pregnancy)
  • Gestational hypertension or pregnancy-induced hypertension (PIH): New onset without the presence of protein in the urine
  • Preeclampsia: Hypertension and proteinuria (have protein in urine)
  • Eclampsia: Hypertension induced onset of seizures
27
Q

What is nail bed capillaroscopy?

A
  • Capillary density as a measurement of vascular rarefaction

* Reduced density could be correlated with pregnancy induced hypertension

28
Q

What is capillary rarefaction associated with?

A
  • Capillary rarefaction is associated with preeclampsia
  • Associated with soluble circulating decoy receptors for VEGF (sFLT-1), and others (e.g. sENG) – they prevent VEGF from binding to its receptor (thus increase hypertension)
29
Q

What is VEGF associated with?

A

maintenance of normal vascular homeostasis

30
Q

What happens if there is impaired VEGF signalling?

A

Impaired VEGF signalling mediated by presence of antiangiogenic factors leads to EC dysfunction

• May lead to reduction in cell numbers and cell death

31
Q

What is found in maternal plasma?

A

In maternal plasma there’s potential mediators that may increase soluble decoy receptor – may be from plasma

  • AT1-AA
  • TNF-a
  • HIF-1a

Cardio and Resp diseases (29 decks)

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