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MCU COLLEGE OF MEDICINE

SY 2022-2023

SUBMITTED BY: GRACE TANGLAO-PEDRO

Case 1:

Amelia, 17 y/o, is due for dental extraction


She is afraid to experience pain. The dentist explained that local anesthetics will be injected prior
to the procedure.
How will you explain based on your knowledge of membrane and action potential how local
anesthetic works?

Generally, local anesthetic drugs interfere with excitation and conduction by action potentials in
the nervous system and in the heart by blockade of the voltage-gated Na channel. Drug affinity
varies with gating state of the channel. The administered drug molecules must diffuse through the
lipid barriers of nerve sheaths and penetrate into or across the lipid bilayers of cell membranes to
reach the acting site on transmembrane proteins.

So, I will explain to the patient that the injection I am holding is an anesthetic drug. Once injected
or put on the skin, the molecules of the drugs will diffuse immediately inside the skin of the gums
and will block the nerves to react. It will give temporary loss of feeling in one small area of the
mouth. He/She stays awake but has no feeling in the area of the body treated with the anesthetic;
thereby, lessening the pain of his/her dental procedures.

Case 2:

What is the difference between isotonic and isometric contraction?


What are the examples of each in relation to your daily life?

An isotonic contraction is one where the muscle shortens without a change in muscle tension.
While in isometric contractions the muscle does not shorten and produces muscle tension without
a change in limb movement.

Examples :

ISOTONIC : A muscle contracts and the joint angle it controls increases and decreases while the
muscle either shortens or lengthens.
ISOMETRIC : Think of holding a weight with your elbow bent to 90 degrees and does not move.

Case 3:

Applying your knowledge on neuromuscular transmission, explain the mechanism behind


Myasthenia Gravis?

Myasthenia Gravis an overall simplification of the postsynaptic folding secondary to NMJ


destruction. It will make your immune system produces antibodies that block or destroy many of
your muscles' receptor sites for a neurotransmitter called acetylcholine. With fewer receptor sites
available, your muscles receive fewer nerve signals, resulting in weakness. results in AChRs and
NaChs depletion, which manifests as neuromuscular transmission failure.
Case 4:

Explain the mechanism based on excitation-contraction coupling mechanism the pathophysiology


of Malignant Hyperthermia?

The state of elevated skeletal muscle metabolism that may occur during general anesthesia in
genetically pre-disposed individuals is call malignant hyperthemia. I will result from altered control
of sarcoplasmic reticulum Ca2+ release. It has been found that there’s a mutation to those MH
susceptible individuals. There are two key proteins of excitation-contraction (EC) coupling, the
Ca2+ release channel of the SR, ryanodine receptor type 1 (RyR1) and the alpha1-subunit of the
dihydropyridine receptor (DHPR, L-type Ca2+ channel). During EC coupling, the DHPR senses
the plasma membrane depolarization and transmits the information to the ryanodine receptor
(RyR). As a consequence, Ca2+ is released from the terminal cisternae of the SR.

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