Jun 22, 2020
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Coronavirus diagnosis
Aggressive testing for coronavirus is one important recommendation for identifying cases of coronavirus. But what are the fundamentals on which the laboratory diagnostic tests for coronavirus are created.
Detection of pathogen
For detecting the pathogens which have infected our body, we need to get an appropriate sample from the body and establish the presence of pathogen in the sample either directly or indirectly. Direct methods mean directly we see either the whole pathogen or recognise a part of it and indirect means we assess the host’s immune response to the pathogen.
Choice of direct method depends on whether the pathogen can be cultured or not. So for cultural pathogens, we can put the obtained sample in a suitable growth medium depending on the suspected pathogen and wait for the pathogen to grow. Then we can stain it and observe the pathogen under the microscope.
For non cultural pathogen, we have to detect the presence of pathogen antigen, which will directly establish the presence of the pathogen. These antigens are basically proteins present on the cell wall of the pathogen. Also, these days we can directly detect the presence of pathogen nucleic acid by genetic tests known as Nucleic acid amplification tests. For DNA viruses we may use Polymerase chain reaction which amplifies the amount of DNA and for RNA viruses we use reverse transcriptase PCR which converts the RNA into its cDNA and then detects the presence of this complementary DNA.
For indirect tests, we detect the host’s immune response to the pathogen. For host’s response we have to look for presence of IgM or IgG antibodies which develop against the host surface antigens or against the toxins produced by them. These are known as serological tests. Generally antibody detection is used for retrospective diagnosis i.e to know whether the person was once infected with the pathogen or not.
So, how the presence of coronavirus is established ?
Well the sample for coronavirus is either nose or throat swab and since coronavirus is an RNA virus, RT-PCR is used to identify its genetic material. There may be some people who got infected but did not show any symptoms or very mild symptoms and were not tested for the presence of the pathogen. So for these people, we need serological tests which will detect the presence of antibodies against the coronavirus implying that the person has already been infected with the virus. So, these serological tests when done on a large scale will tell how many people have been infected , had produced antibodies and are possibly now immune to the infection.
Mechanisms of cardiac arrhythmias | Fundamentals
Arrhhythmias: The arrhythmias may be either bradyaarhythmias or tachyarrhythmias. There are 3 basic mechanisms by which tachyarrhythmias may occur 1. Enhanced automaticity 2. Triggered automaticity 3. Reentry 1. Enhanced automaticity This type of arrhythmias may poccur due to abnormality in the pacemaker cells. Enhanced automaticity may occurif thereis increase in slope of the pacemaker potential or the Resting membrane potential becomes less negative. This may happen in case of excessive sympathetic stimulation and mild kyperkalemia 2. Triggered automaticity This occurs in cells which are not having automaticity but automaticy is being triggered by someting. It involves due to generation of after-depolarization: After depolarizations are of two types: Early after depolarization which occurs during the repolarization phase of cardiac action potential. It occurs whenever action potential gets prolonged. QT interbal prolonation is a sign of prolonationof action potential duration and thus it may lead to early after depolarization and hence predisposes a person to arrhythmias. Delayed after depolarization occur after the repolarization ends i.e in phase 4 of cardiac action potentia. These after depolarization can lead to generation of impulse before the normal impulse reaches the contractile cells. 3. Reentry circuits: Third mechanism for arrhythmias is reentry or movement of an impulse in a circus movement. If an impulse has 2 paths through which it can pass and these conducting paths differe electrically such that one is fast conducting path and th eother is slow conducting path, in that case of renetry of impulse may occur. Reeentry may occur due to an anatomical defect (anatomical reenetry) or may be due to functional difference in the electrical propery of the cells (functional reentry). Wolff-Parkinson syndrome is a type where arrhthmias occur due to anatomical reentry
Ventricular action potential | Ionic basis | Cardiovascular physiology
Phases of ventricular action potential
Stable resting membrane potential is phase 4
Phase of rapid depolarisation (phase 0): Due to opening of voltage gated sodium channels and entry of sodium inside the cells
Phase of early rapid repolarisation , also known as phase 1: Due to opening of voltage gated potassium channels and exit of potassium outside the cells
Plateau phase or phase 2 where there is hardly any change in potential: Both voltage gated potassium channels and voltage gated calcium channels are open. Potassium moves out of the cells while calcium moves into the cells. This balances the poatnetial and the potential is recorded as a plateau.
Phase of delayed rapid repolarization or phase 3: Calcium channels close while potassium channels remain open. Potassium continues to moves out of the cells causing repolarization. Total duration of ventricular action potential is approximately 250 ms.
Mechanism of change in heart rate by autonomic nervous system (chronotro...
Sympathetic and parasympathetic stimulation affect the nodal action potential to change the heart rate Sympathetic stimulation increases heart rateStimulation of sympathetic system releases noradrenaline which binds with beta 1 receptor. Due to this G alpha S gets activated and it causes activation of adenyl cyclase which in turn leads to formation of cAMP. The HCN channels which are responsible for prepotential.. their opening and closing is affected by the concentration cAMP inside the cells. When cAMP increases, the probability of opening of these channels increases. So, in short sympathetic activation leads to more opening of HCN channels, causing more entry of sodium inside the cells leading to faster change in the potential towards threshold. So there is a change in the slope of the prepotential which becomes steeper and due to this SA node generates more number of impulses in the same time and hence it increases heart rate. Parasympathetic stimulation decreases heart rateAcetylcholine released from vagus causes activation of G i type of proteins which inhibits adenyl cyclase leading to decreased production of cAMP. Thus is leads to decreased opening of HCN channels and also T type channels. Hence the slope of pre-potential decreases leading to decrease in the number of impulses generated and hence decreased heart rate. Parasympathetic activation has one more effect. It delays the closure of these potassium channel which are responsible for phase 3. So more potassium moves out which leads to hyperpolarization. that is more negative maximum diastolic potential.
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Pacemaker potential I SA node action potential I Cardiovascular physiology In this video, we differentiate betwwen SA node...
Waves, 3 segments and 5 intervals in ECG (EKG) | ECG basics
ECG waves: P waves, QRS complex, T wave
Segments: Do not include waves (PR segment, ST segment and TP segment )
Do you know the importance of TP segment ? It is used to find whether ST segment elevation or depression is present or not..
Intervals: PR interval, ST interval, QT interval, RR interval (used to calculate heart rate in case of sinus rhythm), P-P interval (used to calculate atrial rate in case sinus rhythm is not present)
Understand the Physiological basis of electrocardiography using vectorcardiogram, the ECG leads (limb leads and chest leads), where ECG lead
Completely understand ECG by viewing videos in this playlist. You will not become an expert but you will gain thinking ability for ECG interpretation