Block 13 Key things to learn

Question 1

What drug do you give to determine if tachycardia is a SVT or ventricular?

Answer 1

Adenosine- it blocks AV node so if it is SVT then it will slow down

Question 2

What happens in a primary TB infection?

Answer 2

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

Question 3

What happens in reactivation of latent TB?

Answer 3

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

Question 4

What are the models of heart failure progression?

Answer 4

Haemodynamic
Neurohormonal
Metabolic
Peripheral

Question 5

What is the haemodynamic model of heart failure?

Answer 5

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

Question 6

What is the neurohormonal model of heart failure?

Answer 6

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

Question 7

What is the metabolic model of heart failure?

Answer 7

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

Question 8

What is the peripheral model of heart failure progression?

Answer 8

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.

Question 9

What is the Vaughan Williams classification of antiarrthymics? Give some examples.

Answer 9

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

Question 10

What are some limitations of Vaughan Williams classification?

Answer 10

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

Question 11

Other than Vaughan Williams how else can antiarrythmics be classified? Give examples.

Answer 11

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

Question 12

What are the 2 types of respiratory failure? and give examples.

Answer 12

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

Question 13

How do you test and treat TB?

Answer 13

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

Question 14

Which ECG leads correspond to which artery?

Answer 14

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

Question 15

What is malignant hypertension

Answer 15

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

Question 16

What are the different types of heart block and their treatments?

Answer 16

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

Question 17

What is LBBB and RBBB?

Answer 17

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

Question 18

What is the different between atrial fibrillation and atrial flutter and how do we treat them?

Answer 18

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

Question 19

What is tachycardia treatment?

Answer 19

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

Question 20

How do we treat heart failure usually?

Answer 20

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

Question 21

What are some other drugs that can help heart failure?

Answer 21

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

Question 22

What drugs need to be avoided in heart failure?

Answer 22

Calcium antagonists- amlodipine
Positive ionotropes- levosimendan
Statins
Aspirin- interferes with ACE inhibitors
Antiarrythmics other than amiodarone

Question 23

What are the usual hypertension treatments and what are some unusual ones?

Answer 23

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