CVD Flashcards
(135 cards)
1
Q
What is the only type of symptomatic high BP and how high is it?
A
Malignant hypertension
180/120
2
Q
What are the symptoms of malignant hypertension?
A
Confusion, visual loss, headache, coma
Evidence of small vessel damage e.g in eyes/ kidneys/ brain
3
Q
What should be the consequence if the blood pressure of a patient is more than 140/90 but less than 180/120?
A
Offer ambulatory bp monitoring or home monitoring or come back three separate times
4
Q
A
4
Q
What is the value for severe hypertension and what is the consequence:
A
180/120
Refer/ admit and treat
Medical emergency
5
Q
What is the value for stage 2 hypertension and what should be the consequence?
A
160/100
Treatment required
6
Q
What is the value for stage 1 hypertension and what should be the consequence of this?
A
140/90
Offer ambulatory (home) BP monitoring
Lifestyle interventions
Assess CV risk and end organ damage
7
Q
What is the value of normal BP for under 80’s and what is the consequence of this?
A
Less than 140/90
Reassess every 5 years
8
Q
What is the value of normal BP for over 80’s?
A
150/90
9
Q
What is the pulse pressure and how do you calculate it?
A
Difference between systolic and diastolic pressure
e.g if bp is 120/80, pulse pressure would be 40mmHg
10
Q
What is the blood pressure value for hypotension?
A
Below 90/60 mmHg
11
Q
What is orthostatic (postural) hypotension?
A
Insufficient compensatory responses to gravitational shifts in blood when person moves from horizontal to vertical position
12
Q
What is pericarditis?
A
When the pericardial fluid becomes infected, virally or bacterially, and there is painful rubbing
13
Q
How do renin inhibitors work and give an example:
A
Not often used alone
Reduce plasma renin activity
Aliskiren- indicated for hypertension alone or in combination
14
Q
What are the benefits of ARB’s compared to ACE inhibitors?
A
More effective as don’t inhibit the breakdown of bradykinin and other kinins fewer side effects then an ACE inhibitor such as a dry cough
15
Q
What are the problems with ACE inhibitors?
A
Dry cough
Caused by inhibition of break down of Bradykinin, where high levels of it are found in the lung
16
Q
What are the three types of calcium channel blockers that act on L- type?
What do they bind to?
A
- Phenylakylamines- verapamil (heart)
- Dihydropryidines- Nifedipine (hypertension)
- Benzothiazepines- Diltiazem
All binding to the a1 subunit
17
Q
What are some side effects of calcium channel blockers and why?
A
Flushing, headaches, ankle swelling, constipation
Due to the blocking of CaV channels in other places
18
Q
Why should you not give a black African Caribbean or a person aged over 55 an ACE inhibitor or ARB as a first line treatment for hypertension?
A
Due to them not producing enough renin, so its better not to involve the renin- angiotensin system
19
Q
What is the process for determining smoking status?
A
Patients who have stopped smoking in previous 5 years should be considered as smokers for CV risk
Risk from smoking more than 5 years ago depends on lifetime exposure and risk will lie somewhere-use clinical judgement
20
Q
What are the baseline assessments before starting a statin?
A
Smoking status
Alcohol consumption
BP
BMI
Lipid profile: total cholesterol, non HDL, HDL and triglycerides
Diabetes status
Renal function
LFTs: transaminase level (alanine aminotransferase or aspartate aminotransferase)
TSH-hypothyroidism, known to increase cholesterol levels and myopathy SEs
21
Q
What are the guidelines/ treatment for primary and secondary prevention in a patient with CKD?
A
Atorvastatin 20mg OD
If target reduction not achieved and eGFR 30 or more then increase dose
If eGFR less than 30 then agree higher dose with renal specialist
22
Q
What are the atorvastatin doses their intensity?
A
10mg= medium
20mg= high
40mg=high
80mg=high
23
Q
What are the aim for % reduction when taking statins?
A
Aim for 40% reduction in non-HDL cholesterol
HDL cholesterol (good) more than 1mmol/L
24
What are the follow up monitoring requirements for taking statins?
At 3 months:
Total cholesterol, HDL and non-HDL cholesterol
LFTs (AST/ALT):
-if more than 3x the upper limit of normal, discontinue and recheck in 1 month
-if less than 3 times the upper limit of normal, continue statin and recheck in 1 month
Creatine Kinase, CK (enzyme released when muscle damage):
-only if develop symptoms of stain related muscle toxicity
Then again at 12 months and then annually
If up titration of dose needed then recheck after 3 months again
25
What are the main side effects of statins?
Stain associated muscle symptoms:
Stain Related Muscle Toxicity (SRM)
-symmetrical pain and/or weakness
-large proximal muscles, nearer to centre of body e.g arms, shoulders, hips
-worsened on exercise
-elevated CK
-resolve with discontinuation
26
What are the other side effects of statins?
GI disturbance- diarrhoea (early stages, tends to resolve)
Hepatotoxicity
New onset T2D- shouldn't stop statin as benefits outweigh risk
Neurocognitive and neurological impairment e.g dementia (conflicted evidence)
Intracranial haemorrhage- (conflicted evidence)
Sleep disturbances e.g nightmares
27
What are the strategies to over come intolerance in statins?
Therapy with a lower dose statin is better than no statin
De-challenge- stop initially to see resolvement
Re-challenge at lower dose of same high intensity statin
Change statin (hydrophilic e.g rosuvastatin instead of lipophilic e.g atorvastatin as less likely to cross into other tissues)
Consider alternative day/twice weekly dosing
Consider alternatives e.g ezetimibe, PC5K9, bempedoic acid, inclisiran
28
What are the types of venous thrombosis?
DVT
Pulmonary embolism (PE)
29
What is stable angina?
Narrowing of coronary arteries due to atheromatous plaques
-chest pain typically provoked by exercise, stress, heavy meals or extremes in temp (as excess demand on heart and blood supply not enough to treat demand)
-relieved by rest (decrease demand) or sublingual GTN
-"demand ischaemia"
-narrowed coronary arteries unable to meet increase O2 demand
30
What are the clinical symptoms of stable angina?
Central crushing chest pain
May radiate to jaw, neck, back or arms
'constricting','choking', 'heavy weight', 'burning', 'stabbing'
Induced by exercise etc and relieved by rest
Lack of ECG and cardiac enzyme changes
31
What is the symptom control management for stable angina?
SL GTN for acute angina- tab or spray under tongue
Antianginals:
1st line-BBs, CCBs
Add on: long lasting nitrate, ivabradine, ran-laziness, nicoradnil
32
What is the secondary prevention for management for stable angina?
Lifestyle changes (smoking/weight loss/diet/excerise etc)
Antiplatelet (aspirin)
Statins (atorvastatin 20-80mg)
33
Name the different forms of Acute Coronary Syndromes (ACS):
MI:
-ST elevated MI (STEMI)
-Non-ST elevated MI (NSTEMI)
Unstable angina (troponin +ve ACS)
34
Describe the results of cardiac enzymes to indicate what diagnosis of ACS it is if at all?
STEMI/NSTEMI means increase troponin levels of more than 99th percentile cut off/ upper reference limit (varies according to specific assay used)
Unstable angina, some changes in troponin level but doesn't meet criteria for MI
< 0.4ng/ml means ACS unlikely
Size of troponin increase is equal to size of infarct- more cells damaged
35
What other causes can increase the level of troponin?
PE
HF
Myocarditis
CKD
Sepsis
36
Describe unstable angina:
Supply ischaemia
Results in decrease of coronary blood flow and decrease oxygen supply due to thrombus formation
Leads to a partial blockage (UA) and complete blockage (STEMI/NSTEMI)
Thrombus forms as a result of plaque rupture and activation and aggregation of platelets
37
What is the main the clinical features of STEMI/NSTEMI?
Severe chest pain, sudden onset, often at rest and constant- not relieved by rest or GTN
20% of AMI have no symptoms- silent MIs are more common in elderly and DM
38
What are the other clinical features of STEMI/NSTEMI?
Sweating
Restlessness
Breathlessness
Pale
N&V
Grey
39
What are the clinical features of UA?
Sudden deterioration in angina symptoms
Often at rest, not relieved by rest of GTN
No ECG changes, small increase in troponin
40
What is the immediate treatment for a STEMI?
Oxygen (if indicated)- releives ischaemia
Diamorphine
-pain relief
-anxiolytic (anxious)
-vasodilation
Antiemetic (e.g cyclizine, metoclopramide)
Aspirin
-300mg STAT asap
Clopidogrel (or Ticagrelor or Prasugrel)
-300mg STAT (or 180mg or 60mg)
PPCI
41
Which antiplatelet should you offer when someone is having a STEMI?
With no reperfusion therapy, just medical management offer ticagrelor
With PCI offer prasugrel if not taking an anticoagulant, offer clopidogrel if already taking an anticoagulant
42
What does PPCI stand for?
Primary Percutaneous Coronary Intervention
43
What is the purpose of PPCI and when should it be administered when a patient has a STEMI?
Thrombolysis
Repurfusion- break down clot and limit damage
Optimal time:
"call to needle"-1 hour
"door to needle"- 30mins
After 6 hours the damage is irreversible
44
Name examples of thrombolysis drugs:
Streptokinase
Alterplase
Tenecteplase
Reletplase
Activates plasminogen to plasmin which breaks down fibrin in the clot
45
What are the CI of thrombolysis?
CVA (Cerebral vascular accident- stroke)
Surgery
Peptic ulcer
Uncontrolled HT
If more than 6 hrs of onset of symptoms
46
What are the SEs of thrombolysis?
Haemorrhage, stroke, repercussion arrythmias, allergy to streptokinase as antigenic
47
What should occur after having thrombolysis?
Heparin for the first 48 hrs after thrombolysis
48
What are the complications of STEMI?
Arrthymias
LVF- left ventricular HF
49
What is the secondary prevention for STEMIs?
5 Gold standard medicines they need to be on:
DAPT (Dual Antiplatelet Therapy):
-Aspirin +ticagrelor/clopidogrel/prasugrel for 12 months , aspirin for life
B blocker- review at 12 months, continue if also HF
ACEi
Statin - Atorvastatin 80mg OD
Lifestyle changes
50
What is the immediate treatment for a NSTEMI or UA?
Oxygen
Diamorphine
Aspirin
Clopidogrel (or ticagrelor or prasugrel)
Fondaparinux- until stable
NO THROMBOLYSIS OR PPCI
51
Describe the use of Fondaparinux for the treatment of NSTEMI/UA:
Injection
Inhibitor of factor Xa- prevent formation of new blood clots
52
What are the further treatments/ investigations that need to be done to someone who presents with an NSTEMI or UA?
Further treatment depends on prediction of 6 month risk of mortality if further CV events
Use GRACE scoring system (Global Registry of Acute Cardiac Events)
If intermediate/high risk >3% they will have an angiogram and PCI
If low risk <3% conservative management (no angiogram/PCI)
53
What is the secondary prevention for NSTEMIs and UA?
Same as STEMI-same 5:
DAPT (Dual Antiplatelet Therapy):
-Aspirin +ticagrelor/clopidogrel/prasugrel for 12 months , aspirin for life
B blocker- review at 12 months, continue if also HF
ACEi
Statin - Atorvastatin 80mg OD
Lifestyle changes
54
What is an angiography?
Thin radiopaque tube (catheter into coronary circulation- normally in wrist/groin)
X-ray contrast material injected into coronary artery
Allows observation of severity of narrowing (stenosis) due to atherosclerotic plaque (looks pale due to reduction in blood flow)
In MI identifies exactly where blood clot present
55
What should a patient be on after they have surgical interventions due to an ACS?
Long term aspirin and 12 months clopidogrel/ticagrelor/prasugrel
56
What is primary PCI and when should it be used?
Gold standard treatment for STEMI (instead of using thrombolysis)
Better outcomes and less people CI compared to thrombolysis
Patient taken straight to angiosuite for angiogram then angioplasty (with or without stenting)
Clot is removed during procedure
"Call to balloon time"= 120mins
"Door to balloon time"= 30 mins
57
What is the correlation between HF and AF?
10% with HF will have AF as a contributory factor
58
What are precipitating factors which cause HF?
Anything that increases myocardial workload:
-arrhythmias
-obesity
-anaemia
-infective endocarditis
-hyperthyroidism
-pulmonary infection
-pregnancy
-change in therapy including poor compliance e.g diuretics can increase urine output so not ideal
59
What is acute HF?
Rapid onset e.g after MI
Contractility immediately drops:
-CO falls
60
What is chronic HF?
Same as acute but decline is progressive rather than a sudden fall
Patients can remain in compensated failure indefinitely:
-severe stress can drive them into decompensation e.g infection, fluid overload, exertion or anaemia
61
What are the 3 major clinical symptoms of HF?
Exercise limitation (fatigue)
Shortness of breath (SOB)
Oedema
62
Describe the symptoms of hypo perfusion:
Effects independent of which side fails
Peripheral vasoconstriction (decrease in blood supply going away from the heart)
-fatigue and exercise intolerance (lack of O2 and nutrient to tissues)
-cold and pale extremities
-fluid and electrolyte retention
-tachycardia and tachypnoea (increase in HR and BR)
63
Describe the symptoms of congestion/ odema in right sided HF:
(Receives deoxygenated to lungs)
*peripheral odema (swollen ankles)
-hepatomegally (enlargement of liver)
-raised jugular venous pressure
-peripheral cyanosis
-fluid and electrolyte retention
64
Describe the symptoms of congestion/ odema in left sided HF:
More common and usually more serious
-pulmonary oedema
*dyspnoea (SOB)
-orthopnoea (SOB lying down)- due to redistribution of fluid to lungs occurs due to abdominal pressure-increases nº pillows
-paroxysmal nocturnal dyspnoea (PND)
-cough/wheeze
-central cyanosis
-tiredness
-breathlessness
65
Name the different New York Heart Association classification of HF symptoms:
NYHA class I, II, III, IV
66
Describe the NYHA class I:
No limitations, ordinary physical activity doesn't cause fatigue, breathlessness or palpitations
67
Describe the NYHA class II:
Mild HF
Slight limitation of physical activity
Such patients are comfortable at rest
Ordinary physical activity results in fatigue, palpitation, breathlessness or angina pectoris e.g walking up the stairs
68
Describe the NYHA class III:
Moderate HF
Marked limitation of physical activity
Although patients are comfortable at rest, less than ordinary physical activity will lead to symptoms e.g walking to the toilet
69
Describe the NYHA class IV:
Severe HF
Inability to carry on any physical activity without discomfort
Symptoms of congestive cardiac failure are present even at rest with any physical activity
Increase discomfort is experienced
70
What are the physical investigations of HF?
Raised jugular vein
Lung sounds
Swelling of ankles and legs
71
Describe how a raised jugular vein can be a sign of AF:
Vein in the side of the neck in somebody with HF becomes visible due to venous distension
e.g Jugular Venous Pressure (JVP) of 5cm- can see it for a length of 5cm above level of sternum
The more visible, the greater the accumulation of fluids
72
What are the tests to assess HF?
Natriuretic Peptides
*Echocardiography
73
Describe the echocardiography test in HF:
Gold standard test
See heart in motion and assess performance as a pump
Measure ejection fraction (EF)
74
Name and describe the different ejection fraction results:
HFrEF- HF with Reduced EF (≤40%)
HFpEF- HF with Persevered EF (≥50%)
HRmrEF- HF with MidRange EF (41-50%)
75
What is the initial treatment in acute HF?
IV diuretics, E.G furosemide 80mg BD
76
Describe the use of thiazide diuretics in HF:
Less potent, used for mild HF
e.g bendroflumethiazide up to 5mg OM (2.5mg in hypertension)
Not effective at eGFR <20ml/min
77
Describe the use of loop diuretics in HF:
Mainstay of treatment
Most common
Potent
e.g furosemide, bumetanide
Can use high doses
Can use IV (furosemide)
78
Describe Metolazone in HF:
Atypical thiazide diuretic
Effective in reduced renal function
Used in combo with loop diuretics in resistant HF
STAT doses 2.5/5mg (normally sufficient)
Short term 2.5-5mg OD for 2-3 days
Long term maintenance (severe HF) 2.5/5mg 2-3 times a week on top of daily loop diuretic
79
What are the pharmaceutical care issues of using diuretics?
Hypotension
Dehydration
Renal impairment
Electrolyte disturbance
Rate of admin of IV furosemide
80
Name the first line treatments for HF:
ACEi/ARBs
B blockers
Aldosterone antagonists (aka MRAs- mineralocorticoid receptor antagonists) e.g spironlactone
81
Name the B blockers licensed in HF:
-bisoprolol -carvediol -nebivolol
82
Name examples of MRAs:
Spironlactone
Eplerenone
83
Name the add on therapies for HF:
Hydralazine/ nitrates
Ivabradine
ARNIs
Digoxin
SGLT2i
84
Describe the use of ivabradine for add on therapies for HF:
Lowers HR- needs to be above 75bpm
Selectively and specifically inhibits if channels in SA node
LVEF less than 35%
85
Describe the use of ARNIs for add on therapies for HF:
Sacubitril and Valsartan (Entresto)
Sacubitril- nepriysin inhibitor (stops degradation of atrial and brain natriuretic peptide)
Valsartan- ARB
Need to stop ACEi/ARB 36 hrs before as 2 ARBs- this decreases chance of severe reaction e.g angioedema
LVEF less than 35%
ESC recommends it joint first line
86
What are the symptoms of cardiac arrhythmias?
Dizzy/ light headed
Palpitations- can feel heart beat
Chest pain
Fatigue
Can also be asymptomatic
Occasionally in severe cardiac arrhythmias decrease in consciousness, small number cardiac arrest (secondary to sudden drop in BP and blood flow)
87
What is the management for bradycardic patients?
Acute- Atropine (increase HR, one off STAT)
Underlying cause (stop drugs, treat disease e.g hypothyroidism)
Permanent pacemaker (PPM)
88
What can cause Torsades de pointes?
Congenital (hereditary)
Hypokalaemia/magnesmia
Drugs:
-Antiarrythmics (class IA or III)
-Erythromycin/clarithromycin
-Tricyclic antidepressants
-Cisapride
-Terfenadine and astemxizole
-Haloperidol
-Lithium
-Phenothiazines
89
Describe how DCCV works:
Application of controlled electric shock across chest wall
-override disordered conduction
-allow SA node to regain control of HR
-pt briefly anaesthetised
90
What is a problem with DCCV and how is this overcome?
Increase risk of thromboembolism so needs anticoagulation for a min of 3 weeks before and 4 weeks afterwards as doesn't always stay
91
What are the cardiac risk factors for AF?
HT, IHD, structural heart diseases
92
What are the non cardiac risk factors for AF?
DM, thyrotoxicosis, increased alcohol, COPD
93
Describe the pathophysiology of AF:
Irregular, rapid atrial rate (300-600bpm) secondary to chaotic conduction within atria
Acute- less 48 hrs
Chronic- more 48 hrs
94
Name and describe the different types of chronic AF:
Paroxysmal- intermittent or self terminating
Persistent- successfully converted by treatment
Permanent- failed or unsuitable treatment
95
What are the common symptoms of AF?
Some asymptomatic
SOB
Dizziness
Fatigue
Palpitations
96
What are the complications of AF?
HF
Angina
Thromboembolism
97
What is the management of AF?
Stroke prevention
Rate control
Rhythm control
98
What have you got to assess in a AF patient in regards to stroke?
Assess stroke risk:
-CHA2DS2VASc stroke risk score
-consider anticoagulant >1men >2 women
Assess bleeding risk:
-ORBIT score to assess risk of bleeding in people who are starting or have started anticoagulation
99
What is another treatment in patients with AF to decrease stroke risk?
Left atrial appendage occlusion
Alternative only if anticoagulation not tolerated or CI
100
What would be the reasons why first line heart rate control in AF wouldn't be appropriate?
Reversible cause e.g infection
HF caused by AF as can worsen HF
New onset of AF (within 48 hrs)
101
What is the treatment for heart rate control in AF?
First line strategy
Standard BB e.g bisoprolol or rate limiting CCB e.g diltiazem, verapamil
Digoxin- only if sedentary lifestyle as doesn't control exercise induced AF
If mono therapy doesn't control, combine 2 of BB, diltiazem or digoxin
102
What is the treatment for rhythm control in AF?
used when rate control isn't successful or still symptomatic
1st line= cardioversion
2nd line= drug therapy
103
Name and describe the drug therapy in rhythm control in AF:
First line: Standard B blocker (+ve as gives both rhythm and rate control)
Others: Dronedarone
Amiodarone (2nd line especially in HF as can make it worse so CI)
104
What is the treatment for paroxysmal AF (PAF)?
"Pill in the pocket" (e.g flecanide) treat attacks only
If frequent, aim to reduce frequency/prevent paroxysms by rate/rhythm control
Not digoxin (increase frequent/rapid and persistant paroxysms)
Abstinence from alcohol/ caffeine
Antithrombotic- needs to be considered as when have paroxysms have increased risk of stroke
105
What are key medications to look out for when a patient has heart block?
Warfarin/ anticoagulants- stop these as patients will have a PPM (surgery)
Rate controlling CCB e.g diltiazem- as can make bradycardia worse
B blockers e.g even eye drops as in elderly enough can get into systemic circulation
106
What is the pre med for a dual chamber pace maker insertion?
Flucloxacillin IV 1g STAT
Co-dydramol IV STAT
107
What is the medication used during the procedure of a dual chamber pace maker insertion?
Gentamicin 80mg STAT injected into the pocket
108
Describe the doses of Amiodarone in rhythm control therapy:
200mg TDS 1 week then 200mg BD for 1 week then 200mg OD maintenance
Half life up to 40-50 days so need a loading dose as takes a while to have an effect
Unlicensed alternative dose: 400mg TDS for 3 days then 200mg OD maintenance
109
What are the doses of Digoxin in rate control therapy?
500mcg x2 STAT doses 6 hours apart
125mcg OD maintenance
110
What are the side effects of amiodarone and therefore monitoring parameters?
Bradycardia
Phototoxicity (need high factor spf)
Slate grey skin
Taste disturbances
Corneal micro deposits-glow (get pt to report any eye sign changes)
Liver dysfunction (initially then every 3 months to monitor)
Thyroid dysfunction (hypo more common)
Pulmonary toxicity (report any breathing problems)
111
What are the SEs of digoxin?
N&V as narrow therapeutic index so chance of toxicity if these symptoms
Blurred vision
Anorexia
Bradycardia
112
Describe a major interaction between rhythm control and rate control therapy and what should be changed?
Amiodarone causes increased levels of digoxin (can double levels) as inhibits Pgp mediated transport of digoxin
Reduce digoxin by 50% if continued use in combo- can use full dose short term, interaction can take 1-4 weeks to occur
Often stop digoxin once ventricular rate is reduced so not often an issue
113
Describe the Wells clinical score as a diagnosis for VTE:
If alternative diagnosis (as likely or greater probability than DVT)
Total above score:
-high probability ≥ 3
-moderate probability 1 or 2
-low probability 0- allows to see whether need for further diagnostic tests
114
Describe a blood test to test for DVT:
D-dimer assay- fibrin degradation product
High -ve predictive value (a low D dimer + a low Wells means a good indicative of -ve DVT)
115
What are the disadvantages of the D-dimer test to diagnose a DVT?
Not as good as positive predictive values as false positives can be present
Increase in trauma, recent surgery, haemorrhage, cancer, sepsis, pregnancy
False positives common in elderly
Affected by heparin use, important to check levels before heparin treatment as can decrease D dimer levels
116
Name the diagnostic imaging used to absolutely diagnose a VTE:
Venography
Duplex ultrasonography (doplus)
Magnetic resonance imaging (MRI)
117
What is the management for VTE?
Identify and treat any underlying cause
Prevent damage to valves of veins
Allow normal circulation to limbs
*Prevent PE
Immediate management with injectable anticoagulant
118
What is the blood test monitoring requirements when using UFH?
Activated partial thromboplastin time (APTT)
Therapeutic and toxic monitoring
Measurement of how long to clot
119
What is the normal APTT for someone not having UFH?
30-40 secs
120
What is the target APTT and APTT ratio for someone using UFH, and what should be the consequences if someone is out of range?
APTT: 80-100 secs
APTT: 1.5-2.5 secs
If below, increase heparin by rate of infusion
If above, then reduce rate of heparin infusion
121
Name examples of Low Molecular Weight Heparin (LMWH):
Enoxaparin
Tinzaparin
122
What are the monitoring requirements for warfarin?
Baseline: clotting screen, Hb, platelets, LFTs, INR, signs of bleeding
123
What is prothrombin time (PT) and international normalised ratio (INR)?
Reference range: 10-14 secs
Relates to changes in extrinsic or common pathways
Expressed as a reference to standard prep
Normal INR= 1-1.2
124
What are the loading dose schedules for warfarin normally?
e.g Day 1 10mg, Day 2 10mg, Day 3 INR
125
In which circumstances is the dose of warfarin decreased?
Increased PT, LFTs, CFF, parental feeding
Elderly, weight less than 60kg
Other drugs which may potentiate INR
126
Describe the main clinical symptoms of PE:
Acute onset chest pain
General malaise
Dyspnoea/ SOB
Haemoptysis (coughing up blood)
127
Describe the other clinical symptoms of PE:
Cough, wheeze, tachypnea (RR>16/min)
Abdominal pain, anxiety, cardiac arrhythmias
Syncope (loss of consciousness)
128
Describe the management for PE:
Supportive therapy- pain relief
Immediate coagulation- as DVT
Fibrinolytics (only in massive PE)
129
Name examples of fibrinolytic drugs:
Urokinase
Streptokinase
Alteplase
Reteplase
130
What are the CI of thrombolytics?
Recent surgery, 'active bleeding sites'
Renal/ liver disease
History of stroke
131
What should occur if a patient is on oestrogen containing contraceptive if they are to have major surgery?
Stop 4 weeks before
132
What types of surgery are high risk?
*Orthopaedic surgery
Cardiac
Vascular
Urological
Thoracic
Gynaecological
Neurosurgery
133
When are patients at high risk for VTE when anaesthetised for surgery?
If under general anaesthetic for more than 90 mins or 60 mins if in the lower limb
Thrombosis after surgery occurs within first 72 hours but can be longer
134
What is the type of mechanical prophylaxis for VTE?
Thigh length graduated compression stockings
From admission until usual level of mobility
