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PMP 201 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

what is cardiovascular disease?

A

diseases of the circulation

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2
Q

what are the main 4 types f CVD?

A

coronary heart disease
strokes and transient ishaemic attacks
peripheral atrerial disease
aortic disease

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3
Q

what are the types of coronary heart disease?

A

angina
myocardial infraction
heart failure

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4
Q

what is coronary heart disease?

A

when there is not enough oxygen to the heart (can be affected by atherosclerosis)

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5
Q

what is angina?

A

not enough oxygen in heart

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6
Q

what is myocardial infraction?

A

tissue death in the heart

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7
Q

what is the long term effect of heart failure?

A

death

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8
Q

what is the cause of transiet ishaemic attacks (TIA)?

A

arteries blocked

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9
Q

what i the cause of perpheral arterial disease?

A

arteries blocked in limbs

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10
Q

what is the cause of aortic disease?

A

aortic muscle gets bigger and bursts

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11
Q

what is epidemiology?

A

the study of health and disease in a defined population

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12
Q

what age and under should be seriously investigated when there is high blood pressure?

A

under 40 years old

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13
Q

what is primary prevention?

A

a strategy to identify and alter modifiable risks to reduce incidence in disease-free individuals or in the population

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14
Q

what is secondary prevention?

A

a strategy to target individuals with established disease, who have usually had an ‘event’ to reduce morbidity and mortality

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15
Q

what relationship in CV disease can we help and interupt from lifestyle and environment factors?

A

acquired vascular

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16
Q

what are the diseases that come under the vascular acquired CV disease?

A

HT
atherosclerosis
coronary disease
isch heart disease
AMI
stroke

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17
Q

what are the myocaardial congenital diseaases?

A

inherited CM
inheretid valce dis
structural abnormalities
inherited conduction defects

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18
Q

most CVDs are acquired, this means…

A

not inherited
most events due to lifestyle
influenced by non-modifiable risk factors

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19
Q

when should a formal risk assesment be carried out ?

A

where 10-year CVd risk i more than 10%

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20
Q

what steps should be taken in primary prevention?

A

lifestyle changes
offer support
tell risk measuremnet
offer medication
keep a record of changes
pharmacological intervention where necessary

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21
Q

what are the lifestyle factors that affect CVD?

A

smoking
overweight
diet and excercise
hypertesion
diabetes
hyperlipidaemia

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22
Q

what is the first line treatment for any/one with hypertension and type 2 diabetes

A

ACEi or ARB

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23
Q

what is the first line tratment for hypertenssion without type 2 diabetes aged under 55 and not african or afro-caribean?

A

ACEi or ARB

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24
Q

what is the first line tratment for hypertenssion without type 2 diabetes aged under 55?

A

CCB

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25
Q

what is the first line tratment for hypertenssion without type 2 diabetes and african or afro-caribean?

A

CCB

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26
Q

what is HbA1c?

A

measures the sugar levels in blood over the last 3 months

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27
Q

what is the pain and discofort in coronary heart disease made from?

A

when coronary arteries becomes narrowed by a build up of atheroma
narrowing is angina and if a blockage occurs it can cause a myocardial infraction

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28
Q

what is NSTEMI?

A

uncomplete blockage that will eventually block fully

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29
Q

what is a STEMI?

A

complete blockage

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30
Q

what is the secondary prevention of ACS, ischaemic stroke, TIA, peripheral artery disease?

A

antiplatelets

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31
Q

what is the secondary treatment for arrythmias?

A

anticoagulants

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32
Q

what is autoregulation?

A

normal resting conditions, redistributes blood as needed by tissues

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33
Q

what is the autoregulation process of low blod pressure?

A

stimulate endothelial cells to release endothelin and platelets are secreted this maakes the precapillary sphincters to vasoconstrict

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34
Q

what is the autoregulation of high blood pressure?

A

stimulate endothelial cells to release NO this causes vasodilation in the precapillary

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35
Q

what is neural regulation of blood pressure?

A

short term regulation of blood pressure, especially in responses to transient changes in arterial pressure, via baroreflex mechanisms

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36
Q

what type of nerves are vagus nerves?

A

parasympathetic which causes the heart to relax

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37
Q

if there is pressure in the aorta where is that signal received?

A

baroreceptors

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38
Q

if there is pressure on carotid sinus where is the signal recieved?

A

baroreceptors

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39
Q

what do the glossopharyngeal nerves connect?

A

carotid sinus to the brain

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40
Q

what do the vagus nerves connect?

A

aortic arch to the brain

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41
Q

what is the neural regulation of low blood pressure?

A

low BP –> aorta baro wide –> brain –> vagul nerve activation slower –> increase heart rate –> increase cardiac output –> BP raised

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42
Q

what is erythropeotin (EPO)?

A

EPO is a vasoconstrictor
that increases the blood viscosity, resistance and pressure
and decreases the blood flow

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43
Q

what does adrenaline/ nor-adrenaline do?

A

enhance and extend the bodys sympathetic activity
increases blood pressure

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44
Q

what does antidiuretic hormone do?

A

increase in tissue fluid osmolarity triggers ADH release

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45
Q

what is the neural regulation of high blood pressure?

A

increase in arterial blood pressure –> baroreceptors firing –> brain–> increase vagal activity –> low heart rate–> low cardiac output–> vasodilation–> low blood pressure

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46
Q

what is the hormonal regulation of high blood pressure?

A

no renin relase= no conversion= sodium excretion= lower osmotic pressure= reduction in vagus return= lower blood pressure

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47
Q

what does atrial natriuetic peptide do?

A

reduce renin= low blood volume= low blood pressure

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48
Q

what does angiotensin 2 do?

A

increases blood pressure
acts as a AT1 receptor

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49
Q

what is the receptor target for angiotensin 2?

A

AT1 (angiotenin 1 receptor)

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50
Q

what is the mechanisms of ACE inhibitors?

A
  1. arterial and venus vasodilation
  2. decrease blood volume
  3. downregulation of sympathetic activity
  4. suppression of hypertrophy (cardiac and vascular)
    (reduces sodium and water reabsorption)
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51
Q

what are the typical names of ACEi?

A

prils

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52
Q

what type of drug is an ACEi?

A

pro-drug
this is an inactive drug that converts to active in the body/ the blood = in the body longer= works in the body longer and has a lasting effect

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53
Q

what are the adverse effects of ACEi?

A

dry, irritant cough
due to the accumulation of bradykinin (release of neurokining and substance P, this causes airway smooth muscle to constrict leading to bronchoconstriction and persistent dry cough. )

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54
Q

whar names are given to most ARBs?

A

sartan

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55
Q

what are ARBs?

A

ARBs are receptor antagonists that block type 1 angiotensin II (AT1) receptors on blood vessels and other tissues such as the heart.

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56
Q

what are the ADME of ARBs?

A

A; readily absorbed
d= binds to plasma protein
m= metaolised in the liver
e= eliminated through the kidney

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57
Q

what is the clinical consideration of ARBs?

A

Patients with bilateral renal artery stenosis may experience renal failure if ARBs are administered.

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58
Q

what is the name given to renin inhibitors?

A

aliskiren

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59
Q

what do renin inhibitirs do?

A

Renin-inhibitors produce vasodilation by inhibiting the activity of renin, which is responsible for stimulating angiotensin II formation.​

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60
Q

what are the names given to calcium channel blockers?

A

dipine

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61
Q

what do calcium channels do?

A

L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (SA and AV nodes) regulate the calcium influx and stimulate smooth muscle and cardiac myocyte contraction. ​

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62
Q

what do thiazide-like diuretics do?

A

inhibit active Na+ reabsorption and accompanying Cl- transport

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63
Q

what name is given to beta blockers?

A

lol

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64
Q

what type of heartbeat is a sign of AF?

A

irregularly irreglar

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65
Q

what heartbeat should be investigated?

A

weak heartbeat

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66
Q

what to do if in clinic the BP is higher than 140/90?

A

take another reading. if very different take another reading and record lower of 2nd or 3rd

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67
Q

what to do if BP is between 140/90 and 180/120?

A

offer ABPM or HBPM

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68
Q

what frequency does ABPM need to be recorded?

A

every 30 mins for 24 hours

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69
Q

how often does home bp monitoring need to be measured?

A

4 times a day for a week (only use last 6 days if its a first time use patient)

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70
Q

what stage of hypertension should be sent to the hospital?

A

stage 3

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71
Q

what is classed as stage 1 hypertension?

A

clinic blood pressure ranging from 140/90 to 159/99 and subsequent ABPM daytime average or HBPM average blood pressure ranging from 135/85 to 149/94

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72
Q

what is stage 2 hypertension?

A

clinic blood pressure of 160/100 or higher but less than 180/120 and ABPM/HBPM 150/95

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73
Q

what is stage 3 hypertension?

A

clinic systolic blood pressure of 180 or higher or clinic diastolic of 120 or higher

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74
Q

what else do we need to do when we investigate for high blood pressure?

A

assess for cardiovascular risk
assess for target organ damage

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75
Q

what assesments are in the tests for target organ damage?

A

blood in urine
protein in urine
measure of blood sugar over last 3 months (HbA1C)
ECG (left ventricle)

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76
Q

what should be presented to the patiemt when discussing their 10 year risk?

A

present individualised risk and benefit scenarios
present the absolute risk of events numerically
use apropiate diagrams and text

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77
Q

what are the modifiable risk factors?

A

smoking
cholestrol
blood pressure
BMI

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78
Q

what are the non-modifiable risk factors?

A

age
sex
FHx
migrane
RA
SLE
severe mental illness

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79
Q

what does anyone with hypertesion and diabetes recieve?

A

ACEi

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80
Q

what needs monitoring whilst on CCB?

A

BP not blood

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81
Q

what ACEi are you most likely to prescribe?

A

ramipril

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82
Q

what CCB are you most likely to prescribe?

A

amlodipine

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83
Q

what TLD are you most likely to prescribe?

A

indapamide

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84
Q

why is lipid modification essential for CVDs?

A

CVD is caused by blood clots or atherosclerosis, which is a build up of fat in the artery restricting blood flow

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85
Q

what is atherosclerosis?

A

is a condition where there is a build up of fatty deposists inside an artery which causes the artery to harden and narrow, restricting the blood flow

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86
Q

what is primary prevention?

A

strategies identify and alter modifiable risks to reduce incidence in disease-free individuals or in the population.​

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87
Q

what is secondary prevention?

A

strategies target individuals with established disease, who have usually had an ‘event’, to reduce morbidity and mortality. ​

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88
Q

how is good cholestrol controlled?

A

by diet and lifestyle

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89
Q

how is bad cholestrol controlled?

A

can be treated

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90
Q

what percentage on the CVD risk should patients be prioritsed for an assessment?

A

10%

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91
Q

what should your HDL ratio be below?

A

5

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92
Q

when should pharmacological treatment be introduced to the patient?

A

after a discussion about the risks and benefits of treatment, co-morbidities, potential benefits from lifestyle interventions and the persons prefereance

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93
Q

if a patient presents with muscle pain from statins what should you do?

A

reduce dose
reassure them that a very small amount of people taking statins actually gain muscle pain

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94
Q

before starting lipid modification therapy, what should be tested?

A

a non-fasting lipid profile
liver function tests
renal function
HbA1c
creatinine kinase
thyroid stimulating hormone

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95
Q

for primary prevention of CVD what should be offered to patients?

A

atorvastatin 20 mg daily

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96
Q

for secondary prevention of CVD what should be offered to patients with exsiting CVD?

A

atorvastatin 80mg daily

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97
Q

what is familial hypercholesterolaemia (FH)?

A

an inherited conition characterized by high cholestrol concentrated in the blood

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98
Q

what are the potential developments of FH?

A

atherosclerosis andcoronary heart disease

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99
Q

what are some chlinica signs of hypercholesterolaemia?

A

tendon xanthomata (highly specific)
xanthelasmata (chlestrol deposits)(low specificity)
corneal arcus (white band before the coloured part of the eye)(highly specific)

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100
Q

what happens if Familial hyperlipidaemia is left untreated?

A

leads to greater than 50% risk of coronary heart disease in men by the age of 50 years and at least 30% in women by the age of 60

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101
Q

how to treat Familial hyperlipidaemia?

A

aggresive early treatment necessary as soon as diagnosed in adults?
in children with homozygous FH- lipid-modifying drug treatment is usually started by the age of 10 years or at the earliest opportunity thereafter, increase as they grow and aggressive treatment whenthey can tolerate it.

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102
Q

wht is the pharmacologicl treatment for hyperlipidaemia?

A

HMG-coA reductase inhibitors (statins)

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103
Q

what type of receptor is a AT! receptor?

A

G coupled receptor

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104
Q

what happens when AT1 is activated?

A

vasoconstriction and aldoterone release
the vasoconstriction increases peripheral resistance
the aldosterone release increases cardiac output
both of these increase blood pressure

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105
Q

what is pharmacokinetics?

A

the movement of drugs within the body, including absorption, distribution, metabolism and excretion

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106
Q

what enzyme system is responsible for metabolising many antihypertensive drugs?

A

cytochrome P450

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107
Q

when do additive interactions occur?

A

when the combination of two drugs produces an effect equal to the sum of their individual effects

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108
Q

when do synergistic interactions occur?

A

when the combination of drugs produces an effect greater than the sum of their individual effects

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109
Q

when do antagonistic interactions occur?

A

when the combination of drugs diminishes or cancels out their individual effects

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110
Q

what are teh ACEi drug-drug interactions?

A

Concurrent use of ACE inhibitors and nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the effectiveness of ACE inhibitors and increase the risk of renal impairment, as NSAIDs can counteract the vasodilatory effects of ACE inhibitors.​

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111
Q

what are ACEi drug-food interaction?

A

Consuming high-sodium meals or foods rich in potassium (such as bananas or oranges) can counteract the effects of ACE inhibitors by potentially increasing blood pressure or interfering with the balance of electrolytes.​

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112
Q

what are ACEi drug-herbal interactions?

A

Taking St. John’s wort (Hypericum perforatum) along with ACE inhibitors may reduce the effectiveness of the medication due to St. John’s wort inducing DME that can accelerate the breakdown of ACE inhibitors.​

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113
Q

what are CYP450 inducers?

A

Concurrent use of rifampin, an antibiotic and a potent cytochrome P450 inducer, with ACE inhibitors can accelerate the metabolism of ACE inhibitors, potentially reducing their effectiveness and requiring higher doses for adequate blood pressure control.​

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114
Q

what are CYP450 repressors?

A

Concurrent use of fluoxetine, a selective serotonin reuptake inhibitor (SSRI) and a cytochrome P450 repressor, with ACE inhibitors can inhibit the metabolism of ACE inhibitors, potentially increasing their blood levels and leading to an increased risk of side effects.​

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115
Q

what are ARB drug-drug interactions?

A

Co-administering beta-blockers with calcium channel blockers can lead to an enhanced blood pressure-lowering effect and an increased risk of bradycardia (low heart rate) due to additive negative chronotropic and negative inotropic effects.​

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116
Q

what are ARB drug-food interactions?

A

Grapefruit juice may inhibit the metabolism of beta-blockers, leading to increased blood levels of the drugs. This can potentially intensify the effects of beta-blockers, resulting in prolonged heart rate reduction and lowered blood pressure.​

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117
Q

what are ARB drug-herbal interactions?

A

Concurrent use of ginseng and beta-blockers may interfere with the blood pressure-lowering effects of beta-blockers. Ginseng can indirectly stimulate the production of adrenaline, which can counteract the beta-blocking activity of these medications.​

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118
Q

what are CCB drug-drug interaction?

A

Simultaneous use of CCB and statin medications can increase the serum levels of statins, potentially leading to statin toxicity e.g. muscle pain and liver toxicity.​

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119
Q

what are CCB drug-food interaction?

A

Consuming grapefruit can interfere with the metabolism of CCBs, leading to increased blood levels of CCBs. This interaction can enhance the hypotensive effects of CCBs.​

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120
Q

what are CCB drug-herbal interactions?

A

Consuming hawthorn (Crataegus) alongside CCBs can cause additive effects on blood pressure reduction. Hawthorn has mild vasodilatory properties and can potentially enhance the antihypertensive effects of CCBs.​

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121
Q

what are TLD drug-drug interactions?

A

Using thiazide diuretics in combination with NSAIDs can reduce the diuretic and antihypertensive effects of thiazides due to NSAIDs inhibiting renal blood flow and decreasing the efficacy of thiazid

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122
Q

what are TLD drug-food interactions?

A

Consuming licorice can lead to decreased potassium levels and increased blood pressure, counteracting the effects of thiazide diuretics. ​

This is due to licorice ​

  • inhibiting the breakdown of cortisol, which can cause sodium and water retention​
  • decrease in potassium levels, as both can lead to potassium loss​
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123
Q

what does AT1 do once activated?

A

vasoconstriction of the smooth muscles
aldosterone release
adrenergic innervations (adrenaline release and inhibit update)
antidiuretic release

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124
Q

what is ACE?

A

a zinc containing dipeptidyl carboxypeptidase enzyme

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125
Q

where is ACE located?

A

on the luminal side of the vascular endothelium

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126
Q

why is ACE found in the lungs as much?

A

the lung has a vast surface area of vascular endothelium, which is rich in ACE

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127
Q

what does ACE do?

A

cleaves the terminal histidyl-leucine from angiotensin 1 to form the ocapeptide angiotensin 2

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128
Q

what is angiotensin 2 ?

A

a peptide hormone, that acts at AT1 receptors, stimulating both vasoconstriction and aldosterone release

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129
Q

what does ACEi do?

A

ACE inhibitors lower blood pressure by reducing the vasoconstriction induced by angiotensin II, thereby decreasing peripheral resistance. Consequently, the lower Ang II level reduces the sodium and water reabsorption and cardiac output. ​

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130
Q

why do ACEi induce a dry cough in some patients?

A

ACEi blocks the breakdown of bradykinin, and increase bradykinin levels, which can contribute to the vasodiator action
accumulation of bradykinin induces sensitation of airway sensory nerves via rapidly adapting stretch receptors and C-fiber receptors that release neurokinin A and substance P
This causes airway smooth muscle to constrict leading to bronchoconstriction and persistent dry cough. ​ (most common adverse effect, 10-20% of patients)​

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131
Q

what should be monitored while on ACEi?

A

serum creatinine and potassium
assess renal structure and function (discontinue ACE inhibitors for patients with bilateral renal artery stenosis)

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132
Q

why are ACEi not reccomended for collagen vascular disease?

A

possible increased risk of agranulocytosis- blood counts recommended

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133
Q

what do ARBs do?

A

receptor agonists that block type 1 angiotensin 2 receptors on blood vessels and other tissues such as the heart

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134
Q

what are the possible adverse effects of ARBs?

A

hyperkalaemia
renal impairment

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135
Q

what is hyperkalaemia?

A

potassium retention

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136
Q

what caused hyperkalaemia from ARBs?

A

the reduction of aldosterone

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137
Q

what is renin?

A

proteolytic enzyme that catalyzes the conversion of angiotensinogen to angiotensin 1

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138
Q

what do renin-inhibitors do?

A

produce vasodilation by inhibiting the activity of renin, which is responsible for stimulating angiotensin 2 formation

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139
Q

what are the 2 classes of CCBs?

A

nondihydropyridines
dihydropyridines

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140
Q

what are dihydropyridines?

A

Dihydropyridine class of CCBs are highly vascular selective and reduce systemic vascular resistance and arterial pressure. ​

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141
Q

what is cholestrol?

A

27 carbon compound with a unique structure with a hydrocarbon tail, a central sterol nucleus made of four hydrocarbon rings, and a hydroxyl groups

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142
Q

what is the use of cholestrol?

A

essential component that makes the cell membrane and modulates membrane fluidity, and critical for cell growth and viability; Precursor for steroid hormones, vitamin D and bile salts​

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143
Q

how is cholestrol absorbed?

A

absorbed from micelles into the intestinal wall through a recently identified protein channel , niemann-pick C1 like 1 protein on the enterocyte plasma membrane

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144
Q

what is the ‘‘de novo’’ synthesis?

A

the cholestrol synthesis in the liver?

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145
Q

are cholestrol and triglycerides insoluble in water?

A

yes
and they require a carrier protein

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146
Q

what are lipoproteins?

A

complex particles that mobilise cholestrol and Triglycerides

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147
Q

what are the functions of apolipoproteins?

A
  1. serving a structural role
  2. acting as ligands for lipoprotein receptors
  3. guiding the formation of lipoproteins
  4. serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins
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148
Q

what is the exogenous pathway of lipid homeostasis?

A

1.The exogenous lipoprotein pathway starts with the incorporation of dietary lipids into chylomicrons in the intestine. ​
2.In the circulation, the triglycerides (TG) carried in chylomicrons are metabolized in the muscle and adipose tissue by lipoprotein lipase (LPL) releasing free fatty acids (FA), which are subsequently metabolized by muscle and adipose tissue, and chylomicron remnants are formed. ​
3.Chylomicron remnants are then taken up by the liver.​

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149
Q

what is the endogenous pathway for lipid homeostasis?

A

1.The endogenous lipoprotein pathway begins in the liver with the formation of VLDL​
2.The triglycerides carried in VLDL are metabolized in the muscle and adipose tissue by lipoprotein lipase releasing free fatty acids and IDL are formed. ​
3.The IDL are further metabolized to LDL, which are taken up by the LDL receptor in numerous tissues including the liver, the predominant site of uptake.​

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150
Q

what is the reverse cholestrol transport?

A

excess cholestrol from cells is brought back to the liver by HDL in a process known as reverse cholestrol transport

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151
Q

what are the steps in reverse cholestrol transport?

A

1.RCT begins with the formation of nascent HDL by the liver and intestine. These small HDL particles can then acquire cholesterol and phospholipids that are effluxed from cells, a process mediated by ABCA1 resulting in the formation of mature HDL. ​

2.Mature HDL can acquire additional cholesterol from cells via ABCG1, SR-B1, or passive diffusion. ​

3.The HDL then transports the cholesterol to the liver either directly by interacting with hepatic SR-B1 or indirectly by transferring the cholesterol to VLDL or LDL, a process facilitated by CETP. ​

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152
Q

what is the pathophysiology of atherosclerosis?

A

1) endothelial dysfunction​

2) formation of lipid layer or fatty streak within the intima​

3) migration of leukocytes and smooth muscle cells into the vessel wall ​

4) foam cell formation​

5) degradation of extracellular matrix​

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153
Q

what are the pharmacological options in lowering lipid?

A
  1. cholestrol syntheisi inhibition
  2. intestinal absorption
  3. lipoprotein lipase activity
  4. HDL
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154
Q

what is used for cholestrol synthesis inhibition?

A

statins

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155
Q

what is coronary artery from?

A

poor supply of oxygen to the heart

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156
Q

what are the conditions that lead to coronary artery disease?

A

hypertension
endothelial dysfunction
atherosclerosis
ischaemia
CAD

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157
Q

when will the heart recieve high oxygen?

A

relaxation (diastole)

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158
Q

why does relaxation still have high pressure in the aortic arch?

A

due to the backflow of the blood, also because the coronary artery is narrower therefore has higher pressure

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159
Q

what is the coronary circulation?

A

two tiny arteries leaving out the aorta
profuse blood to the myocardium
handles high pressure

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160
Q

how does coronary thrombosis develop?

A

thickening of the internal surface of arteries or progression of atherosclerotic lesions, occlude and affect oxygen supply to heart muscles

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161
Q

what is the structure of the coronary artery in stable angina?

A

Atherosclerotic lesions (atheroma/fibrous plaque) narrow coronary arteries and reduce their ability to dilate​

162
Q

what is the structure of coronary arteries in unstable angina?

A

Lesions rupture and stimulate platelet aggregation/thrombus formation. ​

Thrombus occludes the artery and prevents blood flow/supply ​
collagen release from the lesions rupturing causes a blockage in the artery. RBC and platelets adhere to the collagen, this causes thrombus formation​

163
Q

what are antianginal drugs?

A

nitrates
sublingual glyceryl trinitrate (GTN spray)

164
Q

what does GTN do?

A

only frug that directly dilates, can bypass cell membrane

165
Q

what do nitrates do?

A

vasodilate
decrease venous pressure
decreased arterial pressure
reduced preload and afterload
decreased oxygen demand
prevents/ reverses vasospasm
vasodilation

166
Q

what are the 2 types of nitrate drugs?

A

direct and organic
organic needs to be converted to work

167
Q

what are the second line options of antianginal drugs?

A

I(F) current inhibitors

168
Q

what are I(F) current inhibitors?

A

selectively block the Hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels present within the SA nodes and lowers the heart rate without affecting the contractility of the cardiac muscle

169
Q

what could develop from coronary artery disease?

A

thrombosis and lesions rupture
myocardial infarction
reduced contraction
ventricular dilation and remodelling
heart failure
cardiac death

170
Q

what does it tell you when the troponin levels rise in the blood?

A

early signs of MI or heart attack because muscle dying from reduced blood flow/ low oxygen which releases the troponin

171
Q

where is troponin usually located?

A

in the actin-myosin circulation in the smooth muscle

172
Q

what is thrombosis?

A

blood clotting in artery

173
Q

what is embolism?

A

blood clot/endogenous materials moving in the blood and vessels and obstruct blood flow
Embolism are fragments that brake off from the blood clot and is free flowing

174
Q

what are protein c and s ?

A

natural coagulants that are free flowing in the blood, used to regulate coagulations

175
Q

what is polycythaemia?

A

too many cells in the blood, decreases blood flow, increase viscosity

176
Q

what is endothelial injury?

A

complete blockage

177
Q

what are the stages of haemostasis?

A
  1. vascular spasm
  2. platelet activation plug
  3. coagulation patch
178
Q

why is vitamin K important in the coagulation step of haemostasis?

A

Vitamin k dependant , prothrombin activator is activated by vitamin k​
Prothrombin is responsible for activating the thrombin​
Thrombin is responsible for making fibrinogen that makes fibrin used for the coagulation​
​

179
Q

what stage is platelet endothelial activation used?

A

platelet activation plug in haemostasis?

180
Q

what happens durng the platelet endothelial interaction in a healthy patient?

A

In healthy–> High adp–> P2Y1 on endothelial cells sense–>binds to ADP–> release PG12 and NO from endothelial cells –>inhibit platelet activation–> prevent plug formation​

181
Q

what happens during the platelet activation endothelial interaction in a patient with atherosclerosis?

A

With atherosclerosis lesions= no P2Y1 endothelial cells​ =doesnt prevent plug formation

182
Q

what happens in the platelet-fibrin plug formation?

A

Von Willebrand factor acts as a bridge between collagen, exposed in damaged blood vessels, and the glycoprotein receptors, GPIIb/IIIa expressed in activated platelets
Glycoprotein receptors, GPIIb/IIIa binds to fibrinogen and form platelet-fibrin plug​

183
Q

what is an arrhythmia?

A

abnormal rate and /or rhythm of heartbeat

184
Q

what would someone with AFs ECG look like and why?

A

there would be no P waves as AV node is working too fast/ectopic
their right atrium will be chaotic for firing electricity, the AV node will ignore most of that and only receive 1 of them to beat rhythmically

185
Q

what are the common arrythmias?

A

ectopic beats
atrial fibrilation
atrial flutter
ventricular tachycardia
ventricular fibrilation

186
Q

what are the types of atrial fibrilation?

A

paroxysmal AF
petsisteent AF
long-standing persistent AF
permanant AF

187
Q

what are the syptoms of AF?

A

can be asymptomatic
palpitations
tiredness
breathlessness
syncope/ dizziness
chest pain

188
Q

what is the treatment plan of atrial fibrillation?

A

admit if necessary
identify and manage underlying causes and triggers
rate control
rhythm control
stroke prevention

189
Q

what is used to control rate?

A

beta-blockers
rate-limiting calcium channel blockers
digoxin monotherapy

190
Q

what is used to control rhythm?

A

pharmacological cardioversion (flecainide, amiodarone)
electical cardioversion
surgical cardioversion

191
Q

what are the types of anticoagulations?

A

direct-acting oral anticoagulants (DOACs)
vitamin K antagonists

192
Q

what should we know about DOACs?

A

Now much more common than warfarin​
Standard dosing ​
No monitoring of INR required​
A number of interactions have been discovered, more being discovered​
Most common adverse effect is bleeding – more major GI than CNS​
Difficult to reverse the effects – idarucizumab for dabigatran, andexanet alfa for apixaban or rivaroxaban​

193
Q

what are the 5 steps of the patient safety incident reporting?

A

record
learn
shre
act
review

194
Q

what are the six safety competencies included in the ‘safety competencies framework’?

A

1.Recognising the importance of ongoing collaboration and the commitment to advocate for change. ​

2.Demonstrate capabilities and competencies that are essential to efficient, effective and safe collaborative practice.​

3.Effective communication benefits both patients and healthcare providers, builds trust and is a precondition of obtaining patient consent. ​

4.Collect and monitor performance data to assess risk and improve outcomes. ​

5.Optimising the human and environmental factors that support the achievement of best human performance.​

6.Open, honest and empathetic disclosure and appropriate apologies by healthcare providers benefit everyone: patients and families, healthcare providers and their organisations. ​

195
Q

what are the main 7 points in ‘To Err is Human’?

A

1.Prevalence of medical errors​

2.Human errors​

3.Systemic causes​

4.Accountability and reporting​

5.Development of the National Patient safety Agency​

6.Continuous improvement​

7.Patient awareness​

196
Q

what do anticoagulant drugs do?

A

prevent thrombosus formation

197
Q

what does antiplatelet drugs do?

A

prevent platelet activation

198
Q

what do fibrinolytics drugs do?

A

clot retraction

199
Q

what does warfarin do?

A

Inhibit Vitamin K-dependent protein C, natural anticoagulant and may cause pro-coagulant effects before exhibiting anti-coagulant effect.

200
Q

what effect does heparin have in the platelet-endothelial interaction?

A

anti-thrombin heparin complex inhibit thrombin activity (platelet activation is inhibited)

201
Q

why do fibrinolytic drugs activate plasminogen?

A

because the tissue plasminogen activator with the plasminogen create plasmin which digests fibrin (dissolution of clot)

202
Q

what do activated platelets act on?

A

Activated platelets stimulate the release ADP which acts on P2Y12 receptors in platelets to activate positive feedback (more platelet plug formation)​

203
Q

what are the symptoms of an ACS condition?

A

Chest pain​

Pains in other parts of the body

Lightheaded / dizzy​

Sweating​

Shortness of breath​

Feeling sick (nausea) or being sick (vomiting)​

Overwhelming feeling of anxiety / panic​

Coughing or wheezing​

204
Q

what is the character symptom of angina?

A

crushing, squeezing, constriction brought on by physical or emotional exertion

205
Q

what is the unique symptom of unstable angina?

A

brought on by physical or emotional exertion or at rest

206
Q

who has worse symptoms of ACS?

A

women

207
Q

what are the red flags in ACS?

A

Chest pain at rest lasting >15 – 20 mins​

Recent onset of unstable angina symptoms​

Unresponsive to GTN​

Associated with autonomic symptoms:​

Nausea and vomiting​

Sweating ​

208
Q

what are the 3 ways to diagnose ACS?

A

through patient history and identification of patient risk factors
ECG
blood tests

209
Q

what does the ECG look like in STEMI?

A

elevation of ST

210
Q

what does the ECG look like in an unstable angina?

A

normal

211
Q

what does an ECG look like in an NSTEMI?

A

normal

212
Q

in ACS when are troponin levels risen?

A

NSTEMI and STEMI not unstable angina

213
Q

what is the first and second line treatment of angina?

A

antianginal drugs
minimise risk of cardiovascular events

214
Q

what is the initial mnagement of ACS?

A

aspirin 300mg
fondiparinux 2.5mg OD

215
Q

what is a potential initial management of STEMI?

A

pre-cutaneous intervention (PCI)
fibrinolysis

216
Q

what is a PCI?

A

Where coronary arteries have been identified as being stenosed, a drug eluting stent is inserted to widen coronary arteries again

217
Q

what drugs should be used when a patient requires a PCI?

A

aspirin
ticagrelor OR prasugrel
fondiparin

218
Q

what is fibrinolysis?

A

break up the blood clot in the coronary arteries

219
Q

what is acute heart failure?

A

sudden deterioration in HF, which can lead to hospitalisation

220
Q

what is chronic heart failure?

A

established diagnosis of HF or gradual onset of symptoms

221
Q

what is the aim lf heart failure treatment?

A

try and extend the 5 year mortality rate

222
Q

what is the treatment of heart failure with preserved EF?

A

offer loop diuretic

223
Q

what is the treatment for heart failure with reduced ejection fraction?

A

loop diuretic
ACEi
beta blocker

224
Q

what is the treatment for acute decompensated HF?

A

IV diuretics

225
Q

what treatment will all heart failure patient eventually recieve?

A

palliative care

226
Q

what factors affect cardiac output?

A

preganancy
exercise
respiration
age

227
Q

what supplies blood to the heart?

A

the 4 coronary arteries
2 right
2 left

227
Q

how many types of myocardial infarctions are there?

A

5 + injury

228
Q

what is type 1 myocardial infarctions?

A

spontaneous myocardial infarction related to ischaemia due to primary coronary event such as plaque erosion and/or rupture, fissuring or dissection

229
Q

what is type 2 myocardial infarction?

A

secondary to ischaemia due to either increased oxygen demand or decreased supply

230
Q

what is tyoe 3 myocardial infarction?

A

sudden unexpected cardiac death often with symptoms suggestive of myocardial ischaemia

231
Q

what is type 4 myocardial infarction?

A

associated with percutaneous coronary intervention or stent thrombosis

232
Q

what is type 5 myocardial infarctin?

A

associated with cardiac surgery

233
Q

which vessel supplies oxygenated blood to the SAN?

A

right coronary artery

234
Q

what steps are used in setting the basic rhythm?

A
  1. intrinsic cardiac conduction system
  2. gap junctions
235
Q

what is the absolute refractory period?

A

the cell is completely unexcitable to a new stimulus.​

236
Q

what is the effective refractory period?

A

ARP + short segment of phase 3 during which a stimulus may cause the cell to depolarize minimally but will not result in a propagated action potential (i.e. neighbouring cells will not depolarize

237
Q

what is the realtive refractory period?

A

a greater than normal stimulus will depolarize the cell and cause an action potential.​

238
Q

what is the supranormal period?

A

a hyperexcitable period during which a weaker than normal stimulus will depolarize the cells and cause an action potential. Cells in this phase are particularly susceptible to arrhythmias when exposed to an inappropriately timed stimulus, which is why one must synchronize the electrical stimulus during cardioversion to prevent inducing ventricular fibrillation.​

239
Q

what is the sinus node?

A

primary pacemaker
fires at rate of 60-100 depolarisations each minute

240
Q

what is the AV node?

A

base of RA
fires at rate of 40-60 dpm

241
Q

what is the ventricular (bundle of His)?

A

right and left branches
fires at rate of 20-40 dpm

242
Q

what is ventricular (purkinje fibers)?

A

less than 40 dpm

243
Q

what i the typical length of p-q?

A

0.1 sec

244
Q

what is the typical length of qrst?

A

0.3 sec

245
Q

what is the length of tp?

A

0.4 sec

246
Q

what is the PR segment?

A

pause between SA and av nodes

247
Q

what should the st segement be?

A

Should be at isoelectric line if elevated more than 2 small boxes (2mV) could signal issues infarction or ischaemia​

248
Q

what could be preset resulting in an abnormal ECG?

A

Acute impairment of blood flow to the heart (ischemia).​

Prior, or evolving, acute myocardial infarction.​

Abnormally fast, slow or irregular heart rhythms (arrhythmia).​

Aberrant (abnormal) conduction of electrical activity through the heart.​

249
Q

what is the mechanisms of arythmias?

A

The heart’s natural pacemaker (the sinus node) becomes diseased and slows down​

The normal conduction pathway is interrupted​

Another part of the heart takes over as pacemaker​

250
Q

what are the presenting symptoms of arythmias?

A

Palpitations​

Signs of hypotension​

Signs of ↓ brain perfusion​

Tachycardia →Angina​

Sudden cardiac death

251
Q

whata are the causes of arythmias?

A

Ischemia​

Hypoxia​

Acidosis or alkalosis​

Electrolyte abnormalities​

Excessive catecholamine exposure​

Autonomic influences​

Drug toxicity (eg digitalis or antiarrhythmic drugs) ​

Overstretching of cardiac fibres​

The presence of scarred or otherwise diseased tissu

252
Q

what are the most important types of supraventricular arythmias?

A

atrial fibrilation
atrial flutter
paroxysmal superventricular tachycardia

253
Q

what are the most important types of ventricular arythmias?

A

ventricular fibrillation
ventricular tachycardia

254
Q

what are the characteristics of sinus tachycardia?

A

regular rhythm
normal P waves
normal QRS
but HR >100 bpm

255
Q

what are the characteristics of sinus bradycardia?

A

regular rhythm
normal P waves
normal QRS
but HR <60bpm

256
Q

what are the characteristics of atrial fibrillation?

A

no consistent P waves
wavy isoelectronic line

257
Q

what are the characteristics of atrial flutter?

A

Normal atrial rhythm but generally irregular​

Abnormal atrial rate: 150 to 400 beats/minute ​

Normal rate as AV node stops conduction of some APs​

Sawtooth P wave configuration – multiple P waves per QRS​

QRS complexes uniform in shape but irregular in rate​

258
Q

what are the charateristics of supraventricular tachycardia?

A

Extremely fast electrical activity in the ventricles​

Regular​

> 150bpm​

No P waves (?hidden)​

Narrow or normal QRS​

Cant measure ​

259
Q

what are the characteristics of ventricular tachycardia?

A

Extremely fast electrical activity in the ventricles​

Rhythm is usually regular​

Fast rate 120-200bpm​

P wave is blurred in the QRS complex but the QRS complex has no associate with P wave​

QRS complex is wide and bizarre; T wave is in the opposite direction​

PR Interval is not present​

260
Q

what are the characteristics of ventricular fibrillation?

A

Rate is rapid and uncoordinated, with ineffective contractions​

Rhythm is chaotic​

QRS complexes wide and irregular​

P wave is not seen​

PR interval is not seen​

261
Q

what are the order of fatal arythmias?

A

Ventricular Fibrillation (V-fib)​
Ventricular tachycardia (VT)​
Supraventricular tachycardia​
Bradycardia ​
Heart block​
Atrial Fibrillation

262
Q

what do anti-arrythmic drugs act on?

A

supraventricular arrythmias
both supraventricular and ventricular arrythmias
ventricuoar arruthmias

263
Q

what do class 1 antiarrythmic drugs do?

A
  1. Na+ channel blockers​
  2. Influx of Na+ into cardiac myocyte during Phase 0 – slower depolarisation​
  3. Conduction of AP thus wide QRS – slows heart rate​
264
Q

what do antiarrythmic drugs do?

A

treat supraventricular tachycardias

265
Q

what do class 3 antiarrythmic drugs do?

A

treatment of recurrent hemodynamically unstable VT and recurrent VF

266
Q

what are all the diseases where beta blockers are used as drugs?

A

hypertension
arrythmia
angina
MI
CHF

267
Q

what is the structure of catecholamines?

A

catechol group
amine group
it is a G protein coupled receptor

268
Q

what are the targets of catecholamines?

A

norepinephrine
epinephrine

269
Q

where are adrenoreceptors?

A

widely located in various organs and tissues as well as on neurons of both the peripheral nervous system and central nervous system (CNS)​

270
Q

what are the characteristics of beta-1 adrenoreceptors?

A

major in the heart → all β-blockers affinity for β1 → inhibit binding norepinephrine/epinephrine → slow heart rate/decreased myocardium contractility​

in kidney→ all β-blockers affinity for β1 → decrease secretion of renin→ decrease plasma levels of angiotensin II → vasodilatation​

271
Q

what are the characteristics of beta-2 adrenoreceptors?

A

major in CNS→ increased sympathetic activity→ β1- selective drugs can also produce CNS side effects​

vascular, lungs, uterus smooth muscle → arterial dilation, bronchodilation, uterus muscle relaxation. β2- agonist used for alleviating respiratory distress in persons with asthma or used to inhibit uterine contractions in premature labour​

272
Q

what are the characteristics of alpha-1 adrenoreceptors?

A

stimulation of smooth muscle of the peripheral vasculature → constriction causing a rise in blood pressure. α1-antagonist relaxation of the blood vessels and a drop in blood pressure​

273
Q

what are the 3 sections of adrenoreceptors?

A

extracellular
membrane
intracellular

274
Q

what are the 5 binding sites of alpha and beta adrenoreceptors?

A

alcohol
amine
phenols
catechol aromatic ring
alkyl substitution on the side chain

275
Q

what is the characteristics of the alcohol group binding site on the adrenoreceptor?

A

the R-enantiomer is more active than the S-enantiomer. H-bond with Asn293​

276
Q

what is the characteristics of the amine binding site on the adrenoreceptor?

A

normally protonated and ionised at physiological pH. Ionic bond with Asp113.

277
Q

what is the characteristics of the phenol binding site on the adrenoreceptor?

A

important. H-bonds with Ser204 and 207. Groups capable of H-bonding​

278
Q

what is the characteristics of the catechol aromatic ring binding site on the adrenoreceptor?

A

stabilising hydrophobic interaction with Phe290​

279
Q

what is the characteristics of the alkyl substitution on the side chain binding site on the adrenoreceptor?

A

Steric effect which blocks H-bonding to the alcohol​

280
Q

why do we choose beta over alpha adrenoreceptor?

A

extra hydrophobic pocket: N-Alkyl substitution –> receptor selectivity
increasing the size of the N-Alkyl substitutent –> loss of potenty at the a-receptor but an increase in potenty at beta-receptors
beta-adrenoreceptor has a hydrophobic pocket into which a bulky alkyl group can fit

281
Q

what are the characteristics of beta-blockers?

A

Block the binding of norepinephrine and epinephrine (sympatholytic drugs)​
Pharmacological response: dependent on the drug-receptor affinity and selectivity​
Antagonist of β1: atenolol, metoprolol, bisoprolol, and nebivolol (cardio-selective) ​
Antagonists of both, β1 and β2: carteolol, nadolol, penbutolol, pindolol, propranolol, sotalol, and timolol (non selective)

282
Q

what are the two important structureal features of beta blockers?

A

1, two families;arylethanolamines and aryloxypropanolamines

2.stereochemistry of side chain

283
Q

what is the SAR of beta-blockers?

A

At least one aromatic and/or heteroaromatic ring system. Hydrophobic interaction with Phe290​

Alcohol group: H-bond with Asn293. R-enantiomer (arylethanolamines); S-enantiomer (aryloxypropanolaminesm) =R absolute configuration of catecholamines​

Amine: ionised (N+). Ionic bond with Asp113. Essential. Branched bulky N-alkyl substituents (isopropyl and t-butyl groups) for β-antagonist activity (interaction with extra hydrophobic pocket) ​

Majority clinically available selective β1-blockers : phenyloxypropanolamine with para substitutions ​

Replacing O: with S, CH2, or NMe is detrimental. Ok with NH. Substitution on the side chain increases metabolic stability but lowers activity​

284
Q

what are the 4 classes of antiarrhythmic drugs?

A

sodium vhannel blockers
beta-adrenergic blockers
potassium channel blockers
calcium channel blocers

285
Q

what is the MOA of sodium channel blockers?

A

affinity for Na+ channels in the fast action potentia tissue –> decrease the influx of Na+. differ in selectivity, onse of action and offset times

286
Q

what are MOA of beta-adrenergic blockers?

A

Blocking norepinephrine from binding/activating β1-receptors, → significant decrease in sinoatrial (SA) and atrioventricular (AV) nodes automaticity → prolongation of the PR interval. β1-selective antagonist and nonselective β1/β2-antagonist). Esmolol and Propranolol

287
Q

what is the MOA of potassium channel blockers?

A

Block the outflow of K+ → prolong the refractory period and AP duration by prolongation of QT interval.

288
Q

what is the MOA of calcium channel blockers?

A

Non-dihydropyridine Ca2+ channel blockers → decrease the influx of Ca2+ → decrease the slope of phase 0 and prolong the refractory period of the SA and AV nodes → decrease heart rate and prolongation of the PR interval, thus taking longer for the AP to travel from the atrial myocardium to the ventricle. ​

Verapamil and Diltiazem​

289
Q

what are the different types of pharmaceutical powders?

A

dusting powder
oral powder in sachets
powders for reconstitution
inhilation
bulk powders for tablets and capsules

290
Q

what are crystalline structures?

A

regular repeating stuctures

291
Q

what are amorphous structures?

A

irregular order

292
Q

what is polymorphism?

A

different molecular packing arrangments in the crystal lattice

293
Q

what is the affect of x-ray diffraction of a crystal?

A

each crystal has a characteristic pattern of diffraction angles and intensity of the diffracted beam, corresponding to the planes of the crystal

294
Q

what is the outcome of crystalline structures in an x-ray diffraction?

A

scattered only in certain directions

295
Q

what is the outcome of amorphous structure in an x-ray diffraction?

A

scattered in many directions

296
Q

what has higher stability, crystaline or amorphous?

A

crystalline

297
Q

what has higher hygroscopy, crystaline or amorphous?

A

amorphous

298
Q

what has higher soulubility, crystaline or amorphous?

A

amorphous

299
Q

what has higher dissolution rate, crystaline or amorphous?

A

amorphous

300
Q

what is hydrate?

A

if water is present in the crystal lattice

301
Q

what is solvate?

A

if solvents are present in the crystal lattice

302
Q

what does salt form of a drug increase?

A

solubility and dissolution rate

303
Q

what are co-crystals?

A

two or more molecules within the same crystal lattice

304
Q

what is stokes diameter?

A

diameter of a sphere with the same density and settling velocity as the particle

305
Q

what is aerodynamic diameter?

A

diameter of a sphere with the same terminal velocity in air or some other relevant fluid

306
Q

what is hydrodynamic diameter?

A

diameter of a sphere that diffuses at the same rate in liquid as the particle

307
Q

what are the brunguer- emmett-teller theory?

A

powder is filled into a vaccumed sealed chamber
small amount of nirogen gas are added to the chamber
the nitrogen molecules absorb of the powder is covered
pressure transducers sense the amount of gas absorbed from which the surface area can be calculated

308
Q

what is arithmetic mean?

A

regularly spaced out

309
Q

what is geometric mean?

A

irregularly spaced out

310
Q

what is a histogram?

A

incremental distribution
shows how many particles fall within a given size increment

311
Q

what is cummulative distribution?

A

shows how much material lies above or below a particular size

312
Q

how can we show skewed distribution?

A

Skewed distributions may be normalised by replotting the equivalent particle diameters using a logarithmic scale (lognormal distributions)​

313
Q

what is the use of linear-probability paper?

A

Spacing designed such that if you were to plot the cumulative distribution of a data that follows the normal distribution, it would fall on a straight line.​

314
Q

what is the use of log-probability paper?

A

Spacing designed such that if you were to plot the cumulative distribution of a data that follows the lognormal distribution, it would fall on a straight line

315
Q

what is central dispersion?

A

tendancy of the particle size to cluster around a particle value

316
Q

what is the use of coefficient of variation?

A

Normalise the standard deviation through division by the mean​
To compare the degree of variance between multiple sample populations​
Also known as relative standard deviation (RSD)​

317
Q

what is D90/D10 ratio?

A

Used by the pharmaceutical industry to describe polydispersity of powders, regardless of the distribution model.​

Useful measure of dispersion for multimodal distributions​

318
Q

what are the 7 methods of particle sizing?

A

sieving
microscopy
andreasen pipette
electrical sensing zone
laser light diffraction
photon correlation spectroscopy
cascade impactor

319
Q

what is the method of sieving?

A

fill –> seal –> agitate –> weigh

320
Q

what does electical sensing zone do?

A

bigger particles cause more resistance as it passes through
smaler particles cause less resistance as it passes through

321
Q

how does laser diffraction work?

A

The amount of light hitting the outer circles of the bull’s eye detector can be used to calculate the amount of diffracted light and thus the mean particle size​

322
Q

what does cascade impactor measure?

A

particle size of inhaled products

323
Q

what is the disconnection of C-C bond between phenyl ring and C carbonyl group?

A

friedel crafts acylation

324
Q

what is the disconnection of C-C bond between phenyl ring and C aliphatic chain?

A

friedel crafts alkylation

325
Q

what is the disconnection of C-C bond between 2 sp2 carbons?

A

suzuki coupling

326
Q

what is the disconnection of C-N?

A

nucleophilic acyl substitution

327
Q

what is the disconnection of C-O bond?

A

fisher esterification

328
Q

what is the disconnection of C-N (amines)?

A

alkylation of amies by alkyl halides
or reductive amination

329
Q

what is the disconnection of nucleophile-CH2-CH2-OH?

A

opening of epoxide by a nucleophile

330
Q

what is the disconnection of ring-(Br, Cl, NO2, SO3H)?

A

electrophilc aromatic substitution

331
Q

what is the disconnection of C-O ether bond?

A

williamson ether synthesis

332
Q

what is functional group interconversion?

A

Sometimes we need to use one group which leads to another. That means we will not have the “Sacrificial Group” in the final molecule, but it helps to form the TM or it directs the reactivity/selectivity​

333
Q

what is linear synthesis?

A

yield of each stage is the same and goes in one line

334
Q

what is convergent synthesis?

A

lower amount of steps, shorter time, higher yield, better carbon economy

335
Q

what is synthetic step?

A

shows how to convert the epoxide derivative into propanolol

336
Q

what is retrosynthetic analysis?

A

you have to work backwards, as the synthesis was done from right to left

337
Q

what are powders?

A

usually a mixture of fine powders, including active ingredient, colours, flavours and sweetening agents

338
Q

what are granules?

A

comprise powder particles that have been aggregated to from large particles sufficiently robust to withstand handling

339
Q

what are types of pharaceutical granules?

A

colchicine to treat gout
cholecalciferil for oesteoporosis
pyronaridine as antimalaria

340
Q

what is granulation?

A

process by which dry primary powders are processed to adhere to from larger multi-particulate entities

341
Q

why do we granulate?

A

denser
good flowability
uniform
reduce dust

342
Q

reasons for granulation?

A

To prevent segregation of the constituents of a powder mix​

Particles tend to segregate due to differences in the size, shape and density​

To improve the flow properties of the powder mix​

To improve compaction properties and uniformity of the mix​

To reduce toxic dust​

343
Q

what are the steps of wet granulation?

A

blend powder
add binder
moist mass
sieve
moist agglomerated
dry
dried granules
sieve
sized granules

344
Q

what are the limitations of wet granulation?

A

Cost: Granulation is an expensive process because of labour, time, equipment, energy and space requirements​
Stability may be major concern for moisture-sensitive or thermolabile drugs, as well as those exhibiting polymorphisms​
Loss of material during various stages of processing​
Multiple processing steps add complexity and make validation and control difficult​
Incompatibilities between formulation components can be aggravated​

345
Q

what is the equipment used for wet granulation?

A

high shear granulation
fluid bed granulation
extrusion spheronization
spray drying granulation

346
Q

what are the steps of dry granulation?

A

blend powder
compression
slug
mill
granules
sieve
sized granules

347
Q

what are the limitations of dry granulation?

A

High force/pressure involved in compaction​
Greater chances of generation of dust (cross-contamination) and environmental contamination​

348
Q

what are the types of nitrates?

A

direct and organic

349
Q

what drug class is a physiological antagonist of bp?

A

diuretics

350
Q

what is the effect of Nitric Oxide?

A

attatches to cytoplasmic guanylyl cyclase to release [cGMP] which causes more protein kinase G which results in more smooth muscle contractions

PDE isoform breaks down [cGMP]

351
Q

why can you not give ACEi as a first line treatment for hypertension for old and african caribean people?

A

old= age mediated loss of nephrons
afro-caribean= isuuficiency of renin

352
Q

why does ACEi cause hyperkalaemia?

A

blocks aldosterone which lowers sodium reuptake therefore causes retention of potassium

353
Q

why can you not give BB in early diagnosis of Hypertension?

A

non-specific pharmacology interactions

354
Q

why are thiazide diuretics beeter than loop diuretics?

A

thiazides are slower and longer
loop act stronger and shorter

355
Q

what are the characteristics of LDL?

A

enriched in cholesterol
contains 1 apo b-100 molecule (risk of atherosclerosis)

356
Q

what are the characteristics of HDL?

A

contains cholesterol and phospholipids
apo a-1 is at the core (decreased risk)
Role in RCT
(anti-atherogenic)

357
Q

what is the development of atherosclerosis?

A

enothelial dysfunction
formation of lipid layer
migratin of leukocytes and smooth muscle cells
foam cell formation
degradation of extracellular matrix

358
Q

what are fibrates more beneficial for and why?

A

more beneficial for hypertriglycerimia than hypercholesterimia because it activates a class of nucleotic receptors to upregulate expression of lipoprotein lipase which decreases triglyceride levels which increase HDL synthesis for RCT which increase LDL size (not cleared)

359
Q

what is arterial thrombi?

A

mainly platelets and ibrin

360
Q

what is venous thrombi?

A

pooled static blood

361
Q

what is a common ADR from antiplatelets?

A

haemorrhage

362
Q

what is the path of electric wave in the heart?

A

sa to av to bundle of his (collecting duct) to purkinge fibre

363
Q

what part of the heart has no electric conductivity?

A

fibrous midline

364
Q

what causes the blood flow from the heart?

A

atrial kick and cardiac twist

365
Q

what is the structure of the cells in a striated muscle?

A

one nucleus per cell

366
Q

what are the properties of the cardiac striated muscle?

A

elastic muscle
connected by intercalated disks

367
Q

what does ANP do and how is it released?

A

high blood volume and extreme stretching of the cardiac cells trigger ANP which is secreted by cells in the artia of the heart which are antagonists to angiotensin 2, this promotes loss of sodium and water from kidneys

368
Q

where is ACE stored?

A

in the vascular endothelium which is present in the lungs

369
Q

what does vascular selective mean?

A

they prefer to block channels in the blood vessels rather than in the heart

370
Q

how is cholesterol absorbed?

A

from m icelles into the intestinal wall through the niemann pick C1 like protein channel on the entero plasma membrane

371
Q

what does bile do?

A

emulsifies dietary liquids and facilitates absorption

372
Q

what is the de novo synthesis?

A

cholestreol is synthesized in the liver, where 2 acetyl-coa molecules form 1 acetoacetyl coA which then combines with another acetyl coA to form HMG-CoA which forms mevalonate which then forms cholestrol

373
Q

what are chylomicrons?

A

large triglyceride rich particles made by the intestine, which are involved in the transport of triglycerides and cholesterol to peripheral tissues which results in smaller particles called chylomicron remnants

374
Q

what is the exogenous pathway of lipid homeostasis?

A

incorporation of dietary lipids into chylomicrons in the intestine, the triglycerides in chylomicrons are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids that are metabolized by muscle and adipose tissue, chylomicron reminants are then taken up by the liver, where (endogenous pathway) it behins the formation of VLDLs that are then metabolized into LDLs and release free fatty acids to form IDLs

375
Q

where are VLDLs produced?

A

by the liver and are triglyceride rich

376
Q

what are IDLs?

A

the removal of triglycerides from VLDL by muscle and adipose tissue results in the formation of IDL particles which are enriched in cholestrol

377
Q

what is the cause of familial hyperlipidaemia?

A

familial hyperlipidaemia leads to high level of both LDL and triglycerides which develops at a young age and increaes the risk of early coronary heart disease, they contain high levels of apolipoprotein B which is part of the LDL cholestrol

378
Q

what does the liver do to compensate for the melonovate lost when statins are used?

A

the liver recruites more LDL from the circulation resulting to LDL clearance

379
Q

what are anion exchange resins?

A

drug type for hyperlipidaemia which bind to bile salts and are excreted in faeces, which results in reduced cholesterol absorption, cholesterol directed compensate for bile loss, LDL clearance (not used very much as it is very unpallitable and interferes wuth many fat soluble nutrients

380
Q

what does ezetimibe do?

A

blocks the transport protein niemann pick c1 like 1 in the gut wall, which reduces cholesterol absorption without affecting bile

381
Q

what do fibrates do?

A

fibrates elicit complex effects on circulating effects, activates a class of nuclear receptors/ transcription factors to uoregulate the expression of lipoprotein lipase and increase the lipoprotein lipase-mediated lipolysis

382
Q

what does niacin do?

A

reduce the circulation of VLDL and LDL and increase circulating HDL

383
Q

what protein levels go up in the blood if there is a blockage?

A

protein c and s

384
Q

how is heparin produced and what is its role?

A

endothelial cells produce heparin
natural heparin recruits antithrombotic cells as it inhibits thrombin activity

385
Q

what does vitamin k do?

A

activates coagulant factors

vitamin k reductase catalyses vitamin k oxidised into vitamin K reduced so that it is used to activate coagulant factors

warfarin is a vitamin k antagonist

386
Q

what do heparin and LMWH do?

A

binds to antothrombin and block thrombin mediated platelet activation

387
Q

what do NSAIDs do?

A

block cyclo-oxygenase therefore arachodonic acid cannot make endothial cells and platelets which will then reduce plug formation and reduce platelet aggregation on thromboxanes

388
Q

if reduction is not seen with atorvostatin, what else can be given ?

A

ezetimibe 10mg

389
Q

what needs to bemonitored in a patient taking amlodipine and a statin?

A

monitor organ damage as amlodipine has an increase of effect of statins

390
Q

what are class 1 antiarrythmic drugs?

A

block Na+ channels which cause slower depolarisation therefore lowering ap thus widening qrs which slows heart rate (disopyramidine, lidocaine, flecainide)

391
Q

what are class 2 antiarrythmic drugs?

A

beta 1 adrenergic blocker, which reduces ca channel to allow ca into cell therefore lengthes pr interval , good for svt (propanolol)

392
Q

what are class 3 antiarrythmic drugs?

A

potassium channel blockers, amiodarone which slow down the rate of repolarisation and prolongs the qrs duration (used for unstable VT and recuurent VF) (amiodarone, sotalol)

393
Q

what are class 4 antiarrythmic drugs?

A

CCBs to lower myocardial contractility and lower conduction velocity , decrease sinus rate (veapamil)

394
Q

what is digoxin?

A

an unclassified anti arrythmis- it is a cardiac glycoside used in treatment of mild to moderate heart failure and for ventricular respnse rate control in chronic atrial fibrillation

395
Q

what is the normal ejection fraction?

A

50%

396
Q

what is the reduced ejection fraction?

A

40%

397
Q

what is the treatment for acute heart failure?

A

IV diuretics rather than loop
however once stable for 48 hours stop IV and re start usual medication

398
Q

what drugs and drug classes are given for heart failure with reduced ejection fraction?

A

acei -hf w ref
ramipril 2.5mg bd
lisinopril 2.5mg od

beta blocker- hf w ref
bisoprolol 1.25mg od
metoprolol 12.5 mg od

minerocorticoid receptor antagonists- hf w ref
spironolactone 25mg od
epelerone 12.5mg od

sglt-2 inhibitors - hf w ref and ckd
dapagloflozin 10mg od
empagloflozin 10mg od
reversibly inhibit sodium glucose co transporter 2 in renal proximal convulated tubule

399
Q

what should be given for different types of arrythmias?

A

supraventricular arrythmias
verapamil hydrocjloride

supraventricular and ventricular arrythmias
amiodarone hydrochloride

ventricular arrythmias
lidocaine hydrochloride

PMP 201 (4 decks)

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