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AC1 (Izzy) > Week 1: Pathophysiology and Tx HTN 2 > Flashcards

Week 1: Pathophysiology and Tx HTN 2 Flashcards

1
Q

List the classes of drugs to tx. HTN

A

1) Diuretics
2) Beta Adrenoreceptor blockers
3) Calcium channel blockers
4) ACE inhibitors

Angiotensin 11 receptor blockers (ARBS)

Direct renin inhibitors (DRI)

Alpha adrenoreceptor blockers

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2
Q

How do diuretics reduce BP?

A

Diuretics act on the renal tubule, promoting the excretion of Na+ and water, therefore reducing blood volume and blood pressure.

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3
Q

Name two thiazide diuretics

Name two thiazide- like diuretics

A

Thiazide –> Bendroflumethiazide

hydrochlorothiazide

Thiazide- like –> Indapamide

chlortalidone

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4
Q

How do thiazide/ thiazide like diuretics act?

What are two key benefits of thiazide medications?

A

They act at distal convolted tubule

Inhibit Na+/ Cl- transport from the lumen

increase sodium and water excretion

increase potassium loss

Key benefit: Vasodilate by potassium channel activation (therefore reduce BP)

And proven to reduce heart attack and stroke

Adverse effects: high uric acid and gout; low potassium and low sodium, raised glucose and cholesterol

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5
Q

Name two types potassium sparing diuretics

Name two drugs from each class

What are there uses?

What are their side effects?

A
  • Aldosterone antagonist : Spironalactone, eplerenone
  • ENac (Epithelial Na+ channel) blocker: Amiloride, Triamterene
  • They are weak diuretics, useful in combo with other drugs
  • useful against aldosterone excess
  • SE’s:
    • High serum potassium
    • Low sodium
    • Gynaecomastia w spironolactone (Blocks aldosterone by binding MR receptor, but also decreases testosterone production, increases conversion of testosterone to estradiol and displaces estradiol from sex hormone binding globulin.)
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6
Q

What are the effects of beta adrenergic receptor blockers?

A
  • Negative Inotropic effect, decrease contractility
  • Negative chronotropic effect, decreases heart rate
  • AV nodal conduction –> decreases velocity
  • Also promote smooth muscle relaxation –> GI, Vascular, bronchial, ciliary
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7
Q

What are the two types of beta adrenergic receptor?

What are their downstream signalling pw’s?

A

Beta 1 and Beta 2

Beta 1: coupled to GPCR, activates Adenylyl cyclase, converts ATP –> cAMP, activates protein kinase –> Increase force of contraction, HR and AV nodal conduction velocity

Beta 2: coupled to Gs protein, also activates AC, also increases cAMP–> GI, vascular and brocnial/ ciliary SM relaxation

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8
Q

What are the two types of beta adrenergic blockers?

A

1) Cardio selective e.g. just beta 1, atenolol
2) non selective beta 1 and beta 2, e,g, propanolol –> careful w non selective as they can precipitate asthma by blocking bronchial SM relaxation

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9
Q

What is the main use of beta blockers?

Indications of beta blockers?

A

Beta blockers prevent both heart attack and strokes by reducing blood pressure.

Indications: tachycardia, hypertension, myocardial infarction, congestive heart failure, cardiac arrhythmias, +(coronary artery disease, hyperthyroidism, essential tremor, aortic dissection, portal hypertension, glaucoma, migraine prophylaxis)

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10
Q

What are the SE’s of Beta blockers?

A

Beta BLockers Have Really Extreme Ramifications

Bronchospasm

Bad Dreams

Lethargy

Heart Failure

Raynaud’s

Explosive diarrhoea

Reduced HDL cholesterol

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11
Q

Blockade of calcium channels: Where do Ca2+ channel blockers act?

A

Act on:

Vascular SM –> vasodilate, reduction in peripheral resistance

Cardiac myocytes and SAN/AVN –> decreased force of contraction, decreased HR

Renal tubules –> mild natriuretic and diuretic effect

Regulate influx of Ca2+ into cells

Stimulate smooth muscle and cardiac myocyte contraction

Contribute to pacemaker currents and AP’s

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12
Q

By blocking Calcium entry CCB’s cause??

A
  • Vascular SM relaxation
  • Decreased myocardial force generation
  • Decreased HR
  • Natriuresis and diuresis
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13
Q

What are the 3 types of CCB?

A

Dihydropyridines

Diltiazem

Verapamil

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14
Q

Compare and contrast the three types of calcium channel blockers

A

Dihydropyridines: Powerful vasodilators, mild natriuretic effect, tachycardic due to vasodilation (therefore increase preload and HR) increase Sodium/ Water excretion, can work with BB

Diltiazem: Long acting used for BP, vasodilator moderate, no effect on Na+/H2O balance, mild bradycardic effects, good in combination when there is intolerance to others, can work with BB

Verapamil: bradycardic (like beta blocker), cannot be used with beta blocker (contraindication), precipitates Heart block

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15
Q

Verapamil: , class, Two main effects, SE’s

A

Verapamil Class: Type 4 antiarrhythmic agent, Ca2+ channel blocker

Effects: 1) Arterial dilator 2) major cardiac inhibitory effects

Side effects:

Heart failure, Heart block (especially with beta blocker)

Peripheral oedema

constipation

Facial flushing

Headaches

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16
Q

Diltiazem: Main two effects

SE’s

A

Diltiazem: arterial dilator

Moderate cardiac inhibitory effects

Side effects:

  • Facial flushing
  • Headaches
  • Peripheral oedema
  • Heart failure
  • Heart block
17
Q

Name two dihydropyridines

What are their main effects?

SE’s?

A

Nifedipine (fast acting), Amlodipine (slow acting)

Main effects: Arterioselective dilator (no venodilation), and natriuretic

SE’s:

  • Marked facial flushing
  • Headaches
  • Peripheral oedema –> more sensitive in sunlight to dihydropyridines therefore oedema may be worse after a holiday.
  • Polyuria (exacerbate prostatism)
18
Q

What are the long term effects of nifedipine?

A

Long term effect of nifedipine: Reduce sodium balance with fixed sodium intake

19
Q

What is the role of Renin- angiotensin-aldosterone sx?

A
  • Reduces sodium and water losses
  • Maintains blood pressure
  • may contribute to HTN
  • Activated in HF
  • Activated in septicaemia and severe blood loss (hameorrhage)
20
Q

What activates the Renin Angiotensin Aldosterone system?

How is this detected?

A

Activation: 1) low blood pressure or 2) low blood volume (e.g. haemorrhage and hypovolaemic shock or diuretics).

detected via:

  • baroreceptors in both aortic arch (travels via CNX) and carotid sinus (CNIX) detecting low BP –> reduced firing of baroreceptors –> reduced inhibition of SNS (disinhibition) –> increase CO, vasoconstriction PLUS activates renin secretion by JGA (granular) cells:
    • ​Renin –> Angiotensinogen -> ATi –> ACE cleaves to ATii –> vasoconstriction plus stimulation adrenal cortex
    • Adrenal cortex releases aldosterone –> increase in Na+ and H2O uptake by kidney –> increase blood volume –> increase BP
    • Macula densa in distal convulted tubule detects drop in Na+ concentration; releases prostaglandins that vasodilate afferent arteriole and vasoconstrict efferent arteriole, and lead to further Renin release from juxtaglomerular cells.
21
Q

What inhibits RAAS?

A

Inhibition of RAAS 1) High blood pressure 2) High blood volume

High blood pressure –> detected by carotid sinus and aortic arch, increased firing of baroreceptors to the solitary nucleus in medulla oblongata, inhibits vasomotor centre and stimulates vagal output, increased PNS output to decrease cardiac output and vasodilate. Decreased SNS output, SNS does not promote renin secretion

High blood volume --> detected by macula densa, increased flow rate leads to increase NaCl at the distal tubule, inhibits PG release, no stimulation of renin release by juxtaglomerular cells. (Also detected by increased stretch of the smooth muscle of afferent arteriole leading to myogenic autoregulatory contraction of afferent arteriole decreasing GFR).

Decreased Renin –> decreased effects of ATii –> decreased ADH (vasopressin) release from posterior pituitary gland, reduced water uptake via kidney.

Decreased ATii --> less stimulation of aldosterone release, less NaCl and H2O uptake via distal tubule (less ENac, no stimulation Na/K+ ATPase).

Decreased ATii also direct effect of decreaing NaCl and H2O uptake via proximal tubule

22
Q

Name some specific conditions that will inhibit RAAS

A

Any condition that will lead to either high blood pressure or in cases of volume expansion:

E.g. Conn’s syndrome – > adrenal glands over produce aldosterone, leads to increased NaCl and H2O uptake, extreme volume expansion and overloading of the ventricles –> Renin becomes very low to try and compensate

Also: those with persistent HTN, diabetes mellitus with HF with reduced ejection fraction, chronic kidney disease

23
Q

Describe the RAAS cascade

A

Angiotensinogen released from the liver, gets cleaved by Renin released from the kidney to ATi, ATi gets cleaved by ACE in the pulmonary capillaries into ATii –> ATii binds to AT1 receptor (kidney) to have its effects:

  • direct effect on NaCl absorption at the proximal tubule
  • aldosterone secretion from the adrenal cortex
  • binds to vascular smooth muscle leads to vasoconstriction
  • acts on the posterior pituitary to increase ADH secretion –> increased H2O absorption via AQP2
  • Leads to water and salt retention, increase in effective circulating volume, increase in BP

Feedback loop –> AGii negatively feeds back to inhibit renin release by JGA

24
Q

What drugs can be used to block the RAAS system?

A
  1. Beta blockers –> prevent SNS stimulation of Renin release, therefore only useful in patients with HTN and high renin, limited use in african HTN as tends to have low renin
  2. Direct renin inhibitors
  3. ACEi –> inhibit conversion of ATi –> ATii
  4. ARB’s –> block ATii receptor, blocks downstream effects with adddeed advantage of no increase in bradykinins, therefore no SE of dry cough
  5. Aldosterone antagonists (eplerenone, spironalactone), block MR receptor activation and increase in ENac expression and Na/KATPase increase in activity
25
Q

Main action of ACEi’s

Main reason for SE’s

Name examples

Common SE’s

A
  • ACEi’s –> inhibit all formation of ATii
  • inhibit bradykinin breakdown
  • examples: Ramipril, Captopril (drugs list) (enalapril, lisinopril, perindopril)
  • SE’s:
    • Dry cough
    • Angiooedema (swelling of lips and tongue, more common african origin)
    • Hyperkalaemia
    • caution in renal artery stenosis
26
Q

ARB’s L Main action?

Common examples?

SE’s?

A

ARB’s –> Type 1 Angiotensin II receptor blockers

nicknamed the ARB’s, artans, sartans

Examples: Losartan, Valsartan (others = candesartan, telmisartan)

Well tolerated, no dry cough as with ACEi’s

SE’s:

  • Caution in renal artery stenosis ( can precipitate kidney failure)
  • Hyperkalaemia
  • Myalgia (pain in muscles)
  • Raised Creatinine Kinase (CPK)
27
Q

What is the MOA of alpha blockers in HTN treatment?

What other condition may be treated?

Name a long acting alpha blocker

What other a receptor blocker may be used and for what condition?

What are some SE’s of alpha receptor blockers?

A
  • Alpha blockers lower blood pressure by inhibiting the alpha 1 receptors on vascular smooth muscle
  • decreases systemic peripheral vascular resistance therefore reducing BP, exerts minimal effect on HR
  • Can also treat BPH –> blocks alpha 1 adrenoreceptors normally located in prostate gland and bladder neck which cause contraction of regional muscle making an obstruction to urinary flow
  • Long acting Alpha 1 selective blocker = Doxazosin
  • Exception = Phenoxybenzamine for phaeochromocytoma (tumour of adrenal gland leads to too much NA/A)
  • SE’s:
    • First dose hypotension
    • Postural hypotension
28
Q

ACE i:

Indications

Cautions

Contraindications

A

ACE i:

Indications: CHF (prevent fluid overload), CHD, T1D nephropathy (prevents fibrosis of nephrons), secondary stroke prevention, chronic renal failure, T2D nephropathy, proteinuria

Caution: renal impairment, PVD

Contraindication: pregnancy, renovascular disease

29
Q

ARB’s:

Indications

Cautions

Contraindications

A

ARB’ S indications:

ACEi intolerance, T2D nephropathy, LVH (hypertrophy), post MI, CHF, Proteinuria

Cautions: renal impairment, PVD

Contraindications: Pregnancy, renovascular disease

30
Q

Indications, caution and contraindications for:

CCB’s

A
31
Q

Indications, caution and contraindications for:

Diuretics

A
32
Q

Indications, caution and contraindications for: Direct renin inhibitors

A
33
Q

Indications, caution and contraindications for: Beta Blockers

A

Contraindication: Asthma, COPD, heart block

Indicated for: MI, angina, CHF

Caution: HF, PVD, DM

34
Q

Indications, caution and contraindications for: Alpha blockers

A
35
Q

Indications, caution and contraindications for: Anti aldosterone

A

Uses: Conns syndrome, hypertension, CHF

Caution: Hyperkalaemia, gynaecomastia

36
Q
A

AC1 (Izzy) (48 decks)

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