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mpharm year 3 sem 2 > week 1 > Flashcards

week 1 Flashcards

1
Q

name 5 drug properties which affect absorption in CV

A

MW
ionisation
solubility
formulation
liberation

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2
Q

name 3 patient related factors which affect absorption

A

route of administration
gastric pH
contents GIT

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3
Q

describe how malnutrition can affect drug volume of distribution

A

malnutrient leads to a decrease in albumin which increases the free drug volume and thus the volume of distribution of the drug increases

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4
Q

name 5 routes of elimination relating to CVD

A

pulmonary (expired in air)
bile (excreted in faeces)
renal- glomerular filtration, tubular reabsorption, tubular secretion

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5
Q

digoxin indication

A

heart failure
arterial fibrillation/ flutter

  • doses should be reduced in the elderly
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6
Q

describe digoxins half life and VoD

A

T1/2= 26-45 hr
large VoD- it is extensively distributed in tissues

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7
Q

what does digoxin inhibit

A

Na/K ATPase enzyme

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8
Q

renin-angiotensin- aldosterone axis- what does it do

A

regulates BP

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9
Q

how does RAAS regulate BP (5)

A

modulates
- blood volume
- sodium reabsorption
- potassium secretion
- water reabsorption
- vascular tone

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10
Q

what is atherogenesis

A

Atherogenesis is the process of forming plaques in the intima layer of arteries.

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11
Q

how do we reduce atherogenesis

A
  • reduce platelet adhesion
    – we do this by using either aspirin (an irreversible cycloxygenase inhibitor) or clopidogrel (adenosine diphosphate receptor inhibitor)
    these work by blocking thromboxane A2- which is essential in platelet aggregation
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12
Q

how does aspirin reduce platelet aggregation

A

aspirin works by blocking thromboxane A2- which is essential in platelet aggregation

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13
Q

how does clopidogrel reduce platelet aggregation

A

block the ADP (adenosine diphosphate) pathway and suppress its amplifying effect on platelet response

ADP- responsible for platelet aggregation

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14
Q

define efficacy

A

the degree to which a drug is able to produce the desired response

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15
Q

define potency

A

the amount of drug which is required to produce 50% of the maximal response which the drug is capable of inducing
- used to compare compounds within classes of drugs

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16
Q

define effective concentration

A

-ED50
the concentration of the drug which induces a specified clinical effect in 50% of subjects

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17
Q

define lethal dose

A
  • LD50
    the concentration if the drug which induced death in 50% of subjects
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18
Q

define therapeutic index

A
  • measure of the safety of the drug
    calculation - LD50/ED50
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19
Q

define margin of safety

A

margin between therapeutic and lethal doses

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20
Q

give 3 UV/Vis strengths

A
  • easy, cheap, robust
  • quantitative measurements of drugs in formulations
  • routine methods to assess physio-chemical properties of drugs
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21
Q

give 3 UV/Vis limitations

A
  • only moderately selective
  • drug needs to have chromophore
  • not really applicable to analysis of mixtures
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22
Q

define the terms in this equation A=abc

A
  • beer-lambert law

A= absorption
a= absorptivity constant
b= pathlength = 1cm (just size of cuvette)
c= concentration

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23
Q

what are the 2 forms of absorptivity in the beer-lambert law

A

molar E
- absorbance of a 1mol/L solution in 1cm cell
- units= Lmol^-1cm^-1

specific
- absorbance of a 1g/100ml solution in 1cm cell

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24
Q

define the terms in this equation A=log10 (I0/I1)

A

where I0= light intensity transmitted
where I1= light intensity we can see

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25
Q

state the 2 ways of determining the concentration of an unknown solution

A
  • use of literature A(1%, 1cm) or molar (E) values
    – typically used when a pure standard is not available
    – used in many BP assays
  • use of a calibration curve
    – y=mx+c (notes symbols don’t mean the same here as they do in the beer-lambert law)
    – for linear regression- rearrange equation for x (ie unknown concentration)
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26
Q

what stage is a BP of 120-139/ 80-89

A

prehypertensive

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27
Q

what stage is a BP of 140-159/90-99

A

stage one hypertensive

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28
Q

what stage is a BP of 160-179/ 100-109

A

stage two hypertensive

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29
Q

what stage is a BP of >180/>110

A

stage 3 hypertensive

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30
Q

define fibromuscular dysplasia

A

renovascular hypertension- happens when renal blood flow is compromised
more common in younger patients- esp female
relatively rare

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31
Q

what ethnicities are at higher risk of hypertension/ CVD

A

Asian
african
caribbean

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32
Q

what age do men become more at risk of hypertension/ CVD

A

55

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33
Q

what age do women become more at risk of hypertension/ CVD

A

65

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34
Q

name 3 consequences of left ventricle hypertrophy

A

(thickening of muscle wall)- caused by hypertension
- increase workload of LV
- increase after load of LV
- major risk factor for ischemic heart disease (myocardial infarction), arrhythmias, heart failure

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35
Q

CVS - hypertensive impacts (4)

A
  • ventricular hypertrophy (thickening of muscle wall)
  • arrhythmias
  • coronary artery disease (acute MI)
  • arterial aneurysm, dissection, rupture- fatal
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36
Q

kidney- hypertensive effects (3)

A
  • glomerular sclerosis (leads to impaired kidney function and finally end stage kidney disease)
  • reduction in GFR
  • ischemic kidney disease- esp when renal artery stenosis is cause of hypertension (secondary)
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37
Q

long term kidney effects of hypertension (3)

A
  • poor BP control
  • reduced renal pressure (infrarenal redistribution of pressure and increase reabsorption of salt and water)
  • decreased pressure in renal arterioles and sympathetic activity- renin production- angiotensin 2 production
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38
Q

name 2 effects of angiotensin 2 in the kidneys

A
  • causes direct constriction of renal arterioles
  • stimulation of aldosterone synthesis- sodium absorption and increase in intravascular blood volume
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39
Q

describe the importance of RAAS in blood pressure control

A
  • activated in response to reduced blood flow
  • this leads to decrease in GFR- which stimulates more angiotensin 2 and aldosterone- both of which raise BP
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40
Q

ARB

what does it stand for
example of drug
where does it work

A
  • angiotensin 2 receptor inhibitors
  • end in sartan
  • act on AT1 receptors- found in heart, blood vessels, kidneys
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41
Q

name 4 effects of hypertension on the nervous system

A
  • stroke
  • intracerebral and subarachnoid haemorrhage
  • cerebral atrophy
  • dementia
42
Q

name 3 effects of hypertension on the eyes

A
  • retinopathy, retinal haemorrhage and impaired vision
  • vitreous haemorrhage, retinal detachment
  • neuropathy of nerves - leading to extra ocular muscle paralysis and dysfunction
43
Q

effects of hypertension on the heart

A

sympathetic fibres- noradrenaline, B1 receptors, increasing the permeability of the nodal cell plasma membrane to Na+ and Ca2+

parasympathetic - ACh- M2 receptors, increasing the permeability to K+ and decreasing the Na+ and Ca2+ permeability

increased HR- more parasympathetic

44
Q

name 2 receptors involved in the regulation of arterial BP

A

baroreceptor reflex
chemoreceptor reflex

45
Q

name the responsible parties for immediate and long term vascular blood pressure control

A

neural- sympathetic - immediate
hormonal- long term (vasopressin- antidiuretic, angiotensin 2, aldosterone and atrial natriuretic peptide ANP)

46
Q

name the 3 types of diuretics

A

loop
thiazides
potassium sparing

47
Q

what do all diuretics do

A

all indirectly prevent reabsorption of water in the kidneys- they do this by preventing the reabsorption of sodium

48
Q

what kind of diuretic is furosemide
where does it act
how good is it

A

loop
very powerful blocks ~85% of sodium
acts on thick segment- ascending limb of Henle’s loop

49
Q

describe loop diuretic MOA

A

act by inhibiting the Na+/K+/2Cl- co transporter which is responsible for sodium reabsorption- as a result water moves by osmosis- following the higher sodium concentration

(potassium moves out of the cell)

50
Q

name one problem with loop diuretics

A

hypokalaemia - potassium too low

51
Q

what kind of diuretic is bendroflumethiazide
where does it act

A

thiazide
acts on early distal convoluted tubule

52
Q

describe bendroflumethiazide MOA

A
  • inhibits the sodium-chloride transporter in the distal tubule
53
Q

which diuretic is most effective

A

loop

54
Q

name 2 potassium sparing diuretics

A

amiloride
spironolactone

55
Q

describe the MOA of potassium sparing diuretics
- spironolactone
- amiloride

remember these act differently to achieve a similar effect

A

amiloride- distal tubule Na+ channel inhibitor- this leads to excretion of water and sodium and also potassium retention

spironolactone- aldosterone receptor antagonist - competitively binds to aldosterone receptor- inhibiting its effects - this enhanced sodium and water excretion whilst retaining potassium

56
Q

where do potassium sparing diuretics work

A

tubule and collecting duct- distal nephron

57
Q

what do B1 antagonists do

A

reduce sympathetic input-
reduces renin release

58
Q

ACE inhibitors

A

pril ending
angiotensin converting enzyme inhibitors
ie blocks conversion of angiotensin 1 to angiotensin 2

59
Q

decreased angiotensin 2 results in… (4)

A
  • vasodilation
  • decrease blood volume
  • decrease cardiac and vascular remodelling
  • potassium retention
60
Q

increased bradykinin results in.. (3)

A
  • vasodilation
  • cough
  • angiodema (rare)- dilation of blood vessels in the face- puffy face
61
Q

blocking angiotensin 2 action results in.. (3)

A
  • reduced peripheral vascular resistance (after load)- which lowers BP
  • dilates efferent glomerular arteriole- reduces glomerular pressure
  • reducing aldosterone- promotes sodium+ water secretion- can help with venous return (preload) - beneficial effect in heart failure
62
Q

aldosterone antagonists

A

spironolactone (potassium sparing diuretics)
eplerenone
have a direct effect in the kidney (block aldosterone)
competitively bind to aldosterone receptor
promotes Na+ and H2O excretion in collecting tubule and duct

63
Q

where does angiotensin keep NA

A

pre synaptic

64
Q

where do the following drugs act: prazosin, terazosin and labetalol

A

vascular A1 receptors

65
Q

where do the following drugs act: propranolol and metoprolol

A

cardiac B1 receptors

66
Q

where do the following drugs act: clonidine and methyldopa

A

brain stem

67
Q

actions of B adrenergic blockers in hypertension (5)

A
  • Blockade of cardiac beta-1 receptor- decrease HR and contractility- decrease CO
  • Improve efficacy
  • Suppress reflex tachycardia caused by vasodilators
  • Blockade of beta-1 receptors in JG cells in kidney- decrease renin release – decrease RAAS mediated vasoconstriction (angiotensin 2) and volume expansion (aldosterone)
  • Long-term use- decreases peripheral vascular resistance
68
Q

where are B1 adrenergic receptors present

A

cardiac specific

69
Q

why are B adrenergic blockers useful in heart failure

A

they reduce the oxygen requirement by reducing myocardial workload

70
Q

name 2 calcium channel blockers (dihydropyridines)

A

nifedipine
amlodipine

71
Q

first line treatment for hypertension in a 57 y/o male of African decent

A

calcium channel blocker such as amlodipine 5mg once daily initially- can be increased to 10mg daily

72
Q

how do calcium channel blockers work

A
  • block Ca2+ channels in arterioles
    dilate peripheral vessels- which lowers BP
    dilates coronary arteries which increases coronary perfusion
73
Q

why are calcium channel blockers (dihydropyridines) not indicated in patents with cardiovascular disease

A

they increase heart rate and heart force

74
Q

name 2 calcium channel blockers (non dihydropyridines)

A

verapamil
diltiazem

75
Q

calcium channel blockers (non dihydropyridines)

A

can be used for arrhythmias
cardiac selective

76
Q

Of the many types of adrenergic receptors found throughout the body, which is most likely responsible for the cardiac stimulation that is observed following an intravenous injection of Noradrenaline?​

A

β1-adrenergic receptors​

77
Q

From the choices below which ONE drug would have the greatest effect on the adrenoreceptor family?
Isoprenaline​
Adrenaline​
Noradrenaline​
Phenylephrine

A

adrenaline

78
Q

Actions of angiotensin II include which of the following

Vasodilation ​
Increased sympathetic nerve release of noradrenaline​
Inhibition of the reuptake of noradrenaline​
Promotes renal excretion of sodium and water (natriuretic and diuretic effects) ​
Inhibit cardiac and vascular remodelling associated with chronic hypertension, heart failure, and myocardial infarction.​

A

vasodilation

79
Q

what does L-NOARG do

A

blocks NO which in turn increases BP

80
Q

do diabetic patients produce more or less natural NO

A

less

81
Q

first line primary prevention for white male with cardiac risk over 10%

A

atorvastatin 20mg once daily

82
Q

what should a patient who is type one diabetic and; over 40 OR had diabetes for 10+ years OR has established nephropathy OR has another CV risk factors ie is a smoker, be started on

A

atorvastatin 20mg

83
Q

what is the dose for atorvastatin secondary prevention

A

40mg-80mg depending on risk and preveious treatment

84
Q

define rhabdomyolysis

A

abnormal muscle breakdown, which can lead to kidney problems and be life-threatening- very rare
can be caused by stains

85
Q

cholesterol target range

A

no more than 5mmol/L

86
Q

HDL target range

A

should be at least 1mmol/L

87
Q

describe the MOA of ACE (chemistry)

A

ACE hydrolyses the peptide bond between Phe and His (amino acids) in angiotensin 1 to create angiotensin 2

88
Q

name 2 of the main side effects associated with captopril

A

rashes
loss of taste

89
Q

why is enalapril active

A

it is a prodrug- liver esterase enzymes metabolise it into enalaprilat which is active

90
Q

name the three most common hypertension causes

A
  • malfunction of the sympathetic drive (over stimulation of baroreceptors)
  • malfunction of the renin-angiotensin-aldosterone system
  • inflammatory process in endothelium (causes a thickening of arteriole lumen- causing pressure increase)
91
Q

what is the most likely cause of hypertension in a young white patient

A

malfunction of renin-angiotensin- aldosterone system

92
Q

name 6 risk factors for cardiovascular complications

A
  • coronary heart disease
  • stroke
  • heart failure
  • renal failure
  • retinopathy
  • vascular dementia
93
Q

what is ambulatory BP and why is it used

A

a BP cuff that stays on for a few days to monitor BP

  • used to distinguish between the white coat effect and actual hypertension
94
Q

what is the ACD rule

A

1st line= ACEi / ARB
2nd line= calcium channel blocker
3rd line= diuretic (thializide)

95
Q

what is first line treatment for white male, 45 y/o with high renin and hypertensive

A

ACE I such as ramipril 2.5mg OD to start

96
Q

what is first line treatment for a 56 year old women of Caribbean descent with hypertension

A

calcium channel blocker such as amlodipine

97
Q

in what condition is bendroflumethiazide contraindicated

A

gout

98
Q

why are beta blockers no longer preferred treatment

A

less effective in preventing cardiac events- esp stroke

99
Q

why is aspirin 75mg daily only used in secondary prevention

A

unlicensed in primary prevention- no evidence to say it works - higher risk of upper GI damage

100
Q

why should NSAIDs be avoided in hypertension

A

they exacerbate the condition by increasing sodium reabsorption and therefore water reabsorption

101
Q

what drugs should be avoided in hypertensive patients (5)

A
  • NSAIDs
  • oestrogen (oral contraceptives)
  • sympathomimetics (decongestants)
  • corticosteroids
  • antacids with high salt content (gaviscon and peptac)

mpharm year 3 sem 2 (11 decks)

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