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MP323 > L1 - L10 > Flashcards

L1 - L10 Flashcards

1
Q

Pharmacokinetic Terms

  • loading dose, steady state, half-life
A

Loading Dose
- given to help patient reach therapeutic level quickly and safely

Steady State
- drug given = same amount being excreted in one dosing cycle giving constant drug serum level

HalfLife
- time taken for half of drug to be excreted

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2
Q

Pharmacodynamics

  • Potency
  • ED50
A

Potency
- amount of drug required to produce 50% of the max response it is capable of producing

ED50
- conc. of drug that induces specific clinical effect in 50% of subjects

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3
Q

BP Control by Body

A
  1. Blood pressure increases causing inc. firing of Baroreceptors in Carotid Arteries & Aorta
  2. received by sensory neurons in medulla which dec. Symp output & inc. Parasymp output
  3. lower Symp. output = less NA release & less vasoconstriction
    - this decreases peripheral resistance & BP.
    - inc. symp output = more ACh release & less Electrical Impulses, slowing HR and BP
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4
Q

RAAS system

  • angiotensin II effects
A
  1. Ang II increases sympathetic activity, increasing BP
  2. acts on adrenal gland to release aldosterone
    - aldosterone drives Na+ reabsorption & water retention
  3. it promotes release of ADH from pituitary
  4. increases sodium & chloride reabsorption
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5
Q

Electron Transition

  • rotational
  • vibrational
  • electronic
A

electrons only go from non-bonding orbitals to anti-bonding

Electronic transition > vibrational > rotational

Rotation - wide low peak
vibrational - mid peak
electronic - high narrow peak

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6
Q

Hypertensive Stages

  • pre, 1st, 2nd, acute
A

120-139 / 80-89 : pre hypertensive

140-159 / 90-99 : stage 1 hypertension
- advise to avoid risk factors and review in 1yr

160 - 179 / 100-109 : stage 2 hypertension
- treat immediately with statins, hypertensives etc

> 180/110 : acute hypertension needs hospitalisation

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7
Q

BP Calculation

  • Secondary HTN Causes
A

MAP = CO x TPR (total peripheral resistance)

  • renal disease
  • cushings syndrome
  • crohns syndrome
  • coarctation (aorta narrowing)
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8
Q

Renovascular Hypertension

  • Athero
  • Fibromuscular dysplasia
A

Atherosclerosis 75 - 90%
- atherosclerotic plaque build up in arteries

Fibromuscular Dysplasia 10 - 25%
- overgrowth of kidney artery cells causing blockage

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9
Q

HTN & CVD Risk Factors

A

HTN
- ethnicity , smoking , hypercholesterinaemia (high LDL) , obesity , stress , physical inactivity

CVD
- atherosclerosis , Heart Failure , arrythmias , angina - MI

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10
Q

Consequences of HTN

  • Heart
  • Kidney
  • Nervous System
A

Heart - inc. workload in LV from higher afterload

Kidney - can cause sclerosis (scarring)

Nervous System - can cause stroke

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11
Q

Chronotropy & Inotropy

A

chrono - measure of heart rate

ino - measure of force of contraction

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12
Q

Hypertension Mechanisms

  • SA Node parasympathetic Control
A

SA node has muscarinic and B1 receptors:
- BP increases, increasing parasymp output
- more ACh at SA muscarinic receptors which lowers HR

HR decreases on para output , less NA released:
- causes vasodilation of arteries
- lower contraction at myocardial cells

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13
Q

Sympathetic Output on Myocytes

  • Noradrenaline Effects
A
  • increased permeability for Na+ & Ca2+ on nodal cell plasma membranes
  • action potential to be reached quicker as Na+ flows INTO cell to depolarise it
  • causes stronger contraction of heart as Ca2+ enters via Na+/Ca2+ symport from inc. sodium
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14
Q

Parasympathetic Effect on Heart

  • ACh effects
A
  1. lowers permeability of Na+ and Ca2+ in nodal cell membranes
  2. increases permeability of K+
  3. this causes higher ion efflux , extending action potential upstroke and lowering HR
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15
Q

Enzymes as Drug Target

  • Enzyme Use
A
  • enzymes accelerate reactions by lowering energy required for reaction

induced fit:
- active site is close to correct shape for substrate binding
- substrate binding alters enzyme structure which strains the bonds

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16
Q

Pi & Sigma Bonds

A

Pi Bonds
- target for catalysation because susceptible
- 1 bond in a double bond is pi
- weaker bond so this is why it is targeted

Sigma Bond
- strong bonds
- bond present as single bond and one in double

17
Q

Acid/Base Catalysis

  • non-ionised & ionised
A
  • non-ionised bases act as a basic catalyst, accepting protons
  • ionised bases act as acidic catalyst, donating protons to other molecules
  • ionised acid accepts protons
  • non-ionised acid donates protons
18
Q

Types of Enzyme Inhibitors

A

Competitive
- shaped like substrate and binds to active site.
- compensated by higher substrate concentration
- methotrexate is reversible comp. inhibitor

Non-Competitive
- binds to allosteric site to change conformation of active site

Uncompetitive
- inhibitor only binds to enzyme/substrate complex

19
Q

Hypertension Monitoring & Targets

A

< 140/90 - monitor every 1-5 years
- this is target BP for those with hypertension

> 140/90 - treat if they are high risk (existing CVD, diabetes, obese) or if QRISK over 20%
- if they have complicated hypertension (high risk) then BP target should be <130/80 mmHg

20
Q

HTN Management

  • ACE-I (1st line)
  • Enalapril 1st line in HF
  • Ramipril 1st line in MI then HF
A

ramapril , lisinopril

  • blocks ACE enzyme in lung to block conversion of Ang1 to Ang2 , reducing vasoconstriction

S/E
- dizziness, take at night if occurs
- cough (ACE breaks down bradykinin which builds up to cause cough) change med if bad

21
Q

HTN Treatments

  • CCB’s
A

Blocks L-type Ca2+ calcium channels in vessels to reduce contraction and in heart to reduce contraction.

Verapamil + Diltiazem
- rate limiting CCB affects heart. rhythm control for arrhythmias

Amlodipine
- non-rate limiting affecting vessels. used in HTN

S/E - ankle swelling , hot flushes , rash

22
Q

Diuretics

  • Thiazides
  • Loop Diuretics
A

Thiazides
- affects chlorine & sodium reabsorption which reduces water reabsorption to decrease resistance & blood volume
- used in HTN

Loop Diuretic
- NOT USED FOR HYPERTENSION
- used in Heart Failure to clear oedema

23
Q

Alpha Blockers

A
  • blocks effect of sympathomimetic catecholamines
    Noradrenaline & Adrenaline
  • stops vasoconstriction by reducing these, and encourages vasodilation
  • A1 increases constriction in smooth muscle
24
Q

HTN Treatment
- AB/CD therapy

A

<55 & Caucasian - ACE-I first line
- then give CCB or Diuretic if not properly controlled

> 55 or ethnic - CCB
- then give ACE-I or ARB if worsens

25
Q

Beta Blocker

  • 1st line angina
  • not for HTN
  • secondary prevention after MI
A
  • blocks binding of Noradrenaline at beta receptors
  • reduces vasoconstriction and lowers heart rate.

Co-Morbidities
- affects cardiac output so not used for HTN
- DO NOT give with rate limiting CCB or diuretic

26
Q

Aspirin
- secondary CVD prevention

A

secondary - 75mg daily

Antiplatelet Action
- Aspirin is an NSAID, blocking COX-1
- COX-1 produces Thromboxane A2 which is a platelet recruiter and activator
- blocking COX-1

27
Q

HTN Types

  • whitecoat
  • Malignant
A

Whitecoat
- unusually high because of stress in medical setting
- give ABPM reader over 24hrs. limit is 135/85

Malignant
- HTN even when on all drugs (ACE-I, CCB, Thiazide)
- rama 2.5mg OD, amlo 5mg OD, bendro 2.5mg OD
- doesnt have to be max dose of meds, just on 3

28
Q

Statins
- primary and secondary prevention

A

primary
- 10yr CVD risk >20%
- no cholesterol target , used to reduce atherosclerosis

Secondary :
- simvastatin 40mg regardless of BP
- Atorvastatin given if QRISK higher than 10%

29
Q

HTN Exacerbating Drugs

A

NSAIDS - Only used short term
- excreted in kidneys instead of sodium.

Oestrogen - Oral contraceptives only given along with blood tests every 6 months because lead to water retention

Sympathomimetics
- can cause vasoconstriction so need monitoring

Effervescent Tablets & Antacids
- are high in sodium so NOT given to high-risk patients

30
Q

ACE Binding Sites

  • S1
  • S2’
  • S1’
  • Zn2+
A
  1. S1 Terminal - binds with aromatic groups
  2. S2’ Terminal - can bind aliphatic & carboxylate group
  3. S1’ Terminal - can bind to aromatic/aliphatic groups
  4. Zn2+ Terminal - ion that can bind negatively charged groups
31
Q

Enalaprilat Binding
- key features

A

Enalaprit has poor physiochemical properties:
- LogP -0.5 so too hydrophilic to pass through cell membrane
- good bioavailability though once in blood

  1. S1 - binds to aromatic ring
  2. S2’ - binds to aliphatic group and adjoined carboxylate
  3. S1’ - binds to methyl group (aliphatic)
  4. Zn2+ - group will bind to electron rich carboxyl group
32
Q

Captopril Drug History

  • used less because of rash & loss of taste
A
33
Q

Atheroma

  • form in high pressure environments like arteries
A
  • accumulation of intracellular & extracellular lipid in the intima of large and medium arteries
  • NOT found in veins because venous circulation back to heart is low pressure
34
Q

Atherosclerosis (asymptomatic)

  • arterial wall thickening from atheroma build-up over decades
A

main sites: aorta, coronary artery and leg arteries

Monck Berg Atherosclerosis:
- affects small-medium arteries.
- calcium deposits in the middle layer, calcifying arteries independent from atherosclerosis

35
Q

Atheroma Features

  • fatty streak
  • fibrous plaque
  • complicated plaque
A

Fatty Streak
- elevated zone on arterial wall from lipid accumulation. LDL’s become oxidised by free radicals and are then recognised by scavenger monocytes/macrophages and deposited in the arterial wall

Fibrous Plaque
- lipid accumulates & become foam cells. macrophages from foam cells attract SMC from tunica media, forming a cover over the lesion.

Complicated Plaque
- ulcers on fibrous cap rupture to expose plaque contents and leading to thrombosis

36
Q

Atheroma Prevention

  • lifestyle
  • secondary
A

Lifestyle :
- no smoking, diet (low fat), reduce alcohol, regular exercise

Secondary :
- antiplatelet (aspirin)
- statins (atorva 20mg OD)

MP323 (4 decks)

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