1. The document provides 15 multiple choice questions and answers about local anesthesia. It covers topics like the mechanism of action of local anesthetics, the types of nerve fibers blocked first, durations of different local anesthetics, toxic effects at high doses, contraindications of certain techniques, and complications of various nerve blocks. 2. Key points addressed include that local anesthetics work by sodium channel inhibition, that type C nerve fibers are blocked first, that prilocaine can cause methemoglobinemia at high doses, and that bupivacaine is highly cardiotoxic. 3. Different techniques are discussed such as Bier block, pudendal nerve block, and contraindications of certain blocks in conditions

1. By-
Jini Abraham

2. Q1. Local anesthesia acts by
A. Sodium channel inhibition
B. Calcium channel inhibition
C. Magnesium channel inhibition
D. Potassium channel inhibition
Answer – A. Sodium channel inhibition

3.  Local anesthesia blocks the sodium channel from
inside the cell membrane and raises the threshold of
the channel opening
 LA decreases the rate of depolarization in response
to excitation, preventing the achievement of the
threshold potential.

4. Q2. Afferent nerve fibre affected by local
anesthesia first
A. Type A
B. Type II – B
C. Type C
D. Type II
Answer – C. Type C

5.  Smaller diameter fibres and non myelinated fibres
are blocked more easily and at low concentration,
than thicker myelinated fibres.
 Larger diameter correlates with more rapid nerve
conduction.
 Sequence of block – Autonomic preganglionic
sympathetic (1st)  sensory (in order of pain,
temperature, touch and pressure)  motor

6. Q3. Shortest acting local anesthetic agent is
A. Procaine
B. Lidocaine
C. Tetracaine
D. Bupivacaine
Answer – A. Procaine

7.  Procaine and chloroprocaine are the shortest acting
agents (15 – 30 minutes)
 Lidocaine, mepivacaine and prilocaine have slightly
longer duration of action (30 – 75 minutes)
 Longer acting agents are tetracaine ( 2 – 3 hours),
bupivacaine ( 2 – 4 hours) and etidocaine ( 2 – 3
hours).

8. Q4. Maximum dose of lignocaine with
adrenaline is
A. 3mg/kg
B. 4mg/kg
C. 5mg/kg
D. 7mg/kg
Answer – D. 7mg/kg

9.  Maximum dose of lignocaine without epinephrine is
4.5mg/kg (upto 300mg), effective for about 30 – 60min.
 Maximum dose of lignocaine with epinephrine is
7mg/kg (upto 500mg), effective for about 90min.
 Used for infiltration, peripheral block, epidural and
spinal anesthesia
 Produces local vasoconstriction, which limits systemic
absorption of local anesthetic and prolongs the duration
of action while having little effect on the onset of
anesthesia.

10. Q5. Lignocaine in high dose produces all except
A. Convulsion
B. Respiratory depression
C. Hypotension
D. Cardiac arrest
E. Hypothermia
Answer – E. Hypothermia

11.  CVS – Bradycardia, arrythmia, hypotension and
cardiac failure
 CNS – Depression, restlessness, vertigo, tremor,
convulsion
 RS – Depress hypoxic drive, apnoea
 Allergic reaction – Bronchospasm, urticaria and
angioedema

12. Q6. Local anesthesia causing meth
haemoglobinemia
A. Procaine
B. Prilocaine
C. Bupivacaine
D. Cocaine
Answer – B. Prilocaine

13.  Prilocaine undergoes rapid metabolism and low
acute toxicity.
 Administration of high doses (>600mg) may result in
clinically significant accumulation of metabolite,
ortho-toludine, an oxidizing compound capable of
converting hemoglobin to methemoglobin.
 This effect can be reversed by administration of
methylene blue ( 1 to 2 mg/kg IV over 5 minutes)

14. Q7. Cardiac or central nervous system toxicity may
result when standard lidocaine doses are
administered to patients with circulatory failure.
This may be due to the following reason:

15. A. Lidocaine concentration are initially higher in
relatively well perfused tissues such as brain
and heart
B. Histamine receptors in brain and heart gets
suddenly activated in circulatory failure
C. There is a sudden out-burst of release of
adrenaline, noradrenaline and dopamine in
brain and heart
D. Lidocaine is converted into a toxic metabolite
due to its longer stay in liver

16. Answer – A. Lidocaine concentration are initially
higher in relatively well perfused tissues such as
brain and heart
The highly perfused organs (such as brain, lung, liver,
kidney) are reponsible for initial rapid uptake which is
followed by slower redistribution to moderately
perfused tissues (muscle and gut)
Decreased hepatic function or blood flow  Reduce
metabolic rate  Systemic toxicity

17. Q8. Anesthetic agent with vasoconstrictor is
contraindicated in?
A. Finger block
B. Spinal block
C. Epidural block
D. Regional anesthesia
Answer – A. Finger block

18.  Epinephrine should be avoided when performing
peripheral nerve blocks in areas that may lack
collateral flow (e.g., digital blocks).
 Absolutely contraindicated for injection close to end
arteries (ring blocks of fingers and toe digits, pinna
and penis).

19. Q9. Bier’s block is
A. Subarachnoid block
B. Infiltration and surface block
C. Intravenous block
D. Peripheral nerve and nerve root block
Answer – C. Intravenous block

20.  Intravenous regional neural anesthesia (Bier block) is
a method of producing anesthesia of the arm or leg.
 It involves intravenous injection of large volumes of
dilute local anesthetic solutions into an extremity
after occlusion of the circulation by a tourniquet.

21. Q10. Which anesthetic modality is to be avoided
in sickle cell disease?
A. General anesthesia
B. Brachial plexus block
C. IV regional anesthesia
D. Spinal anesthesia
Answer – C. IV regional anesthesia

22.  IVRA is contraindicated in situations in which
tourniquets are contraindicated e.g., sickle cell
disease, Raynaud’s disease and scleroderma.
 During tourniquet application in IVRA, blood flow
slows down and can precipitate acute hemolytic crisis
in patients with sickle cell disease.

23. Q11. Pneumothorax is a complication of
A. Axillary block
B. Brachial plexus block
C. Epidural block
D. High spinal block
Answer – B. Brachial plexus block

24.  Brachial plexus block can be anesthetized along 4
anatomic locations – interscalene, supraclavicular,
infraclavicular and axillary.
 Common complication of supraclavicular block is
pneumothorax, because of the close proximity of the
lung to the brachial plexus at the level of the clavicle.
Other complications are subclavian artery puncture,
spread of local anesthetic to cause paresis of stellate
ganglion, phrenic nerve and recurrent laryngeal
nerve.

25. Q12. Pudendal nerve block involve
A. L1L2L3
B. L2L3L4
C. S1S2S3
D. S2S3S4
Answer – D. S2S3S4

26.  Pudendal nerve block commonly used in the practice
of obstetrics to relieve pain during the delivery of
baby by forceps.
 Anesthesia is produced by blocking the pudendal
nerves near the ischial spine of the pelvis.

27. Q13. Most common complication of coeliac
plexus block:
A. Pneumothorax
B. Postural hypotension
C. Retroperitoneal haemorrhage
D. Intra-arterial injection
Answer – B. Postural hypotension

28.  Most common complication of coeliac plexus block is
postural hypotension due to lumbar sympathetic
chain blockade leading to upper abdominal vessel
dilation and venous pooling.
 Intravenous fluids are required preblock to reduce
the risk.

29. Q14. From which of the following routes
absorption of local anesthetic is maximum?
A. Intercoastal
B. Epidural
C. Branchial
D. Caudal
Answer – A. Intercoastal

30.  Systemic absorption is directly proportional to blood
supply. Local anesthetic is absorbed very rapidly in
intercoastal blocks due to close location of blood
vessels around the nerve.

31. Q15. Which one of the following local anesthetic
is highly cardiotoxic?
A. Lignocaine
B. Procaine
C. Mepivacaine
D. Bupivacaine
Answer – D. Bupivacaine

32.  Bupivacaine, like lidocaine, blocks the sodium
channels, this block being more slowly reversible.
 Disturbance of sodium channels throughout heart 
decreased conduction speed throughout the
conduction system
 Bupivacaine, at toxic levels, has direct effect on
contractility.