Cardiology Flashcards
Ejection systolic murmur
- louder of expiration (2)
- louder on inspiration (2)
- also (1)
louder on expiration - aortic stenosis - hocm louder on inspiration - pulmonary stenosis - atrial septal defect also: tetralogy of Fallot
Pansystolic/holosystolic
- louder on inspiration (1)
- louder on expiration (1)
- also (1)
mitral/tricuspid regurgitation
- (high-pitched and ‘blowing’ in character)
- tricuspid regurgitation becomes louder during inspiration unlike mitral stenosis
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)
Late systolic murmur (2)
mitral valve prolapse
coarctation of aorta
Early diastolic murmur (2)
aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)
Mid to late diastolic (2)
Mid-late diastolic
mitral stenosis ('rumbling' in character)
Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)Continuous machinery like murmur
Continuous machine-like murmur
patent ductus arteriosus
Congenital heart disease
Acyanotic - most common types
1. Most common
& 4 others
Acyanotic - most common causes ventricular septal defects (VSD) - most common, accounts for 30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis
Cyanotic CHD
- most common & when does it present
- which is most common at birth
Cyanotic - most common causes
tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia
Fallot’s is more common than TGA. However, at birth TGA is the more common lesion as patients with Fallot’s generally presenting at around 1-2 months
pharm cardiovert of af - 2 options
Cardiovert AF: amiodarone or flecainide
- Amiodarone if structural heart disease
rate control of AF
1st line
2nd line
1: B-blocker or rate limiting CCB (EG diltiazem)
2: If 1 doesn’t adequately control rate: combo with any 2 of - b-blocker, diltiazem and digoxin
what do you use to calculate risk of stroke?
can you write it out and say when to give anticoag (what score
CHA2DS2-VaS Congestive heart failure 1 Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2 Age 65-74 years 1 D Diabetes 1 S2 Prior Stroke, TIA or thromboembolism 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1 S Sex (female) 1
SCORES:
0 No treatment
1 Males: Consider anticoagulation. Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation
can you give verapamil and b-blockers together?
why?
NEVER
can cause bradycardia, heart block and fatal arrest or congestive cardiac failure
normal heart anatomy?
what does s1 and s2 represent
svc > RA > TV > RV > PV > pulm arteries
pulm veins > LA > MV > LV > AV > aorta
s1: M and T valves shut
S2: P and A valves shut
which murmurs are accentuated with inspiration? and which with expiration?
right sided murmurs: inspiration
rIght = Insp
bcos venous return to heart is increased
left sided: expiration
what is diastole?
whats systole?
D: ventricles relaxed and filling with blood
S ventricles contracting
aortic stenosis
- murmur
- pulse/pulse pressure?
- what heart sounds can you get?
- presentation?
- causes
ESM radiating to carotids (crescendo-descresendo)
Narrow pulse pressure, slow rising pulse
Can get a soft/absent S2, a reversed split S2 and an S4
presents: SOB, syncope, chest pain
causes: calcification >65, bicuspid <65, williams syn, rheumatic fever, HOCM
aortic regurg
- Early diastolic murmur
- Collapsing pulse, wide pulse pressure, nailbed pulsation + head bobbing
- Causes: aortic root dilation (dissection, HTN, syphilis, marfans, ehler-danlos), valve disease (rheumatic fever, IE, CTDs, bicuspid valve)
mitral stenosis
• Mid-late diastolic murmur (rumbling)
• Best heard in expiration & at apex w pt in left lat position
• Essentially need to rule out rheumatic fever (main cause)
• Loud S1, opening snap; low volume pulse
Malar flush
mitral regurg
Pansystolic blowing murmur- best heard at apex, radiates to axilla.
S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
ECG may show a broad P wave, indicative of atrial enlargement
Causes: Post-MI, MV prolapse, IE, rheumatic fever, Congenital
cyanotic CHD which way is the shunt? why?
R to L shunt
blood is skipping the lungs so not getting oxygenated
acyanotic CHD (5)
• VSD 30% • ASD • PDA • Coarctation of aorta • AS NB in adults, ASD more common new diagnosis as usually present later
cyanotic CHD (3)
Tetralogy of fallot
Transposition of great arteries
Tricuspid atresia
hypertension mx
<55y old or type 2 diabetes
1. A (ACEi or ARB) 2. Add in C or D: A+C or A+D (d=thiazide-like diuretics)
55 or older with no T2DM or black african/afro-caribbean
1. CCB 2. Add in A or D: C+A or C+D (if black: consider ARB in pref to ACEi)
Step 3: A+C+D
Step 4 =resistant - 1st confirm high clinic BP with ABPM or HBPM. Check for postural hypotension. Discuss adherence. - Seek advice or start 4th drug ○ K<4.5: low dose spironolactone K >4.5: a or b-blocker
hypertension stages and tx targets
STAGES
1. Clinic >= 140/90
and then ABPM daytime av or HBPM average BP >= 135/85 mmHg
- Clinic BP >= 160/100
And ABPM/HBPM av BP >= 150/95 mmHg
Severe:Clinic systolic BP >= 180, or diastolic BP >= 110
TREATMENT TARGETS
<80y old: Clinic BP 140/90 mm; ABPM/HBPM 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg
when to treat htn
Clinic reading 140/90 or higher»_space; ABPM or HBPM
- 135/85 or higher: tx if <80 and any of:
○ Target organ damage
○ Established CV disease
○ Renal disease
○ Diabetes
○ 10y CV risk of 10% or higher
○ NB *consider tx if <60 and 10y risk <10%
If 150/95 or higher»_space; treat
ecg changes - which artery
ECG; Coronary artery
Anterior: V1-V4 Left anterior descending
Inferior II, III, aVF Right coronary
Lateral I, V5-6 Left circumflex
angina tx
All: aspirin + statin + sublingual GTN
1. B-blocker or CCB (verapamil or diltiazem)
a. Increase to max tol dose
2. B-blocker + CCB (if together then CCB needs to be nifedipine)
Alt: if on B or C and can’t tolerate B+C, can add in:
- Long-acting nitrate
- Ivabradine
- Nicorandil
- Ranolazine
If on B+C, only add 3rd drug whilst a/w PCI or CABG
causes of long QT
Drugs
A – AntiArrhythmics (Amiodarone, Sotalol, Flecainide)
A – AntiAnginals (Ranolazine)
B – AntiBiotics (Fluoroquinolones, Macrolides, Aminoglycosides)
C – AntiCychotics (Haloperidol, Quetiapine, Risperidone)
D – AntiDepressants (SSRIs, TCAs)
D – Diuretics
E – AntiEmetics (Ondansetron)
- antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
- TCAs
- Antipsychotics: haloperidol
- chloroquine
- terfenadine
- Erythromycin, clarithromycin
- Methadone
Electrolytes
- Low calcium - Low `K - Low Mg
Medical problems
- Hypothermia - Myocarditis - SAH - MI/sig active myocardial ischaemic
Congenital
- Jervell-Lange-Nielsen syndrome - Romano-Ward syndrome
HF tx
1: ACEi + b-blocker
- Start one at a time
- B-blocker options: bisoprolol, carvedilol, and nebivolol.
- NB these drugs have NO effect on mortality if there is preserved ejection fraction
2nd line: aldosterone antagonist (mineralocorticoid rec antag)
- Spironolactone and eplerenone - Monitor K (as these drugs + ACEi cause hyperkalaemia)
3rd line: specialist should choose
Other • Annual influenza vaccine • One off pneumococcal vaccine ○ Usually need just one dose ○ but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years
warfarin
- major bleeding?
- INR >8, minor bleeding
- INR >8, no bleeding
- INR 5-8, minor bleeding
- INR 5-8, no bleeding
Major bleeding
- Stop warfarin
- Give IV vitamin K 5mg
- Prothrombin complex concentrate - if not available then FFP*
INR > 8.0; Minor bleeding Stop warfarin Give intravenous vitamin K 1-3mg Repeat dose of vitamin K if INR still too high after 24 hours Restart warfarin when INR < 5.0
INR > 8.0 No bleeding
Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
INR 5.0-8.0 Minor bleedin
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
INR 5.0-8.0 No bleeding
Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
pulmonary arterial htn
- how do you decide on tx?
- tx options for each?
If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers
If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil
is LBBB ever normal?
fts?
causes?
WiLLiaM MaRRoW
• in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
• in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
Causes: • MI • HTN • AS • cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
1st line antihypertensive for diabetic
ACEi/ARB
dipyridamole mech of action
phosphodiesterase inh
heart block
- definitions of 1,2, 3
- features of complete incl effect on heart sounds
1st degree HB: prolonged PR interval (>0.2s)
2nd
- Type 1/mobitz 1/wenckebach: progressive prolongation of PR until there's a dropped beat - Type 2: constant PR interval but often no QRS after a p wave
3rd degree/complete: no ass between P and QRS
Complete HB features - Syncope - HF - Regular bradycardia (30-50bpm) - Wide pulse pressure - JVP cannon waves Variable intensity S1
rheumatic fever
- dx
- mx
- histology
- cause
Mx:
- Oral penicillin V - NSAIDs - Tx of comps
Diagnostic
Evidence of strep inf &
- 2 major
- 1 major + 2 minor
Strep infection
- Positive throat swab culture or strep antigen test - High or rising strep Ab titre
Major
- Carditis and valvulitis (must be endocarditis/murmur) - Polyarthritis - Sydenham's chorea - Erythema marginatum - SC nodules
Minor - Arthralgia - Fever - high CRP or ESR Long PR interval
· Group A strep (pyogenes) infection Aschoff bodies (granuloma with giant cells) and Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus) are seen in rheumatic heart disease.
3rd heart sound causes (4)
- Caused by diastolic filling of ventricle
- Normal if <30y old
Caused by: LV failure, constrictive pericarditis + MR
- Normal if <30y old
4th heart sound - 3 causes
- AS, HOCM, HTN
- Cause: atrial contraction against stiff ventricle - so at same time as p wave on ECG
1st heart sound
- cause
- soft in (2)
- loud in (1)
caused by closure of MV + TV
- Soft if MR or long PR
Loud in MS
where to listen to each of the valves
Pulmonary valve
Left second intercostal space, at the upper sternal border
Aortic valve
Right second intercostal space, at the upper sternal border
Mitral valve
Left fifth intercostal space, just medial to mid clavicular line
Tricuspid valve
Left fourth intercostal space, at the lower left sternal border
infective endocarditis abx management
- initial blind mx for native valve, pen allergic, prosthetic valve?
- if staph what to give for native valve & penallergic
- if strep: full sensitive, or less sensitive?
Initial blind tx:
• Native valve: amox (+ gent)
• Pen-allergic, MRSA or severe sepsis: vanc + gent
• Prosthetic valve: vanc + gent + rifampicin
Staph
• Native valve: flucloxacillin
○ pen-allergic or MRSA: vanc + rifampicin
• Prosthetic: flucloxacillin + gent + rifampicin
○ pen-all or MRSA: vanc + gent + rifampicin
Strep
• Fully-sensitive: benpen (pen-allergic: vanc + gent)
Less sensitive: benpen + gent (pen-allergic: vanc + gent)
aortic dissection ass w 9
• hypertension: the most important risk factor
• trauma
• bicuspid aortic valve
• collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
• Turner’s and Noonan’s syndrome
• pregnancy
Syphilis
Glycoprotein 2b/3a rec antagonists (3)
: tirofiban, abciximab, eptifibatide
pericarditis
- most specific ecg marker?
pr depression
HOCM poor prognosis 6
- Syncope
- FHx of SCD
- Young age at presentation
- Non-sustained VT on 24 or 48h holter monitor
- Abn BP change on exercise
Increased septal wall thickness
causes of long QT
Drugs
- antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs - TCAs - SSRIs (esp citalopram) - Antipsychotics: haloperidol - chloroquine - terfenadine - Erythromycin, clarithromycin - Methadone - Ondansetron
Electrolytes
- Low calcium - Low `K - Low Mg
Medical problems
- Hypothermia - Myocarditis - SAH - MI/sig active myocardial ischaemic
Congenital
- Jervell-Lange-Nielsen syndrome - Romano-Ward syndrome
ICD indications
• long QT syndrome • HOCM • previous cardiac arrest due to VT/VF • previous MI w non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35% Brugada syndrome
BNP - below what level is HF unlikely high bNP (4) low BNP (3) produced by? BNP actions (5) uses (3
BNP <100: HF unlikely
NOTES
High BNP: HF, MI, valvular disease, CKD
Lower BNP: ACEi, ARB, diuretics
Produced mainly by LV myocardium - in response to strain
BNP actions:
- vasodilator - diuretic and natriuretic - suppresses sympathetic tone + renin-angiotensin-aldosterone system
Uses
- Rule out HF in acute SOB
- Good marker of prognosis in chronic HF
Guides tx: effective tx will lower BNP levels
ecg fts of hypokalaemia (5)
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
ECG features • U waves • small or absent T waves (occasionally inversion) • prolong PR interval • ST depression long QT
indicators for temporary pacemaker
- Symptomatic or haem unstable bradycardia not responding to atropine
- Post-anterior MI: type 2 or complete heart block
Trifascicular block before surgery
- Post-anterior MI: type 2 or complete heart block
Post-inferior MI complete HB is common
- If asym and haem stable, mx conservatively (usually self-resolve)
ebsteins anomaly
Cause: taking lithium whilst pregnant
Clinical features
- cyanosis - prominent 'a' wave in distended JVP - hepatomegaly - TR - RBBB → widely split S1 and S2
Ass:
- WPW - PFO or ASD in 80% (so shunt from R to L atria)
DETAILS
= low insertion of TV»_space; large atrium and small ventricle (‘atrialisation’ of RV)
Ecg hypothermia
bradycardia 'J' wave - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias
what drug type to avoid in RV MI?
nitrates
what to do if pts on warfarin need emergency surgeyr
Pts on warfarin undergoing emergency surgery:
- If can wait 6-8h: give 5mg vit K IV
If can’t wait: give 25-50units/kg 4 factor prothrombin complex concentrate
adenosine
- what drug enhances effect and what reduces effect
- avoid in what condition
- use?
- adverse effects (4)
- mech of action
Dipyridamole: enhances effect
Aminophylline: reduces effect
Avoid in asthma (bronchospasm)
NOTES
Use: stop SVT
Adverse effects • chest pain • bronchospasm • transient flushing • can enhance conduction down accessory pathways > increased ventricular rate (e.g. WPW syndrome)
DETAILS
Mechanism of action
• causes transient heart block in AVN
• agonist of A1 receptor in AVN > inhibits adenylyl cyclase > reducing cAMP and causing hyperpolarization by increasing outward potassium flux
Short half life
• very short half-life of about 8-10 seconds
ideally be infused via a large-calibre cannula due to it’s short half-life,
dentistry procedures in pts on warfarin - mx?
check iNR 72h before, proceed if INR <4
Naftidrofuryl - mech of action; use
Naftidrofuryl: 5-HT2 rec antagonist
peripheral vascular disease
dipyridamole mech of action
what drug is CI with it
· Dipyridamole = non-specific phosphodiesterase inh > decreases cell uptase of adenoside > increases effects of adenosine
Dipyridamole
= antiplatelet
- Non-specific phosphodiesterase inhibitor
- Decreases cell update of adenosine
- NB use of adeonsine if CI (eg for SVT)
Detail
mainly used with aspirin after an ischaemic stroke or TIA
Mechanism of action
- inhibits phosphodiesterase (these usually break down cAMP)> higher plt cAMP levels > lower intracellular calcium levels - Also reduces cell uptake of adenosine & inhibits thromboxane synthase
paradoxical embolisation
- describe
- most common cause? and its ass
- 2nd most common cause
- dx?
· PFO is the most common cause: Ix w TOE
○ PFO ass w migraines
· Dx: ECHO
NB if stroke + DVT = paradoxical embolisation
- Venous thrombus breaks off > IVC > R heart > L heart > brain
NOTES
For a right sided thrombus (eg dvt) to cause a left sided embolism (stroke), it must pass from R to L side of the heart
Causes:
1. Patent foramen ovale (20% of pop): ass w migraines 2. ASD (much less common)
Mx of ps with PFO who’ve had a stroke remains controversial
Options include antiplatelet therapy, anticoagulant therapy or PFO closure.
when is adenosine CI
whats the alt tx for SVT
asthma
verapamil
HOCM inheritance avoid what 3 drug classes mx 2 most common mutations poor prog factors
· Usually mutation in gene encoding beta myosin heavy chain protein or myosin binding protein C
· Thick ventricular wall.
· Avoid ACEi
• Can’t give things that reduce preload/afterload (ACEi, nitrates, nifedipine like CCBs) as can aggravate outflow tract obstruction
• If see a non-sustained VT on 24h ecg»_space; ICD
• Poor prognosis/assessing risk of sudden death: syncope, young age at presentation, FHx of sudden death, abn BP changes on exercise, non-sustained VT on holter, increased septal wall thickness
NOTES
AD
Most common cause of SCD in young
Avoid: nitrates, ACEi, inotropes
Mx
1. Amiodarone 2. B-blockers or verapamil for symptoms 3. Cardioverter (ICD) 4. Dual chamber pacemaker 5. Endocarditis prophylaxis
NB if have AF too = need anticoag (regardless of chadvasc)
ecg change w high calcium
short qt
loop diuretics - 2 eg - where do they work what do they act on uses (2) adverse effects (10)
- Work at thick ascending limb
NOTES
· Furosemide and bumetanide
· inhibit Na-K-Cl cotransporter (NKCC) in thick ascending limb of the loop of Henle, reducing the absorption of NaCl.
Indications
• HF: acute (usually IV) and chronic (usually PO)
• resistant hypertension, esp if renal impairment
Adverse effects
- Low BP - Low Na, low K, low Mg - Low chloride alkalosis - ototoxicity - Low calcium - renal impairment (from dehydration + direct toxic effect) - hyperglycaemia (less common than with thiazides) - gout
DETAILS
2 variants of NKCC
- loop diuretics act on NKCC2, which is more prevalent in the kidneys.
ASD
- 2 types - diff and which is more common
fts of ASD generally (2)
Most likely CHDs to be found in adulthood
Sig mortality - 50% dead by 50
Ostium secundum (70%)
- Ass w holt-oram syn (tri-phalangeal thumbs) - RBBB w RAD
Ostium primum
- Present earlier - Ass w abn AV valves - RBBB w LAD, long PR interval
ASD fts
- ESM, fitxed splitting of S2 - Paradoxical embolism (passes from venous system to L side of heart > stroke)
statin - ci (2)
CI: macrolides (erythromycin/clarithromycin), pregnancy
ebstein’s anomaly
- characteristic murmur
- ass w (3)
- cause
- fts
· Tricuspid regurg (pan/holosystolic murmur, louder on inspiration)
Ebstein’s can > WPW (slurred upstroke on ECG)
NOTES
Cause: taking lithium whilst pregnant
Clinical features
- cyanosis - prominent 'a' wave in distended JVP - hepatomegaly - TR - RBBB → widely split S1 and S2
Ass:
- WPW - PFO or ASD in 80% (so shunt from R to L atria)
DETAILS
= low insertion of TV»_space; large atrium and small ventricle (‘atrialisation’ of RV)
mech of action of thiazide /thiazide-like diuretics
thiazide: common SE (9), rare (4)
Thiazide and thiazide-like diuretics inh Na reabs by blocking Na-CL symporter at start of DCT
Common SE
- Dehydration, postural hypotension - Low Na & K; hypercalcaemia (hypocalciuria) - gout - impaired glucose tolerance - Impotence
Rare adverse effects - thrombocytopaenia - agranulocytosis - photosensitivity rash pancreatitis
amiodarone
- why do you check U&E before you start
actions (2)
use limited by (4)
adverse effects (10)
U&E before start to check for hypokalaemia (can cause arrhythmia and hypokalaemia sig increases this risk)
Main action: blocks K channels > prolong AP
- But also blocks Na channels
Use limited by
- Very long half life - Thrombophlebitis - so give into central vein - Lengthens QT interval > arrhythmia - P450 inhibitor
Adverse effects • thyroid dysfunction: hypo and hyper-thyroidism • corneal deposits • pulmonary fibrosis/pneumonitis • liver fibrosis/hepatitis • peripheral neuropathy, myopathy • photosensitivity • 'slate-grey' appearance • thrombophlebitis and injection site reactions • bradycardia lengthens QT interval
brugada - ecg changes? giving what makes them more apparent mutation in what is most common? - mx? - inheritance -
· more common in asians
· ECG: convex ST elevation in V1-3 followed by a negative T wave w partial RBBB
○ Changes become more apparent after flecainide
· Mutation in SCN5A gene (encodes myocardial Na channel)
NOTES
· AD
Mx: ICD
ECG changes
• convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
• partial RBBB
• changes may be more apparent after having flecainide or ajmaline = Ix of choice in suspected cases of Brugada syndrome
BNP
- increase levels (11)
- decrease levels (5)
INCREASE Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis
DECREASE Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists
MI 4ds after previous MI - best marker?
CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)
digoxin ecg changes (4)
• down-sloping ST depression (‘reverse tick’, ‘scooped out’)
• flattened/inverted T waves
• short QT interval
arrhythmias e.g. AV block, bradycardia
malignant htn
- fts
- mx
Papilloedema: indication for IV - eg IV nitroprusside
NOTES severe hypertension (e.g. >200/130 mmHg)
Features
• severe headaches, N&V, visual disturbance
• Chest pain, SOB
• papilloedema
• severe: encephalopathy (e.g. seizures)
Management
• reduce diastolic no lower than 100mmHg within 12-24 hrs
• bed rest
• most patients: oral therapy e.g. atenolol
if severe/encephalopathic: IV sodium nitroprusside/labetolol
hydralazine
- mechanism
- CI (3)
- adverse effects (6)
MECH: increases levels of cGMP»_space; smooth muscle relaxation (to a greater extent in arterioles than veins)
NOTES
CI: SLE, IHD/cerebrovascular disease
Adverse effects • tachycardia • palpitations • flushing • fluid retention • headache • drug-induced lupus
DETAILS
increased levels of cyclic GMP > activation of protein kinase G >phosphorylates and activates myosin light chain phosphatase.
- This dephosphorylates myosin light chains
- and prevents their binding to actin
and therefore prevents the smooth muscle from contracting
