Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 31 Cardio-respiratory > PPT > Flashcards

PPT Flashcards

1
Q

what is ambulatory BP?

A

measures BP throughout day and night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

after ambulatory blood pressure monitoring (ABPM) a patient may be described as normotensive, what does this mean?

A

ABPM daytime average below 135/85mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

after ambulatory blood pressure monitoring (ABPM) a patient may be described as stage 1 hypertensive, what does this mean?

A

ABPM daytime average 135/85 or higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

after ambulatory blood pressure monitoring (ABPM) a patient may be described as stage 2 hypertensive what does this mean?

A

ABPM daytime average above 150/95

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

a patient after having ABPM is shown to have readings at day and night of less than 10% difference, what does this suggest?

A

blood pressure would normally dip at night

could be an underlying cause such as sleep apnoea for why this is happening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

after having ABPM a patient is found to have a daytime average below 135/85 yet a clinical blood pressure persistently over 140/90. what does this suggest?

A

white coat hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

a patient is 75 and has ABPM of 140/90. when should antihypertensive drug treatment be given?

A

the patient is under 80 with stage 1 hypertension. these patients should be given treatment if they have any of the following:

  • target organ damage
  • established CVD
  • renal disease
  • diabetes mellitus
  • 10 yr CV risk 20% or higher
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

a patient is found to have hypertension, what assessment should be offered?

A
  • albumin:creatinine ratio
  • test for haematuria using a reagent strip
  • plasma glucose
  • electrolytes and creatinine
  • estimated glomerular filtration rate
  • serum total cholesterol and HDL cholesterol
  • examine the fundi for the presence of hypertensive retinopathy
  • 12-lead electrocardiograph
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what drugs are used in the treatment of hypertension (8)?

A
  • ACE Inhibitors
  • Angiotensin receptor blockers
  • Beta blockers
  • Calcium channel blockers
  • Thiazide-like/thiazide diuretics
  • Spironolactone (aldosterone antagonist)
  • Alpha-receptor blockers
  • Loop diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the step approach of hypertension treatment and what are the exceptions to this?

A
  1. ACE inhibitor/ARB
    • calcium channel blocker
    • thiazide diuretic
  4. spironolactone

except in patients older than 55 or of afro-caribean origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how long should you wait before evaluating the therapeutic effect of hypertension treatment and what BP should be aimed for?

A

1 month
<140/90 in clinic
<135/85 at home

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a typical drug and dose given in the inital treatment of hypertension in a white patient under 50?

A

ramipril 2.5mg oral daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what would be the first step of hypertension treatment in a patient over 55 or of afro-caribbean origin?

A

calcium channel blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the potential side effects of ACE inhibitors?

A
  • dry cough (bradykinins)
  • hypotension (usually on first dose)
  • angioedema (sporadic and unpredictable)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when are the use of ACE inhibitors cautioned?

A

patients with renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the potential drug interactions of ACE inhibitors?

A
  • with spironolactone-hyperkalaemia

- with NSAID-AKI in patients with renal disease due to reduced perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

are there any sick day rules for antihypertensives?

A

yes

don’t take if unwell due to dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe cholesterol management in primary prevention of CVD?

A

QRISK >10%

atorvastatin 20mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What class of drugs are statins?

A

HMG-CoA reductase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe the main pathway of lipoprotein formation and metabolism?

A
  • lipids and fatty acids in gut emulsified by bile acids
  • transported in chylomicrons to liver
  • circulated as cholesterol and triglycerides to tisses in VLDL
  • endothelial LPL liberates FFA in adipose and muscle for storage or metabolism
  • this LDL is returned to hepatocytes via LDL receptors or taken up by LDL receptors in extrahepatic tissues
  • here they are oxidised and contribute to atherogenesis
  • HDL pool comes from chylomicrons following action of LPL and the reverse cholesterol pathway returns HDL to liver via receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when should patients on statins take it?

A

simvastatin and pravastatin-short half life-taken before bed to maximise effect as HMG-CoA reductase more active at night
atorvastatin and rosuvastatin-longer half life so can be taken when convenient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the mechanism of action of statins?

A
  • inhibit HMG-CoA reductase
  • reduces intracellular cholesterol
  • activates a protease
  • this cleaves sterol regulatory element binding protein (SREBPs) from ER
  • these translocate to nucleus and upregulate expression of LDL receptor gene
  • increases receptor mediated endocytosis of LDL and lowers serum LDL
  • HMG-CoA reductase also reduces intracellular levels of isoprenoids which are intermediates of cholesterol biosynthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the most common side effects of statins?

A

-headache
-GI disturbances
-muscle-aches, myopathy, rhabdomyolysis
rise in liver enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

in what patients should statins be used in with caution?

A
  • hepatic impairment
  • excreted by kidneys so dose should be reduced in patients with renal impairment
  • avoided in pregnancy (stop if trying to conceive)
  • avoid if breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what drugs can reduce the metabolism of statins?

A 
cytochrome P450 inhibitors such as
-amiodarone
-diltiazem
-itraconazole
-macrolide antibiotics
-protease inhibitors
accumulation of statin in body-increased risk of adverse effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the maximum dose of simvastatin when given with amlodipine?

A

20mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

a patient on statins is started on clarithromycin, what action should be taken?

A

statin discontinued temporarily until the antibiotic is finished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the most common concern for drug interaction between statins and another drug and when is this risk increased?

A

induced muscle injury

increased for statins metabolised by cytochrome P450 3A4 (simvastatin and atorvastatin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what statins are preferred if the patient is unavoidably on another strong inhibitor of CYP3A4?

A

fluvastatin

rosuvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what compund is in grapefruit juice that is a potent inhibitor of cytochrome P4503A4?

A

furanocoumarins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

when prescribing drugs to a patient what do you need to explain to them?

A
  • side effects
  • cautions
  • interactions
  • how to take the drug
  • when to seek advice
  • sick day rules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

when prescribing statins would do you need to explain to the patient?

A
  • seek advice if muscle symptoms
  • blood tests in 3 and 12 months
  • alcohol to a minimum
  • avoid grapefruit juice
  • sick day rules don’t apply to statin use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what other drugs can be used to treat high cholesterol?

A

fibrates

specific cholesterol absorption inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the Well’s criteria?

A

score of 3 or more suggests DVT

  • if high probability of PE=CT
  • if low probability of PE=D-dimer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what drugs can be used for immediate anticoagulation?

A
  • unfractionated heparin
  • LMWH
  • direct inhibitors of factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how do unfractionated heparin, LMWH and fondaparinux have their anticoagulant affect?

A

fondaparinux bind to antithrombin via a pentasaccharide sequence and accelerate its inhibition of various coagulation proteases, primarily inhibition of Factor Xa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is fondaparinux?

A

synthetic analogue of the naturally occurring pentasaccharide sequence found in heparin molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what other coagulation effect do heparin molecules with a molecular weight over 5400 have?

A

bridging antithrombin and thrombin and acting as a catalytic template.
Most heparin chains in UFH are long enough to exert this effect, but at least 50% of the heparin chains in LMWH are too small, hence LWMH exert most of their anticoagulant effect via indirect inhibition of factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what affect does fondaprinux have on antithrombin?

A

no effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

dosage of LMWH is dependent on…

A
  • condition used to treat

- body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what heparins are usually administered by infusion pump?

A

unfractionated hepatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what heparins are usually administered by SC injection?

A

LMWH

fondaparinux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what monitoring is needed in a patient of heparin and fondaparinux?

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q
  1. what is the potential side effect of heparins?

2. what drugs should be stopped when taking heparin?

A
  1. bleeding

2. stop NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

give examples of direct acting oral anticoaglants (DOACs)?

A

dabigatran
apixaban
rivaroxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the vitamin K dependent coagulation factors?

A

II (prothrombin)
VII
IX
X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the mechanism of vitamin K antagonists?

A

-blocks function of vit K epoxide reductase complex in the liver so less reduced vit K that is a cofactor for gamma carboxylation of vit K dependent coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is epoxide reductase needed for?

A

recycle vit K between reduced and epoxide forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what happens to vitamin K dependent factors without gamma carboxylation?

A

the vitamin K-dependent factors, including factors II (prothrombin), VII, IX, and X, are immunologically detectable, but they cannot function because they cannot adequately bind calcium and phospholipid membranes needed for their haemostatic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

describe Gamma carboxylation of glutamic acid residues and how does this affect desired anticoagulant effects of vit K antagonists?

A

occurs at the time of protein synthesis; it does not affect the structure or function of existing proteins. Thus, the ultimate anticoagulant effect of VKAs is delayed until the previously synthesized, functional clotting factors are cleared from the circulation. Depletion of both factor X and factor II (prothrombin) is important for clinical efficacy, and factor II has the longest half-life of the vitamin K-dependent factors (approximately three days). Thus, the desired anticoagulant effect of a VKA does not occur for at least three days after drug initiation despite prolongation of the prothrombin time (PT) at earlier time points.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why does warfarin have a transient procoagulant effect during the first day or 2 of use?

A

VKAs also inhibit vitamin K-dependent gamma carboxylation of the anticoagulant factors protein S and protein C, which inhibit activated factors VIII and V. Thus,warfarinhas a transient procoagulant effect during the first day or two of use. This is rarely of clinical significance, with the possible exception of patients who receive “loading doses” of warfarin (especially those with inherited protein C deficiency) who may (rarely) develop warfarin-induced skin necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what should you do initially when prescribing warfarin?

A

continue a LMWH for at least 5 days
Warfarin does not have an effect on the function of biologically-active, circulating factors that have already been synthesised – only the inhibition of new factors.
In addition to inhibiting the formation of procoagulant factors 2, 7, 9, 10 – warfarin also inhibits formation of anticoagulant proteins C & S. All the factors have varying half-lives which also carries a risk of warfarin potentially exerting an initial pro-coagulant effect if the presence of circulating anticoagulant factors are depleted prior to procoagulant factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why should aspirin be avoided in patients on warfarin?

A

potential for GI bleed which could be dangerous on warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what mechanisms can medications interact with vitamin K antagonists?

A

prolonged prothrombin time
increased bleeding risk independent of PT/INR
reduced anticoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

describe how medications can interact with VKAs by prolonging prothrombin time (PT)/INR?

A
  • Altered intestinal flora, with reduced intestinalvitamin Ksynthesis
  • Inhibition of hepatic CYP2C9, with reduced warfarin metabolism
  • Displacement ofwarfarinfrom albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

describe how medications can interact with VKAs by increasing bleeding risk independent of PT/INR?

A
  • Injury to gastrointestinal mucosa
  • Interference with platelet function
  • Other (incompletely characterized)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

describe how medications can interact with VKAs by reducing anticoagulation?

A
  • Induction hepatic CYP2C9, with increased warfarinmetabolism
  • Bypasswarfarineffect via large amounts ofvitamin K
  • Incompletely characterized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what drugs interact with warfarin by altering intestinal flora, with reducing intestinalvitamin Ksynthesis?

A

Antibiotics, especially cotrimoxazole, metronidazole, macrolides and fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what drugs interact with warfarin by Inhibition of hepatic CYP2C9, with reducedwarfarinmetabolism?

A

Many agents (e.g. fluconazole, metronidazole, amiodarone, gemfibrozil and sulfamethoxazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what drugs interact with warfarin by Displacement ofwarfarinfrom albumin?

A

Any medication that binds albumin; however, this effect is usually minor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what drugs interact with warfarin by injuring GI mucosa?

A

Aspirinand nonsteroidal anti-inflammatory drugs (NSAIDs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what drugs interact with warfarin by interference with platelet function?

A

Anti-platelet drugs, includingaspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what drugs interact with warfarin by Induction hepatic CYP2C9, with increasedwarfarin metabolism?

A

Rifampin,carbamazepine,phenytoin,primidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what drugs interact with warfarin by bypasswarfarineffect via large amounts ofvitamin K

A

Some vitamin and calcium supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how can the efficacy of warfarin be monitored clinically?

A

reducedsymptomsof breathlessness in heart failure, or improvedblood pressurecontrol in hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

how can safety of warfarin be tested?

A

checkelectrolytesandrenal functionbefore starting treatment. Repeat these 1–2 weeks into treatment and after increasing the dose. Biochemical changes can be tolerated provided they are within certain limits: the creatinine concentration should not rise by more than 30%, the eGFR should not fall by more than 25%, and the potassium concentration should not rise above 6.0 mmol/L. If any of these limits are exceeded, you should stop the drug and seek expert advice.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

in what instance is the therapeutic index INR level higher than nornal?

A

patients with arteficial heart valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the usual therapeutic level INR levels?

A

2-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

If the INR is too low or too high what are the consequences?

A

too low-thromboembolic

too high-haemorrhagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what should be explained to a patient before they start taking warfarin?

A 
Potential side effects
Cautions-avoid grapefruit, kale, if bleed get medical help
Interactions
How to take the drug
When to seek advice
Sick day rules?-medical help
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the issues with using DOACs?

A

not as easily reversed as warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

give examples of DOACs?

A

Factor Xa inhibitors:

  • Apixaban
  • Edoxaban
  • Rivaroxaban

Direct thrombin inhibitor:
-Dabigatran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what would you give to reverse warfarin?

A

Vitamin K1
Prothrombin complex concentrate
(fresh frozen plasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what would you give to reverse dabigatran?

A

Idarucizumab (monoclonal antibody fragment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What would you give to reverse factor Xa inhibitors?

A

Andexanet alfa (awaiting approval in UK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

describe the drug therapy used in a patient with acute coronary syndrome

A

Aspirin
Clopidogrel / Ticagrelor
Fondaparinux (or LMWH)
Avoid O2 unless O2 sats < 90% (cause reflex constriction of coronary arteries)
-Avoid IV morphine unless pain unacceptable (10mg in 10mL titrate slow)
-Beta-blocker (improves prognosis)
-Statin (secondary prevention)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

give examples of classes of antiplatelet drugs?

A
  • cyclo-oxygenase inhibitors
  • phosphodiesterase inhibitors
  • adenosine diphosphate receptor antagonists
  • glycoprotein IIb/IIIa receptor antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

give an example of a cyclo-oxygenase inhibitor?

A

aspirin (inhibits generation of thromboxane A2(TXA2) by COX-1 which otherwise causes platelet aggregatoin and upregulation of GPIIb and IIIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

give an example of a phosphodiesterase inhibitor?

A

dipyridamole (inhibit activation of platelets and downregulate glycoprotein receptors by increasing cAMP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

give examples of adenosine diphosphate receptor antagonists?

A

clopidogrel
tricagrelor
(inhibit ADP (P2Y12) receptors and prevent ADP induced upregulation of glycoprotein GPIIb/IIIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

give examples of glycoprotein IIb/IIIa receptor antagonists?

A

abciximab (antibody)

tirofiban (non-peptide inhibitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what dose of aspirin is required to have an antithrombotic effect and how?

A

low doses
75-81mg/day
irreversibly acetyate serine 530 of COX-1 and inhibit platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what doses of aspirin can cause analgesic and antipyretic effects and how?

A

intermediate doses
650mg-4g/day
inhibit COX-1 and COX-2 blocking PG production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what doses of asprin can result in anti-inflammatory effects for rheumatic disorders and how?

A 
high doses
4-8g/day
PG dependent (COX-2 dependent PGE2) and independent factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

in what ways is aspirin toxic at high doses?

A

tinnitus
gastric intolerance
bronchospasm (potential side effect)
(if a patient has overdosed and has tinnitus you know they have taken a significant dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

how does high dose aspiring result in GI problems/

A

it is a non specific blocker of prostaglandin synthesis

PG2 causes GI problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

why should aspirin not be given in children <16 and what it the exception?

A

greatly increases the risk of Reye’s syndrome (rapidly progressing encephalopathy)
except in Kawasaki disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is the mechanism of action of adenosine diphosphate receptor antagonists?

A

clopidogrel-irreversibly inhibits P2Y12 receptor and ticagrelor binds to a different site on the receptor and causes reversible inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

how do the effects of clopidogrel and ticagrelor differ?

A
  • clopidogrel-considerable interindividual variability in the degree of platelet inhibition and slow onset of action (about 5 days for full effect) without a loading dose.
  • Ticagrelor- more predictable inhibitor of platelet activation than clopidogrel, and more rapid onset of action.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what is the mechanism of action of ticagrelor?

A

Ticagrelor acts directly and via an active metabolite (TAM) with both non-competitive antagonism of activation by ADP and inverse agonism at P2Y12. In addition, ticagrelor and TAM weakly inhibit ENT1 leading to increased extracellular adenosine that acts via adenosine receptors such as A1and A2Areceptors, the latter mediating platelet inhibition

91
Q

what is the mechanism of action of dipyridamole?

A

phosphodiesterase inhibitor

  • inhibits cellular reuptake of adenosine
  • increased plasma concentration of adenosine
  • activate cell surface adenosine A2 receptors stimulating intracellular adenyl cyclase and production of cGMP and cAMP which inhibit expression of cell surface GPIIb/IIIa receptors
  • inhibits platelet aggregation
  • also causes vasodilation and inhibits PDE3 and 5 resulting in increased cGMP and cAMP
92
Q

what is the mechanism of action of abciximab and tirofiban?

A
  • Abciximab binds irreversibly to the GPIIb/IIIa receptors and blocks the binding of fibrinogen – reduces platelet aggregation by 90%. (monoclonal antibody fragment)
  • Tirofiban is a nonpeptide reversible antagonist of the GPIIb/IIIa receptor.
  • GPIIb/IIIa antagonists are given by IV bolus to achieve rapid inhibition of platelets, followed by continuous IV infusion.
93
Q

how do beta blockers help in angina?

A

-Decrease heart rate
-Reduce the force of cardiac contraction
-Lower blood pressure by reducing cardiac output
-Overall effect is to reduce myocardial oxygen demand
-Slower heart rate increases diastole and gives more time for coronary perfusion so effectively improving myocardial oxygen supply
(-ve chronotrope, +ve ionotrope)

94
Q

how can you easily tell if a patient is on beta blockers?

A

their pulse is usually about 60bpm

95
Q

what are the potential drug interactions of beta blockers?

A

other antihypertensives

96
Q

what are the potential side effects of beta blockers?

A
  • raynaud’s phenomenon
  • bradycardia (avoid in older patients)
  • heart block/hypotension
  • may cover up hypoglycaemia in diabetics
  • impotence
97
Q

how do calcium channel blockers help in angina?

A
  • Peripheral arterial dilation (dihydropyridines most potent)
  • Coronary artery dilation
  • Negative chronotropic (and -ve ionotrope) effect (diltiazem and verapamil only)
  • Reduced cardiac contractility (esp verapamil)
  • Overall effect is to reduce myocardial oxygen demand
98
Q

describe calcium regulation in cardiac myocytes and blood vessels?

A
  • Calcium conc. under influence of different mechanisms.
  • Calcium entry through voltage-gated L-type Ca2+channels stimulates ryanodine receptors (RyR) in the sarcoplasmic reticulum, releasing stored Ca2+(Ca2+-induced calcium release, CICR).
  • Intracellular Ca2+is also regulated by exchange with Na+via the Na+/Ca2+ exchangers (NCX) in the cell membrane.
  • Vascular smooth muscle cells have ATP-sensitive inward rectifier K+channels (KIR) which combine with sulfonylurea receptors to form ATP-sensitive K+channels (KATP).
  • Hyperpolarisation of the cell by drugs which open KATPchannels, such as nicorandil, closes voltage-gated L-type Ca2+channels and causes relaxation.
99
Q

what are the types of calcium channel blocker?

A

Dihydropyridine

Non-dihydropyridine

100
Q

describe the differences of Dihydropyridine vs Non-dihydropyridine?

A
  • Verapamil and diltiazem (non-dihydropyridines) exhibit frequency-dependent receptor binding and gain access to the Ca2+channel when it is in the open state.
  • Dihydropyridines preferentially bind to the channel in its inactivated state.
  • More Ca2+channels are in the inactive state in relaxed vascular smooth muscle than in cardiac muscle ☛ dihydropyridines selectively bind to Ca2+channels in vascular smooth muscle.
  • Relative vascular selectivity of the dihydropyridines
  • Antiarrhythmic properties of verapamil and diltiazem
101
Q

give examples of nitrates used clinically?

A

GTN

isosorbide mononitrate or dinitrate

102
Q

what is the mechanism of nitrates?

A
  • mimic NO
  • mainly effect venous system
  • Nitrates are vasodilators causing vascular smooth muscle relaxation by mimicking the vasodilator effects of endogenous NO.
  • Dilation of: Venous capacitance vessels, Arterial resistance vessels, Coronary arteries
103
Q

what are the adverse effects of nitrates?

A
  • peripheral vasodilation which can cause collapse

- headaches

104
Q

describe how nitrates should be administered?

A
  • GTN-sublingual
  • develop tolerance to nitrates so affects when should be taken
  • morning dose and then 8 hours later so that at night there is a 16 hour withdrawal and tolerance less likely
105
Q

what may be a potential issue for a patient that uses GTN spray occasionally?

A

it has a short half life so needs replacing regularly (every 3 months)

106
Q

List some other classes of drugs that can be use for angina treatment other than GTN and calcium channel blockers?

A
  • potassium channel openers
  • specific sinus node inhibitors
  • late sodium current inhibitors
107
Q

give an example of a potassium channel opener?

A

nicorandil

108
Q

what is the mechanism of action of nicorandil?

A
  • potassium channel opener
  • Nicorandil opens KATPchannels in vascular smooth muscle cells ultimately leading to vasodilation in systemic and coronary arteries
  • Lower blood pressure reduces myocardial oxygen demand
  • Preventing coronary vasospasm can improve myocardial perfusion
109
Q

give an example of a specific sinus node inhibitor/

A

ivabradine

110
Q

what is the mechanism of action of ivabradine/

A
  • specific sinus node inhibitor
  • Ivabradine is a specific inhibitor of theIfcurrent, and its major effect is to slow the rate of firing of the sinus node.
  • The efficacy of ivabradine increases with the frequency of channel opening and is greatest at higher heart rates.
111
Q

give an example of a late sodium current inhibitor/

A

ranolazine

112
Q

what is the mechanism of action of ranolazine?

A
  • late sodium current inhibitors
  • Ranolazine attenuates the late transcellular Na+current in ischaemic myocardial cells and reduces Ca2+accumulation and lowers wall tension.
  • Lower wall tension in the ventricles reduces myocardial oxygen demand
  • It also reduces compression of small intramyocardial coronary vessels, potentially improving myocardial perfusion in diastole
113
Q

what are the potential issues with using nitrates, nifedipine and nicorandil in angina treatment and how can this be overcome?

A

can cause reflex tachycardia due to a rapid fall in BP

this isn’t a problem with nondihydropyridines diltiazem and verapamil which constantly slow heart rate

114
Q

what are the major sites of action of antianginal drugs?

A

reduce cardiac work and myocardial oxygen demand either by peripheral vasodilation (which reduces afterload and preload) or by reducing heart rate and/or myocardial contractility. Myocardial oxygen supply may also be enhanced, either by coronary artery dilation or due to increased diastolic filling time.

115
Q

how can reflex tachycardia to nifedipine be avoided?

A

modified-release formulation, or a more slowly acting dihydropyridine such as amlodipine can be used

116
Q

what are the common presentations of heart failure/

A

acute pulmonary oedema (acute LVF)
congestive cardiac failure (chronic)
sudden weight loss is due to water loss

117
Q

what drug is commonly used in the treatment of acute pulmonary oedema?

A

furosemide

118
Q

give examples of loop diuretics?

A

furosemide

bumetanide

119
Q

how are the loop diuretics administered?

A

furosemide - IV/oral

bumetanide - oral

120
Q

describe how the differing administration of loop diuretics affect its affects?

A

When injected intravenously, furosemide releases vasodilator prostaglandins, such as prostacyclin, into the circulation and produces a short-lived venodilation - helps in LVF

Bumetanide is more completely and reliably absorbed than furosemide from the GI tract

121
Q

what electrolyte imbalance could be expected in a patient on loop diuretics?

A

hypokalaemia
hyponatraemia
hypochloraemia

122
Q

what are the potential side effects of loop diuretics?

A

ototoxicity (given IV)
acute hypertension
kidney failure

123
Q

what drugs can cause hearing loss?

A

loop diuretics (IV)
gentamycin
erythromycin

124
Q

what are the main drugs used for the treatment of chronic heart failure?

A

loop diuretics
ACE inhibitors
ARBs
(others-aldosterone antagonists, beta blockers)

125
Q

which drugs help reduce symptoms and reduce morbidity and mortality from chronic heart failure?

A

beta blockers with ACE inhibiters

126
Q

what drugs are used for treatment of atrial fibrillation/

A
  • beta blockers
  • digoxin (only works if sedentary)
  • non-dihydropyridine calcium channel blocker (verapamil)
  • anticoagulation (DOACs vs warfarin)
127
Q

why may anticoagulants for AF treatment be stopped?

A

may come a point in a patients life where the risk of being on an anticoagulant is greater than issues with AF (falls/injuries)

128
Q

how can you predict the risk of stroke in patients with non-rheumatic atrial fibrillation?

A

CHADS2 (CHA2DS2VASc) score

129
Q 
Vaugn williams classification of antidysrhythmics: 
what class (1,2,3 or 4) works at point 0 on the cardiac action potential?
A 
class 1
sodium channel blockers
130
Q 
Vaugn williams classification of antidysrhythmics: 
what class (1,2,3 or 4) works at point 2 on the cardiac action potential?
A 
class 4
calcium channel blockers
131
Q 
Vaugn williams classification of antidysrhythmics: 
what class (1,2,3 or 4) works at point 3 on the cardiac action potential?
A 
class 3
potassium channel blockers
132
Q 
Vaugn williams classification of antidysrhythmics: 
what class (1,2,3 or 4) works at point 4 on the cardiac action potential?
A 
class 2
beta blockers
133
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class Ia drugs and give examples?

A

sodium channel blockers (intermediate association/ dissociation)
quinidine, procainamide

134
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class Ib drugs and give examples?

A

sodium channel blockers (fast association/dissociation)

lidocaine, phenytoin

135
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class Ic drugs and give examples?

A

sodium channel blockers (slow association/dissociation)
flecainide
propafenone

136
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class II drugs and give examples?

A 
beta blockers (propanolol also has some class I action)
propanolol, metoprolol
137
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class III drugs and give examples?

A 
potassium channel blockers (amiodarone has class I, II, III and IV activity)
amiodarone, sotalol (beta blocker)
138
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class IV drugs and give examples?

A

calcium channel blockers
verapamil
diltiazem

139
Q

Vaugn williams classification of antidysrhythmics:

what is the mechanism of class V drugs and give examples?

A 
unknown mechanisms (direct nodal inhibition)
adenosine, digoxin
140
Q

what drugs can be given during resuscitation?

A

adrenaline

amiodarone

141
Q

what medical treatment can be given to a patient with bradycardia?

A

atropine OR
transcutaneous pacing OR
isoprenaline, adrenaline

142
Q

what would sats of 91% indicate?

A

hypoxic

respiratory failure

143
Q

what would a Capillary refill time in a patient presenting acutely indicate?

A

circulatory shock

144
Q

what would you expect to see on X-ray in a patient with left basal pneumonia?

A

left lower zone shadowing

silhouette sign at left cardiac border meaning heart edge is visible suggests infection in left lower zone

145
Q

what is the risk stratification scoring system used in pneumonia?

A

CURB65

146
Q

what would a CURB65 score of 3 or more indicate and what action should be taken?

A

high risk of death

review by senior physician and managed as having high severity pneumonia

147
Q

How would a CURB65 score of 4 or 5 affect treatment?

A

should be assessed with specific consideration to the need for transfer to a critical care unit (high dependency unit or intensive care unit)

148
Q

what does a CURB65 score of 2 suggest and what action should be taken?

A

moderate risk of death

considered for short stay inpatient treatment or hospital supervised outpatient treatment

149
Q

what does a CURB65 score of 0-1 suggest and what action should be taken?

A

low risk of death

may be suitable for treatment at home (social circumstances and wishes should be taken into consideration)

150
Q

what are the clinical features involved in the CURB65 scoring system?

A 
confusion
urea >7
resp rate >30
BP (systolic <90, diastolic <60)
age over 65
151
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 0/1 in the community?

A

oral amoxicillin 500mg 8-hrly

152
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 0/1 orally in hospital?

A

oral amoxicillin 500mg 8-hrly

153
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 0/1 in hospital if IV is needed?

A

IV amoxicillin 500mg 8-hrly

154
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 2 in hospital?

A

oral dozxcycline 100mg 12-hrly or oral amoxicillin and clarithromycin
if IV needed - iv benzylpenicillin 1.2g 6hrly + IV clarithromycin 500mg 12-hrly

155
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of >3 in hospital?

A

IV co-amoxiclav 1.2g 8hrly and IV clarithromycin 500mg 12 hrly

156
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 0/1 in patients with penicillin allergy?

A
  • Community treatment oral doxycycline 100 mg 12-hrly
  • Hospital treatment oral doxycycline 100 mg 12-hrly
  • If IV needed -IV clarithromycin 500 mg 12-hrly
157
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of 2 in patients with penicillin allergy?

A

=Hospital treatment oral doxycycline 100 mg 12-hrly
or oral clarithromycin 500 mg 8-hrly
-If IV needed IV clarithromycin 500 mg 12-hrly

158
Q

what treatment would be given to a patient with pneumonia with a CURB65 score of >3 in patients with penicillin allergy?

A

Hospital treatment IV cefotaxime 1 g 8-hrly + IV clarithromycin 500 mg 12-hrly

159
Q

what pneumonias are associated with highest mortality rates?

A

pneumococcal infection and legionnaires disease

160
Q

resistance amongst pneumococci is the result of…

A

alterations in one or more penicillin-binding proteins, thus reducing affinity for penicillin this in turn leads to a requirement for higher drug concentrations to bring about death of organism

161
Q

what type of antibiotics are not widely used in treatment of CAP?

A

tetracyclines

162
Q

describe susceptibility of different pneumonias to antibiotics?

A

In Strep pneumoniae 94% of bacteraemia isolates and 92% of respiratory isolate being fully susceptible to penicillin and 85% and 88% of blood and respiratory isolates, respectively, susceptible to erythromycin and, by implication, other macrolides.

163
Q

what is antimicrobial stewardship?

A

The term ‘antimicrobial stewardship’ is defined as ‘an organisational or healthcare-system-wide approach to promoting and monitoring judicious use of antimicrobials to preserve their future effectiveness’.

164
Q

describe the basic principles of how antibiotic resistance happens?

A
  • lots of drugs and a few are drug resistant
  • antibiotics kill bacteria
  • the drug resistant bacteria grow and take over
  • some bacteria give drug resistance to other bacteria
165
Q

what are the basic principles of antimicrobial stewardship?

A
  • prescribing the shortest effective course
  • the most appropriate dose
  • route of administration
166
Q

what are the 6 recommendations of the British thoracic society regarding antimicrobial stewardship?

A
  • diagnosis of CAP and antibiotic therapy initiation should be reviewed by senior clinician (no barrier to stopping antibiotics if not indicated)
  • indication documented in notes
  • need for IV antibiotics reviewed daily
  • de-escalate from IV to oral ASAP
  • narrow spectrum when pathogens identified
  • specify stop dates
167
Q

what are the principles of antimicrobial prescribing?

A
  • right antibiotic
  • right patient
  • right time
  • right dose (renal, hepatic function)
  • right route (oral?)
  • least harm (spectrum, duration, side effects)
168
Q

what antibiotics are more frequently implicated in predisposition to C. diff?

A

fluoroquinolones, clindamycin, and broad-spectrum penicillins and cephalosporins

169
Q

what factors contribute to incidence of C.diff infection?

A

use of broad-spectrum antimicrobials, use of multiple antibiotic agents, and increased duration of antibiotic therapy

170
Q

what are extended spectrum beta lactamases (ESBL)?

A

enzymes that confer resistance to most beta-lactam antibiotics, including penicillins, cephalosporins, and the monobactam aztreonam. ESBLs have been found exclusively in gram-negative organisms, primarily in Klebsiella pneumoniae, Klebsiella oxytoca, and Escherichia coli but also in Acinetobacter, Burkholderia, Citrobacter, Enterobacter, Morganella, Proteus, Pseudomonas, Salmonella, Serratia, and Shigella spp.

171
Q

describe carbopenem resistant enterococci?

A

Carbapenem antibiotics have an important antibiotic niche in that they retain activity against the chromosomal cephalosporinases and extended-spectrum beta-lactamases found in many gram-negative pathogens. The emergence of carbapenem-hydrolyzing beta-lactamases has threatened the clinical utility of this antibiotic class and brings us a step closer to the challenge of “extreme drug resistance” in gram-negative bacilli. The most clinically important of the Class A carbapenemases is the Klebsiella pneumoniae carbapenemase (KPC) group. These enzymes reside on transmissible plasmids and confer resistance to all beta-lactams. Use of broad spectrum cephalosporins and/or carbapenems is an important risk factor for the development of colonization or infection with carbapenemase-producing organisms, although prior receipt of carbapenems is not essential for acquisition of these strains.

172
Q

what are the sepsis 6?

A

give; antibiotics, oxygen, fluid

take; urine, lactate, blood

173
Q

give examples of atypical pneumonia?

A

Legionella
Mycoplasma pneumoniae
Chlamydophila pneumoniae
C burnetii

174
Q

what is atypical pneumonia?

A

radiological pattern associated with patchy inflammatory changes, often confined to thepulmonary interstitium, most commonly associated with atypical bacterial aetiologies such as
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Legionella pneumophilia
Viral and fungal pathogens may also create the radiological and clinical picture of atypical pneumonia.

175
Q

what is the treatment for TB?

A

Treatment consists of combination antibiotic therapy for at least six months. The agents isoniazid, rifampicin, ethambutol, and pyrazinamide are considered first-line antituberculosis agents.

176
Q

what is multidrug resistant TB?

A

Multidrug-resistant TB (MDR-TB) is defined as disease caused byM.tuberculosisresistant to at least isoniazid and rifampicin. Treatment is a challenge and involves second-line therapies for up to two years.

177
Q

what is extensively drug resistant TB?

A

progresses very rapidly and can be fatal within weeks. XDR-TB is defined as TB that has developed resistance to at least rifampicin and isoniazid, plus any agent of the fluoroquinolone family, plus at least one of the aminoglycosides or polypeptides

178
Q

what are the 4 drugs used in treatment of TB?

A

Rifamycins
Isoniazid
Pyrazinamide
Ethambutol

179
Q

what are the 2 phases of TB drug therapy?

A

an intensive phase (two months) followed by a continuation phase (four to seven months); most patients receive six months of treatment (intensive phase of two months and continuation phase of four months)

The intensive phase usually consists of four drugs (isoniazid,rifampin,pyrazinamide, andethambutol) administered for two months.

The continuation phase (regimen beyond the first two months) usually consists of two drugs (isoniazidandrifampin) administered for at least four additional months, for a total of six months.

180
Q

what is the mechanism of rifampicin and what are the interactions?

A

induction of cytochrome P450 isoenzymes (including CYP2C9, CYP3A4) and other drug-metabolising enzymes in the liver can reduce plasma concentrations of oestrogen in those taking oral contraceptives and of many other drugs including warfarin, phenytoin and sulphonylureas
Can cause hepatoxicity

181
Q

what drugs should be stopped if a patient starts taking clarithromycin?

A

statins

182
Q

what is isoniazid?

A

It is a pro-drug activated by catalase–peroxidase activity within the mycobacteria.
The active product inhibits enzymes involved in the synthesis of long-chain mycolic acids, which are unique to the cell wall of mycobacteria, and also inhibits enzymes required for nucleic acid synthesis.
Isoniazid is bactericidal against dividing mycobacteria, but bacteriostatic on resting mycobacteria.
In the UK it is considered an essential drug, along with rifampicin, for the treatment of tuberculosis.
Can cause hepatotoxicity and peripheral neuropathy

183
Q

what is pyrazinamide?

A

Resistance results from mutations in the gene that codes for pyrazinamidase and develops rapidly if pyrazinamide is used as a sole treatment for tuberculosis.
Can cause hepatotoxicity and a rise in plasma bilirubin usually requires cessation of treatment; regular monitoring is recommended.
Crosses blood-brain barrier and good in tuberculous meningitis

184
Q

what are the adverse effects of ethambutol?

A

Visual disturbances: optic neuritis produces initial red-green colour blindness, then reduced visual acuity; these effects are dose-related but usually reversible. - Visual acuity should be tested before treatment.
Peripheral neuritis
Hyperuricaemia, gout
Nephrotoxicity

185
Q

how long is antibiotic treatment for endocarditis?

A

8 weeks

186
Q

what is the treatment for endocarditis?

A

Streptococci (e.g. viridans)
Penicillin G adjusted to MIC – often combined with gentamicin
Antibacterial synergy by combination therapy

Staphylococci – depends on MSSA vs MRSA

Synergistic gentamicin is recommended in initial treatment of native valve endocarditis due to enterococcal and streptococcal species and in prosthetic valve endocarditis of all aetiology including staphylococci.

187
Q

what does exercise induced asthma suggest about the patients condition?

A

expression of poorly-controlled asthma and regular treatment including inhaled corticosteroids should be reviewed

188
Q

what defines complete control of asthma?

A
  • no daytime symptoms,
  • no night-time awakening due to asthma,
  • no asthma attacks, no need for rescue medication,
  • no limitations on activity including exercise,
  • normal lung function (in practical terms forced expiratory volume in 1 second (FEV1) and/or peak expiratory flow (PEF) > 80% predicted or best)
189
Q

what non pharmacological treatment should you suggest to a patient with asthma?

A 
Life style advice 
Weight loss 
Smoking cessation
Avoiding triggers
Breathing exercise programs
190
Q

what initial pharmacological treatment should be offered to a patient with asthma?

A

SABA (short acting beta2 agonist)
and
inhaled corticosteroid

191
Q

what is the mechanism of action of SABA?

A

Activation of β adrenergic receptors leads to relaxation of smooth muscle in the lung, and dilation and opening of the airways.
β adrenergic receptors are coupled to a stimulatory G protein of adenylyl cyclase. This enzyme produces the second messenger cyclic adenosine monophosphate (cAMP).
They also inhibit mediator release from mast cells and TNF-a release from monocytes and increase mucus clearance by cilia.

192
Q

what are the side effects of SABA?

A

Angioedema; arrhythmias; behavioural disturbances; collapse; fine tremor (particularly in the hands); headache; hyperglycaemia (especially when given intravenously); hypersensitivity reactions; hypokalaemia (with high doses); hypotension; ketoacidosis (especially when given intravenously); muscle cramps; myocardial ischaemia; nervous tension; palpitation; paradoxical bronchospasm (occasionally severe); peripheral vasodilation; rash; sleep disturbances; tachycardia; urticaria

Tremor & tachycardia are the most frequent side effects seen in clinical practice.

193
Q

What is the mechanism of action of inhaled corticosteroids and give examples?

A

potent inhibitors of inflammatory processes
Clinicians should be aware that higher doses of inhaled corticosteroids may be needed in patients who are smokers or ex-smokers.
Beclometasone, Fluticasone

194
Q

if inhaled corticosteroid and SABA so not control asthma what potential treatments can be given next?

A

leukotriene or LABA

check adherence and inhaler technique and offer spacer if needed

195
Q

give examples of LABA’s ?

A

Salmeterol, Formoterol

196
Q

what patients are combined inhalers not recommended in?

A

• guarantee that the long-acting β₂ agonist is not taken without inhaled corticosteroid • improve inhaler adherence

197
Q

describe the features of salbutamol?

A 
hydrophilic
fast action
short duration
partial agonist
accesses active site directly from the aqueous extracellular compartment
198
Q

describe the features of formoterol?

A 
moderately liphophilic
fast onset
long action
full agonist
forms a depot in cell membrane and progressively leach out
199
Q

what 3rd line treatment could be offered in asthma if symptoms weren’t controlled?

A

long acting muscarinic receptor antagonist

ipatropium

200
Q

describe the mechanism of action of long acting muscarinic receptor antagonist

A

Ipratropium binds non-selectively to all five subtypes of muscarinic receptor (M1to M5). The recommended dose is determined by unwanted effects and is well below the dose that produces maximal bronchodilation.

Tiotropium and other long-acting antimuscarinics are functionally selective for the M3receptor due to a higher affinity for binding to the receptor or due to lower reversibility of binding at M3than at other muscarinic receptors.

The main benefit of muscarinic antagonists is in COPD. They are of less value for bronchodilation in acute mild to moderate asthma, but ipratropium has a place when added to aβ2-adrenoceptor agonist in severe exacerbations of asthma.

201
Q

what is theophylline and when is it indicated?

A

amiophyline
A methylxanthine
Inhibits phosphodiesterase and block adenosine receptors.
Indication : IV – status asthmaticus, PO – sustained-release

202
Q

what are cysteinyl leukotriene receptor antagonists

A

montelukast

Compete with cysteinyl leukotrienes at CysLT receptors in respiratory mucosa and infiltrating inflammatory cells.

203
Q

what is the problem with prescribing theophylline?

A

Theophylline has a narrow therapeutic window – can result in cardiac arrythmias, seziures and GI disturbance.
Metabolised by P450 in liver so liver dysfunction & viral infections increase plasma concentration and half-life.
Also lots of drug interactions!!

Aminophylline – combo of theophylline with ethylenediamine to increase its solubility in water

204
Q

how should asthma medication be maintained?

A

Regular review of patients as treatment is decreased is important. When deciding which drug to decrease first and at what rate, the severity of asthma, the side effects of the treatment, time on current dose, the beneficial effect achieved, and the patient’s preference should all be taken into account.

Patients should be maintained at the lowest possible dose of inhaled corticosteroid. Reduction in inhaled corticosteroid dose should be slow as patients deteriorate at different rates. Reductions should be considered every three months, decreasing the dose by approximately 25–50% each time.

205
Q

what are the features of moderate acute asthma?

A
  • increasing symptoms
  • PEF >50-75% best or predicted
  • no features or acute severe asthma
206
Q

what are the features of acute severe asthma?

A

any one of:

  • PEF 33-50% best or predicted
  • respiratory rate >25
  • heart rate >110
  • inability to complete sentences
207
Q

what are the features of life threatening asthma?

A

-PEF <33% best or predicted
-SpO2 <92%
-PaO2 <8kPa
-normal PaCO2
-altered conscious level
-exhaustion
-arrythmia
-hypotension
-cyanosis
silent chest
-poor respiratory effort
-

208
Q

what are the features of near fatal asthma?

A

raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

209
Q

what is involved in the initial assessment of a patient with asthma?

A 
clinical features
PEF or FEV1
pulse oximetry
blood gases
chest X-ray
210
Q

how would you deliver oxygen to a patient with an asthma attack?

A

non-rebreath mask
The non-rebreather face masks can deliver an FIO2 up to around 80%. It is a mistake to label a patient with any loose-fitting face mask as receiving an “FIO2 of 100%.” (Again, 100% oxygen can only be delivered with a ventilator or tight-fitting face mask.)

211
Q

How should inhaled beta 2 agonists be given in a patient with acute asthma?

A

oxygen driven nebuliser

212
Q

how should steroid therapy be given in a patient with acute asthma attack?

A

Prednisolone 40mg for 5 days minimum till symptoms improve orally, IV hydrocortisone only for those unable to take oral medication.

213
Q

what should be added to beta 2 agonist for patients with acute severe or life threatening asthma or with poor response to beta 2 agonists?

A

Add nebulised ipratropium bromide (0.5 mg 4–6 hourly)

214
Q

what other medication may you consider giving to a patient having an acute asthma attack?

A

IV magnesium under specialist supervision – inhaled MG2+ not recommended in adults.Magnesium sulphate (1.2–2 g IV infusion over 20 minutes

215
Q

when should patients be admitted for asthma attack?

A

Admit - Admit patients with any feature of a life-threatening or near-fatal asthma attack. patients with any feature of a severe asthma attack persisting after initial treatment.
Patients whose peak flow is greater than 75% best or predicted one hour after initial treatment may be discharged from ED, unless there are other reasons why admission may be appropriate.

216
Q

what non-pharmacological measures would be suggested for a COPD exacerbation?

A
  • Smoking cessation reduces the progressive decline in lung function
    Pulmonary rehabilitation. Involves physical training, disease education, and nutritional, psychological, and behavioural interventions tailored to the person’s needs.
    Encourage physical activity
  • Pneumococcal and influenza vaccination to reduce risk of infection
217
Q

what pharmacological measures would be suggested for a COPD exacerbation?

A

Trial ICS. Meets criteria with 2 moderate exacerbations and daily symptoms. Increased risk of pneumonia in patients taking ICS. Review in 3 months and if no benefit consider discontinuing.
Mucolytic (carbocisteine) may help with secretions
- Theophylline could also be considered, before or after a trial of ICS. There is evidence that theophylline improves lung function, but it does not result in a statistically significant difference in symptoms (wheeze, breathlessness, or walking distance), use of rescue medication, or exacerbation frequency compared with placebo. The higher rate of adverse effects with theophylline needs to be balanced against any benefits.

218
Q

what are the fundamentals of COPD care?

A
  • offer treatment and support to stop smoking
  • offer pneumococcal and flu vaccine
  • offer pulmonary rehabilitation
  • co-develop self management plan
  • optimise treatment for comorbidities
219
Q

for patients with COPD inhaled therapies should only be started in?

A

all other inverventions have been offered and inhaled therapies are needed to relieve breathlessness and people have been trained to use inhalers
offer SABA or SAMA

220
Q

if a patient is limited by symptoms or having exacerbations despite treatment with no asthmatic features what treatment would be offered?

A

offer LABA and LAMA
and if patient has day to day symptoms consider 3 month trial of LABA + LAMA +ICS and if no improvement revert to LABA +LAMA
or if patient has1 severe or 2 moderate exacerbations a year consider LABA + LAMA +ICS

221
Q

if a patient is limited by symptoms or having exacerbations despite treatment with asthmatic features what treatment would be offered?

A

consider LABA +ICS

if patient has day to day symptoms of 1 severe or 2 moderate exacerbations a year offer LABA+LAMA+ICS

222
Q

what is an oxygen alert card?

A

An oxygen alert card is sometimes given to patients who have had T2RF. It shows the oxygen saturations required during previous exacerbations. Patients and their carers should be instructed to show the card to emergency healthcare providers in the event of an exacerbation.

223
Q

what is noninvasive ventilation?

A

refers to the administration of ventilatory support without using an invasive artificial airway (endotracheal tube or tracheostomy tube).

Block 31 Cardio-respiratory (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions