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Unit 12 week 4 > Pharmacology of HF > Flashcards

Pharmacology of HF Flashcards

1
Q

What is heart failure

A

Reduced cardiac output to the point that there is end organ failure due to the inadequate blood supply.

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2
Q

What is the classification sytem for HF?

A
  1. No limitation on physical activity. Ordinary physical activity does cause undue fatigue, palpitation, dyspnoea. (pre heart failure)
  2. Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea.
  3. Marked limitation on physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation of dyspneoa.
  4. Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.
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3
Q

Symptoms of left sided heart failure

A
  • Dyspnoea
  • Orthopnoea: dyspnoea on lying down
  • Paroxysmal nocturnal dyspnoea
  • Pulmonary congestion and oedema (Crackles)
  • Exercise intolerance
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4
Q

Symptoms of right sided heart failure

A
  • Oedematous swelling of feet, ankles and legs
  • Hepatomegaly: enlarged, palpable, tender liver
  • Ascites: increase in abdominal fluid
  • Excessive nocturnal urination
  • Increase to jugular venous pressure
  • Exercise intolerance

backing up from vena cava

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5
Q

what is the name for HF that affacets both sides of the heart

A

biventricular failure

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6
Q

vicious cycle (diagram of how injury causes increased preload and afterload)

A
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7
Q

final diagram overview of heart failure *important*

A
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8
Q

Classes of drugs used to manage heart failure

A
  • ACE1 (-pril) (hyp)
  • ARB (-sartan) (hyp)
  • B blockers (-lol) (hyp)
  • Diuretics
  • SGLT2 inhibitors (-gliflozin)
  • Nephrilysin inhibitors (-tril)
  • Cardiac glycosides (ANTI-DYSRHYTHMIC)
  • Ivabradine (ANGINA)
  • Vasodilators (ANGINA)
  • Calcium-channel blockers- mostly not for CHF (hyp)
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9
Q

Chronic heart failure diagnosis

A

Take a detailed history and perform and clinical examination.

A) Measure NT-proBNP (precursor to BNP released by both the atria and ventricles- raised in symptomatic and non-symptomatic left ventricular failure). If it is >2,000 ng/L refer urgently.

B) Perform ECG consider chest X-ray, blood tests, urinalysis, peak flow or spirometry.

3) Specialist clinical assessment including transthoracic echocardiography.

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10
Q

management of heart failure

A

1) Offer diuretics for symptoms and fluid retention – offer ACE1 and BB if symptoms continue, consider hydralazine and nitrate if intolerant of ACE1 and ARB)
2) Manage comorbidities such as hypertension, atrial fibrillation, ischaemic heart disease and diabetes

  • Offer a personalised exercise-based cardiac rehabilitation
  • Digoxin for heart failure with sinus rhythm
  • Cardiac resynchronisation therapy
  • Implantable cardioverter defibrillator
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11
Q

which part of the neprhon does the majority of sadium reabsorption take place in

A

proximal convuluted tubule

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12
Q

most diuretics are what

A

natriuretics

makes you reabsorb less and therefore excrete more sodium

where sodium goes wter follows

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13
Q

what part of the nephron reabsrobes the second most amount of sodium

A

Loop of henle

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14
Q

Acetazolamide

A

CLASS: Carbonic anhydrase inhibitor (CAI)

CHEMSITRY: Small molecule

PHARMACOLOGY: target- Carbonic anhydrases Activity- Competitive inhibitor

PHYSIOLOGY-↓ Na reabsoroption in PCT – ↑urine flow

1/3 PCT Na+ reabsorption is through Na+/H+ antiporter

Diuretic effect is mild and self-limiting

– ↓preload –↓venous congestion– sympotamtic relief

Heavy loss of HCO3- – alkaline urine/ metabolic acidosis – ↓diuresis

↑Na+ at DCT – ↑K+ loss – hypokalaemia

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15
Q

How does competitively inhibiting carbonic anhydrase lead to a diuretic effect

A

The main way that the kidney controls ECF and therefore BV is via reabsorption of Na+.

This is done in the PCT via Na+/H+ antiporters (Na+ entering tubule epithelial cells and H+ leaving into lumen).

The H+ required for this is gained from carbonic anhydrase converting carbonic acid into its ionic forms.

The only way for carbonic acid to enter tubule epithelial cells is to use CA to convert it to H2O and CO2 and then to use CA again to convert it back to carbonic acid.

Therefore, if you antagonise CA, you stop carbonic acid entering the epithelial cells and also block its conversion into H+ for Na+ transport.

Na+/K+ -ATPase “sodium pump” on the apical side allows for Na+ to be transported out of tubular epithelial cells to the basolateral side.

Na+/HCO3- co-transporter allows Na+ to also be transported to the basolateral side

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16
Q

name 2 pumps that transfer Na from within tubule epithelial cells to the basolateral side

A

Na+/K+ -ATPase “sodium pump”

Na+/HCO3- co-transporter

17
Q

what are the 3 ways that CO2 is transported in the blood

A

10% dissolved in plasma

20% bound to Hb

79% converted to H2CO3

18
Q

Hydrochlorothiazide

A

CLASS: Thiazide diuretic

CHEMISTRY: Small molecule

PHARMACOLOGY: Target- NCC = Na+ Cl- symporter Activity- Inhibition

PHYSIOLOGY:

↓Na+ reabsorption in DCT – ↑urine flow

Mild diuretic action

Some loss of HCO3- – metabolic alkalosis

↑K+ loss – hypokalaemia

Secreted by OAT (organic anionic transporter)  uricaemia  ↑risk of gout

CLINICAL: Hypertension; oedema

19
Q

Furosemide

A

CLASS: Loop (“high ceiling”) diuretic

CHEMISTRY: small molecule

PHARMACOLOGY: target: NKCC2= Na+-K+-Cl- symporter on the apical side Activity: Inhibitor

PHYSIOLOGY:

  • ↓Na+ reabsorption in thick ascending loop of Henle – ↑ urine flow
  • Potent diuretic action (up to 15% of filtered load)
  • ↑ K+ loss – hypokalaemia (and metabolic acidosis)
  • Secreted by OATs in PCT – ↑ concentration in tubules
  • ↓ uric acid secretion (competes for OATs) – uricaemia – ↑ risk of gout
20
Q

spironolactone

A

CLASS: K+ sparing diuretic or MRA (mineralocorticoid receptor antagonist)

CHEMISTRY: small molecule- steroid so acts intracellularly

PHARMACOLOGY: Target- Mineralocorticoid receptor Activity: Competitive antagonist

PHYSIOLOGY:

  • Antagonises action of aldosterone in late DCT/CD
  • ↓ expression of ENaCs and Na+/K+ -ATPase
  • Weak diuretic effect (most Na+ is already absorbed at this point)
  • causes K+ retention- hypertension
21
Q

why is spirinalactone often used in conjunction with thiazide?

A

offsets the loss of K+

22
Q

Amiloride

A

CLASS: k+ sparing diuretic

CHEMISTRY: small molecule

PHARMACOLOGY: target: epithelial Na Channel (ENaCs) activity: channel blocker

PHYSIOLOGY:

  • ↓Na+ entry from lumen of DCT into cell
  • Rate-limiting step of Na+ reabsorption
  • Weak diuretic effect (most Na+ already reabsorbed by this point)
  • K+ retention – hyperkalaemia

CLINICAL: used with thiazide (balances K+) for odeema and heart failure

23
Q

what is a ROMK

A

renal outer medullary K channel

k+ leaves via channel to balance charge when Na+ enters

24
Q

Mannitol

A

CLASS: Osmotic diuretic

CHEMISTRY: Small molecule- natural sugar

PHARMACOLOGY: Target- NONE Activity- NONE

PHYSIOLOGY:

  • Does not cross membranes
  • Raises osmotic pressure – draws water towards itself
  • Response directly proportional to concentration ←the effect does not saturate

CLINICAL:

  • Used ACUTELY  rapid loss of fluid e.g., cerebral oedema
  • NOT used in chronic hypertension or congestive heart failure
  • Very potent diuretic
  • Substantial K+ loss
  • Also: laxative, mucolytic
25
Q

what is an osmotic diuretic

A

Osmotic diuretic- inhibits the reabsorption of water by increasing the osmolarity of blood and renal filtrate

26
Q

Dapagliflozin

A

CLASS: SGLT2 inhibitor (-gliflozin)

CHEMISTRY: small molecule- modified sugar

PHARMACOLOGY: Target- SGLT2 (sodium/ glucose transporter 2) Activity- Competitive inhibitor

PHYSIOLOGY:

↓ glucose reabsorption in PCT - glycosuria -osmotic diuresis

↓ Na+ reabsorption in PCT - natriuresis

↓ blood glucose

CLINICAL: diabetes mellitus (mostly type 1) ,Congestive heart failure

27
Q

SGLT2 receptors

A
  • Na+ / glucose co-transporter
  • Expressed in early PCT
  • 1 Na+ in: 1 glucose in
  • 1* function in kidney
  • = reabsorption of glucose (~90%)
  • Low affinity/ high capacity
28
Q

SGLT1 co-transporter

A

Na+/ glucose co-transporter

Expressed in late PCT

In intestine + kidney – glucose absorption

2Na+: 1 glucose in

Also in kidney = reabsorption of glucose (~10 %)

High affinity/ low capacity

29
Q

sacubitril

A

CLASS: Nephrilysin inhibitor (-tril)

CHEMISTRY: prodrug: active metabolite= sacubitrilat

PHARMACOLOGY: Target- Nephrilysin (enzyme)- neutral endopeptidase Activity- Competitive inhibitor

PHYSIOLOGY:

  • Nephrilysin cleaves/ degrades ANP and BNP (also enkephalins, AT-1 and AT-II)
  • Hence, sacubitril ↑ ANP/BNP levels

CLINICAL: used in combination with valsartan (ARB) = ARNI

Congestive heart failure

30
Q

ANP and BNP

A

CLASS: Natriuretic peptides

CHEMISTRY: Endogenous peptides produced when the atria (ANP) and ventricles (BNP) are distended (Hypertension of CHF)

PHARMACOLOGY: Target- Natriuretic Peptide Receptor 1= NPR1 (also NPR2 and NPR3) Enzyme- Transmembrane guanlyl cyclase Activity: agonist

PHYSIOLOGY:

  • NPR1 widely expressed, including kidney
  • Guanylyl cyclase converts GTP - cGMP - ↑PKG activity
  • -inhibition of ENaC and Na+/K+-ATPase in collecting duct
    • ↑ GFR ↓ renin release - ↓ ECF
  • Oppose action of AT-II and aldosterone (e.g., decrease expression of eNaCS)

CLINICAL: Sacubitril effectively ↑ activity of ANP/BNP

31
Q

Digoxin

A

Low priotiry????

CLASS: cardiac glycoside

CHEMISTRY: natural molecule

PHARMACOLOGY: Target- Na+/ K+-ATPase (sodium pump) transporter Activity: Competitive inhibitor (K+ bonding sites)

PHYSIOLOGY:

  • Na+/ Ca2+ exchanger (NCX) removes Ca2+ from cytoplasm during diastole
  • ↑ [Na+]I  ↑ driving force for Ca2+ extrusion  ↑[Ca2+]I  ↑force of contraction +ve inotropic effect
  • ↓oedema
  • TOXIC- low therapeutic index

CLINICAL:

  • Atrial fibrillation: ↓ AVN conduction
  • Formerly congestive HF
32
Q

Ivabradine

A

CLASS: xxx

CHEMSITRY: small molecule, structurally similar to vermapril

PHARMACOLOGY: Target- HCN channels (“funny” current)

PHYSIOLOGY: Inhibiting If (funny) current  ↓HR  ↓ cardiac work

CLINICAL: Angina, congestive heart failure (last ditch)

33
Q

Hydralazine

A

CLASS: vasodilator

CHEMISTRY: small molecule

PHARMACOLOGY: not well understood

PHYSIOLOGY: Vasodilator

May block IP3-dependant Ca2+ release from SR

CLINICAL: anti-hypertensive, congestive heart failure (used with nitrates)

34
Q

nitrovsodilators

A
  • Sodium nitroprusside
  • Isosorbide dinitrate
  • Isosorbide mononitrate
  • Glyerceryl trinitrate

Pharmacology of nitrates:

Varying pharmokinetics: duration of action, route of admission etc…

Each compound break down/ is metabolised to release nitric oxide

NO activates NO sensitive soluble guanylyl cyclase (ANP an BNP)

 ↑cGMP  ↑PKG  vasodilation and other responses…

Unit 12 week 4 (3 decks)

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