Block 13 Key things to learn Flashcards
What drug do you give to determine if tachycardia is a SVT or ventricular?
Adenosine- it blocks AV node so if it is SVT then it will slow down
What happens in a primary TB infection?
TB enters lungs and is recognised by macrophage- create phagosome
Cant kill it so wall it off in granuloma
Area of granuloma with caveating necrosis is ghon focus
TB also goes to hilarious lymph nodes- more caveating necrosis- all called ghon complex
Area in granuloma becomes fibroses and calcified- now called ranke complex
May be completely killed or may be latent
What happens in reactivation of latent TB?
Ghon focus gets reactivated and bacteria spreads upwards
Memory T cells kick in- lots of areas of caveating necrosis
Cavitates so TB can disseminate and spread
Spreads in lungs and via vascular system- systemic military TB: Hepatitis of liver Kidneys- sterile pyuria Meningitis Adrenal glands- Addison's disease
What are the models of heart failure progression?
Haemodynamic
Neurohormonal
Metabolic
Peripheral
What is the haemodynamic model of heart failure?
As left ventricle fails, bp falls, kidneys sense it and activate RAAS- increase fluid volume- more afterload-
chronic heart failure with dilated heart due to excess fluid volume
What is the neurohormonal model of heart failure?
In heart failure all hormonal systems are abnormal-
RAAS activated, increased ADH, increased endothelin.
Cause increased fluid volume and vasoconstriction which makes heart failure worse.
ANP and BNP also released to try to counteract, so naturetic peptides are diagnostic of heart failure
What is the metabolic model of heart failure?
People with heart failure have higher BMR and become resistant to anabolic substances like insulin which help you gain muscle, fat and maintain bone
Patients have more catabolic than anabolic activity so lose muscle bulk
What is the peripheral model of heart failure progression?
Get abnormal skeletal muscle, enhanced ergo reflexes which tell brain to increase resp rate on exercise, and get decreased chemo and baroreflexes so have more sympathetic outflow which makes heart failure worse.
What is the Vaughan Williams classification of antiarrthymics? Give some examples.
Classify by where they act in cardiac action potential Class 1 - act on phase 0 Class 2- act on phase 4 Class 3- act on phase 3 Class 4 - act on phase2
Drugs that work on phase 0 all block sodium channels: class 1a- disopyramide for SVT and VT to prolong depolarisation class 1b- lidocaine- for VT to shorten depolarisation class 1c- flecainide- for SVT/ VT- no effect on action potential
Drugs on phase 2 blocks calcium channels to prolong conduction and refractory time in SA and AV nodes:
Verapamil, Diltiazem- SVT
Drugs on phase 3 block potassium channels to prolong action potential duration
amiodarone- SVT/ VT
Drugs on phase 4 act to reduce background sympathetic tone and reduce automatic discharge to slow heart:
beta blockers- stall, atenolol- SVT
What are some limitations of Vaughan Williams classification?
Some drugs act across multiple classes: Amiodarone- acts like class 1,2 and 3 drug Sotalol acts as class 2 and 3 drug
Also vaughan Williams doesn’t include some drugs:
Adenosine- k channel activator, slows AV conduction, used for SVT
Digoxin- slows AV conduction- AF and flutter
Magnesium- Calcium Chanel blocker, used for VF
Atropine- antimuscarinic, increase SA firing and AV conduction- treats bradycardia
Other than Vaughan Williams how else can antiarrythmics be classified? Give examples.
By site of action:
SA node- Adenosine Atropine Digoxin Verapamil
Atrium-
Amiodarone
Digoxin
Accessory tract- Adenosine Sotalol Amiodarone Feraininide
AV node-
beta blockers
Digoxin
Verapamil
Ventricle-
Amiodarone
Lidocaine
What are the 2 types of respiratory failure? and give examples.
Type 1- hypoxameic- low oxygen, normal CO2
Type 2- hypercapnic- low oxygen, high CO2
Acute asthma see type 1
Severe asthma see type 2
COPD is type 2, but may be compensated by HCO3
IPF see type 1
Restriction due to chest wall deformity see type 2
How do you test and treat TB?
Acid fast- stains red with ziehl-nielson stain
Tuberculin test- but doesn’t differentiate active or latent infection or just immunity from bcg vaccine
Interferon gamma release assay testing for interferon specific to TB
Latent TB- isoniazid for 9 months
Active- combination of rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months until not infectious,
then rifampicin and another for 7 months until clear
Which ECG leads correspond to which artery?
Issue in leads I, II and AvF = inferior MI- right coronary artery
Leads V1-V4- anteroseptal MI- LAD
Leads V5, V6 and AvL- lateral MI- left circumflex artery
What is malignant hypertension
Recent significant elevation over baseline blood pressure and associated with end organ damage
Very rare- affects- men, smokers, people with secondary hypertension
Histological changes:
fibrinoid necrosis of small arteries
damage to rbcs as they go through vessels obstructed by fibrin- haemolytic anaemia
Die due to intracerebral effects of raised ICP due to cerebral oedema
What are the different types of heart block and their treatments?
1st degree- regular QRS complexes but delay between P and QRS complex- no issue
2nd degree-
Mobitz type 1 -wenkenbach- PR interval increases in length for 3 beats, then a QRS complex is skipped. Repeats. No issue
Mobitz type 2- 2 P waves for every QRS complex- need monitoring and pacing
Type 3- QRS complies regular, but unrelated to P waves- need epinephrine and pacing
What is LBBB and RBBB?
LBBB- suggests issue with left ventricle, may need resynchronisation therapy, seen on ECG as WilliaM- W seen in V1 lead and M seen in V6
RBBB- Usually benign but may suggest a lung disease, seen on ECG as MarroW- M is seen in V1 and W seen in V6
What is the different between atrial fibrillation and atrial flutter and how do we treat them?
Irregular trace with absent P waves often seen with AF. Pulse is irregularly irregular, treat with controlling ventricular rate- digoxin, verapamil and beta blockers, plus anticoagulants to reduce clot risk
Atrial flutter is where atria flutter and contract at around 300bpm but AV node stops most of it getting through to ventricles. Atria too fast, but not disordered like AF. P wave seen as saw tooth appearance. Need to anticoagulant and may treat by cardioversion or electroablation
What is tachycardia treatment?
Sinus tachycardia- just need to remove cause
Stable SVT-
vagotonic manoeuvres
rapid adenosine bolus
cardioversion if collapse
Stable VT-
check if low k or mg- torsades de pointes
iv amiodarone
cardioversion
How do we treat heart failure usually?
Diuretics for symptoms ACE inhibitors ARBs Beta blockers Mineralocorticoid receptor antagonist
Triple therapy- best- doubles life expectancy- ACE inhibitors, beta blockers and mineralocorticoid receptor antagonist
What are some other drugs that can help heart failure?
Ivabradine- works on IF funny current responsible for depolarisation in pacemaker cells
Block IF- slows down rate of spontaneous depolarisation so slows heart rate
Used in heart failure if hr is still over 70bpm when on triple therapy
Drugs that help keep nature tic peptides around- Candoxatril- blocks NEP, so ANP and BNP can’t be broken down so get longer vasodilation and diuresis
Alikerin- direct renin inhibitor
What drugs need to be avoided in heart failure?
Calcium antagonists- amlodipine Positive ionotropes- levosimendan Statins Aspirin- interferes with ACE inhibitors Antiarrythmics other than amiodarone
What are the usual hypertension treatments and what are some unusual ones?
ACE inhibitors
Beta blockers
Calcium channel blockers
Diuretics
Alpha blockers-doxasosin
Central agents- stimulate central alpha receptors to reduce sympathetic outflow- clonidine, methydopa
Minoxidil- vasodilation by blocking K channels, rarely used, have to be used with beta blockers and diuretic if using for hypertension
