Bipolar transistors are made of alloyed materials and can be of two types - NPN and PNP. A transistor has three terminals known as emitter (E), base (B) and collector (K). The figure below shows an NPN transistor where, in the main operating modes (active, saturation, cutoff), the collector has a positive potential, the emitter is negative, and the base is used to control the state of the transistor.

The physics of semiconductors will not be discussed in this article, however, it is worth mentioning that a bipolar transistor consists of three separate parts, separated by two p-n junctions. A PNP transistor has one N region separated by two P regions:

An NPN transistor has one P region sandwiched between two N regions:

The junctions between the N and P regions are similar to the junctions in , and they can also be forward biased or reverse biased p-n junctions. These devices can operate in different modes depending on the type of displacement:

• Cut-off: work in this mode also occurs when switching. No current flows between the emitter and collector, practically an “open circuit”, that is, “the contact is open”.
• Active mode: The transistor operates in amplifier circuits. IN this mode its characteristic is almost linear. A current flows between the emitter and collector, the magnitude of which depends on the value of the bias (control) voltage between the emitter and the base.
• Saturation: works when switching. There is practically a “short circuit” between the emitter and the collector, that is, “the contact is closed.”
• Inverse active mode: As in active mode, the transistor current is proportional to the base current, but flows in the opposite direction. Very rarely used.

In an NPN transistor, a positive voltage is applied to the collector to create a current from the collector to the emitter. In a PNP transistor, a positive voltage is applied to the emitter to create a current from the emitter to the collector. In NPN, current flows from the collector (K) to the emitter (E):

And in PNP, the current flows from the emitter to the collector:

It is clear that the directions of current and voltage polarity in PNP and NPN are always opposite to each other. NPN transistors require a supply with positive polarity relative to the common terminals, and PNP transistors require a negative supply.

PNP and NPN work almost identically, but their modes are different due to the polarities. For example, to put NPN into saturation mode, U B must be higher than U K and U E. Below is short description operating modes depending on their voltage:

The basic operating principle of any bipolar transistor is to control the base current to regulate the flow of current between the emitter and collector. The operating principle of NPN and PNP transistors is the same. The only difference is the polarity of the voltages applied to their N-P-N and P-N-P transitions, that is, to the emitter-base-collector.

Polyneuropathy– a clinical syndrome that occurs as a result of the influence of various etiological factors on peripheral nerves and is characterized by heterogeneous pathogenetic mechanisms.

Polyneuropathy(PNS) occupy second place in the structure of diseases of the peripheral nervous system, second only to vertebrogenic pathology, but significantly exceeding it in the severity of clinical manifestations and disabling consequences.

Currently, three leading pathomorphological mechanisms underlying the formation of PSP have been established:
Wallerian degeneration
primary demyelination
primary axonopathy

There are several pathogenetic theories of the development of the disease:
1.Vascular theory is based on the involvement of the vasa nervorum in the process, which provides blood supply to the peripheral nerves, as well as a change in blood rheology, which leads to their ischemia.
2.Oxidative stress theory explains the development of PSP from the standpoint of disturbances in the metabolism of nitric oxide, which changes the potassium-sodium mechanisms underlying the formation of excitation and conduction of impulses along the nerve.
3.The theory of decreased activity of nerve growth factors suggests a deficit in axonal transport with subsequent axonopathy.
4.Immunological theory explains the development of PSP as a result of cross-production of autoantibodies to PNS structures with subsequent autoimmune inflammation and necrosis.

The causes of the development of PSP are varied and numerous, but even modern research allows us to establish the etiological factor of the disease only in 40-75% of patients.

Nevertheless, the most common systematization of PSP is based on etiological principles.

Classification of polyneuropathies

Autoimmune:
Acute inflammatory demyelinating PSP
Chronic inflammatory demyelinating PSP
Multifocal motor PSP
Paraneoplastic PSP
PNP for systemic diseases
Inflammatory:
Diphtheria PNP
Leprosy PNP
Lyme borreliosis PNP
HIV-associated PSP
Dysmetabolic:
Diabetic PNP
Nutritional PNP
Alcoholic PNP
PNP critical illness
Hereditary:
Sensorimotor PSP type I
Sensorimotor PSP type II
Dejerine-Sottas disease
Refsum disease
PSP with a tendency to pressure paralysis.
Toxic(medicinal or due to intoxication with household or industrial poisons).
PSP caused by exposure to physical factors.

Autoimmune polyneuropathies

1. Acute inflammatory demyelinating PSP(AIDS, Guillain-Barré syndrome) occurs with a frequency of 1-2 cases per 100 thousand population, more often in men, and has two peaks of incidence: at 20-24 and 70-74 years.
It is characterized by the appearance of acute (or subacute) progressive symmetrical weakness in the limbs with loss of tendon-periosteal reflexes. In 70% of cases, ARDP is preceded by various infections suffered the previous day (1-3 weeks before). In other cases, the disease develops for no apparent reason.
Typically, AIDP begins with pain in the calf muscles (cramps) and paresthesias in the fingers and toes, which are then quickly replaced by the development of flaccid paresis of the limbs.

Weakness and wasting of muscles predominate in the proximal sections, pain in the nerve trunks on palpation and positive symptoms of radicular tension (Lasegue, Neri symptoms) are noted.

An early decrease in the Achilles and knee reflexes is an obligatory sign of the disease.

In 25% of cases, there is a disorder of superficial types of sensitivity in the form of “gloves” and “socks”. Less commonly, deep sensitivity is impaired with the development of sensitive ataxia. In 30% of patients, the disease is ascending in nature with damage to the cranial nerves (most often VII, IX, X), with impaired swallowing and breathing.

Pelvic disorders are not typical for AIDP.

There are options for OVDP in the form:
pandysautonomia (heart rhythm disturbances, blood pressure instability)
with exclusively motor impairments in the limbs
Miller Fisher syndrome (manifested by ataxia, areflexia and ophthalmoplegia).

In the majority of patients (80-90%), the disease proceeds benignly with complete or almost complete recovery, and restoration of lost functions always occurs in reverse order: dysfunction of the cranial nerves regresses first, then the upper and lower extremities. In 18% of patients, motor deficits or sensory impairments that limit ability to work persist.

In the diagnosis of ARDP it is important:
Detection of protein-cell dissociation in the cerebrospinal fluid, which is detected in 60-90% of patients 7-10 days after the onset of the disease.
The results of electroneuromyography (ENMG) indicate the demyelinating nature of the lesion, which is manifested by a significant (>80%) decrease in the speed of impulse conduction in at least two motor nerves.
The modern approach to diagnosing ARDP is to conduct enzyme immunoassays to detect an increased titer of antibodies to gangliosides GM1 and GQ1b in Miller Fisher syndrome.

2. Chronic inflammatory demyelinating PSP(CIDP) is characterized by slow (more than 2 months) development of motor and sensory disorders in the extremities.

Men suffer 3-4 times more often than women. The disease occurs with a frequency of 1-2 cases per 100 thousand population. There are two peaks of the disease: 40–50 years (more pronounced) and over 70 years.

The most consistent symptoms of CIDP are:
hypo- or areflexia
muscle hypotonia
hypotrophy in the limbs

Also typical:
Frequent signs of the onset of the disease are numbness or paresthesia in the limbs
Every third patient has cramps in the calf muscles at the onset of the disease

1. Patients with distal tetraparesis predominate (40%).
2. In 80% of patients, sensitive polyneuritic and autonomic (sympathetic) disorders in the limbs are detected.
3. In 20% of cases, the clinical picture of CIDP contains signs of damage to the central nervous system (pyramidal, pseudobulbar, cerebellar symptoms).
4. In 17% of patients, the cranial nerves are involved in the process (usually the facial or caudal group).

Pelvic and respiratory disorders are not typical.

The course of CIDP can be:
monophasic progressive
monophasic regressive
recurrent

After a year, 50% of patients have signs of partial or permanent disability.

In diagnostics diseases are helped by:
detection of protein-cell dissociation in the cerebrospinal fluid (in 40-60% of cases)
high titer of antibodies to myelin associated with glycoprotein
ENMG reveals a decrease or partial block of conduction in two or more motor nerves
with a biopsy of the sural nerve, the identification of a pattern of demyelination or remyelination, endoneurial edema, proliferation of Schwann cells with the formation of “onion heads” in 4 out of 5 nerve fibers is of diagnostic significance.

3. Multifocal motor PNP (MMP) with conduction blocks(Sumner-Lewis syndrome) occurs in a wide age range, predominant in men.

The onset of the disease is subacute or chronic, often without visible reasons.

The neurological picture consists of:
distal asymmetric paresis, mainly in the arms
crumpy
fasciculations
rapid formation of pronounced amyotrophies
the lower extremities are affected later and to a lesser extent
tendon reflexes decrease, but may be normal

Sensitive, bulbar, respiratory, pelvic, pyramidal, and autonomic symptoms are not typical.

The course of MMP is progressive.

Diagnostics:
ENMG results - detection of conduction blocks outside the zones of typical nerve compression
cerebrospinal fluid often does not change
in some patients, an increase in the titer of antibodies to gangliosides GM1, GA1, GD1b is possible

4. Paraneoplastic PSP(Denny-Brown syndrome) can develop with different localization of the tumor process (usually in lung cancer), which often precedes (several years) the manifestation of the oncological process.

1) Sensory variants of the disease predominate, which are manifested by numbness, paresthesia, dysesthesia and pain in the distal extremities. Usually all types of sensitivity are affected, but disorders of vibration and deep muscle sense dominate, up to severe sensory ataxia.
2) Deep reflexes gradually decrease.
3) Orthostatic hypotension and other autonomic disorders are often observed.

The course of the disease is slowly progressive with the transition to a plateau phase.

Diagnostics:
identification of the primary oncological process
detection of antibody titer to ANNA1, Hu
ENMG - characterized by an axonal type of damage to peripheral nerves, which is manifested by a significant decrease in the amplitude of the M-response at normal impulse conduction speed

5. PNP for systemic rheumatic diseases nyahs occur when:
polyarteritis nodosa
scleroderma
dermatomyositis
Wegener's granulomatosis
Sjögren's disease
antiphospholipid syndrome
primary and secondary vasculitis

Variants of the disease:
1) simultaneous or sequential damage to individual nerves in different limbs
2) symmetrical sensorimotor PSP

Neurological manifestations are always combined with signs:
systemic damage to internal organs (kidneys, lungs, heart, gastrointestinal tract), skin, joints, ENT organs
weight loss
general intoxication manifestations

Diagnostics:
increased ESR
detection of C-reactive protein
increased titer of cardiolipin antibodies to lupus anticoagulant and antibodies to the cytoplasm of neutrophils (specific for Wegener's granulomatosis)

Inflammatory polyneuropathies

1. Diphtheria ANPs appear:
early (from the 3-4th day of illness) development of bulbar symptoms (dysphagia, dysphonia, dysarthria)
oculomotor disorders (diplopia, mydriasis, ptosis, limited mobility of the eyeballs, weakened pupillary reactions to light, accommodation paralysis) due to damage to the caudal and oculomotor nerves
after 1-2 weeks, peripheral paresis of the limbs usually appears, predominant in frequency and severity in the legs
Disorders of superficial types of sensitivity of the distal type are characteristic

These symptoms are often accompanied by general intoxication symptoms.

Restoration of lost functions occurs in the reverse order: Bulbar and oculomotor disorders regress first over several weeks, then gradually (over the course of a year) motor and sensory disorders in the limbs, which rarely leave a motor deficit.

Diagnostics based on:
epidemic data
bacteriological studies of the pharynx mucosa (isolation of Corinebacterium diphtheriae)

2. Leprosy PNPs.
Neurological manifestations diseases:
loss of superficial types of sensitivity (pain, temperature) in the areas of innervation of individual nerves (usually the ulnar and peroneal), as well as in places of skin manifestations of leprosy
soreness and thickening of individual nerves (usually the greater ear)
limited muscle atrophy, predominant in the thenar, hypothenar, interosseous muscles and early development of contractures of the fingers
vegetative-trophic disorders: dryness and flaking of the skin, hypo- and anhidrosis, hair loss, hypo- and hyperpigmentation, striations and brittleness of the nail plates, cyanosis of the hands and feet, trophic ulcers and mutilation of individual phalanges
paresis of the facial muscles occurs, especially the upper part of the face (“St. Anthony’s mask”).

The course of the disease is progressive and ends with severe motor loss.

3. Lyme borreliosis ANPs are often neurological complications of the disease.
The most common are:
neuropathy of the facial nerves (possible diplegia facialis)
sensory PNP
sensorimotor PSP

Clinically they manifest are characterized by paresthesia and severe pain in the limbs, followed by amyotrophy. The upper extremities are always affected more often and more severely. Deep reflexes are lost on the hands while the knee and Achilles are preserved.
The course of the disease is regressive with frequent residual motor deficits.
IN diagnostics disease, a diagnostically significant increase in the titer of specific antibodies in the blood and cerebrospinal fluid is important.

4. HIV-associated PSP most often (30%) it manifests itself as distal symmetrical weakness in the limbs.

First signs- numbness and moderate pain in the legs. In 60% of cases, distal paresis develops in the legs, Achilles reflexes decrease (or fall out), pain, vibration, and rarely temperature sensitivity decreases. These symptoms develop against the background of other manifestations of HIV infection: weight loss, fever, lymphadenopathy, etc.
The course of the disease is slowly progressive.

Dysmetabolic polyneuropathies

1. Diabetic PNP occurs in 60-80% of patients with long-term diabetes mellitus and high hyperglycemia, more often in men.

1) The most common manifestation of the disease is the distal sensorimotor form.
2) The disease begins gradually, with paresthesias and dysesthesias in the distal parts of the extremities, like “gloves” and “socks”.
3) An early symptom is loss of Achilles reflexes.
4) As the disease progresses, pain in the legs appears, which occurs or intensifies at night, all superficial types of sensitivity are disrupted (pain, temperature, tactile, vibration).
5) Subsequently, weakness of the foot muscles, typical deformities of the fingers (hammer, claw), trophic ulcers and osteoarthropathy develop.
6) Autonomic symptoms are characteristic: orthostatic hypotension, impotence, violation heart rate, gastroparesis, diarrhea, disorders of sweating and pupillary reactions.
7) Cranial nerves may be affected (usually III, VI, VII). The course of the disease is regressive and is clearly related to the level of glycemia in the blood. ENMG reveals the axonal nature of the lesion.

2. Nutritional ANP due to:
insufficient intake of vitamins B, A, E as a result of malnutrition or unbalanced nutrition or impaired absorption in the gastrointestinal tract
in patients with achylia or achlorhydria after gastrectomy operations
for diseases of the liver, kidneys, thyroid and pancreas, dysproteinemia

The clinical picture is dominated by:
paresthesia
dysesthesia
burning sensation in the lower extremities
knee and Achilles reflexes decrease or disappear
Amyotrophy is observed mainly in the distal limbs
movement disorders are not typical
more than 50% of patients develop heart pathology, including cardiomegaly and atrial fibrillation, swelling in the legs, orthostatic hypotension, weight loss, anemia, stomatitis, glossitis, cheilesis, dermatitis, diarrhea, corneal atrophy

3. Alcoholic PNS- a variant of nutritional PNP. Associated with a deficiency of vitamins B1, B2, B6, B12, B15, A, PP, E due to exposure to ethanol, as well as its direct toxic effect on metabolism in neurons.

The disease most often manifests itself as distal symmetrical vegetosensory PSP.

Characteristic:
pain in the legs of varying severity
crumpy
dysesthesia
vegetative-trophic disorders are represented by changes in skin color, hypo- or anhidrosis of the hands and feet, hair loss on the legs
symmetrical decrease in vibration, tactile, pain and temperature sensitivity in the distal parts of the legs, their moderate amyotrophy
loss of Achilles, less often knee reflexes
frequent combination with cerebellar ataxia expressed exclusively in the legs (Marie-Foy-Alajuanin syndrome), Gaye-Wernicke polyencephalopathy, Korsakoff syndrome, epileptic seizures, chronic hepatitis

Movement disorders occur rarely, cranial nerve damage not typical.

The course of the disease is regressive.
ENMG reveals the classic axonal type of nerve damage.

4. PNP critical conditions develops with severe infections, injuries or intoxications, accompanied by multiple organ failure. Prolonged loss of consciousness and significant severity of the patient’s condition masks the symptoms of PSP, which can be suspected in the case of:
loss of deep reflexes
early (after 1-3 weeks) development of amyotrophy and muscle contractures in the distal limbs
lack of spontaneous breathing when mechanical ventilation is stopped, which cannot be explained by existing pulmonary and cardiovascular pathology

In surviving patients, the disease manifests itself as nonspecific symptoms of severe asymmetric distal sensorimotor PSP.

The course of the disease is regressive, often with moderate residual effects.
ENMG records the axonal nature of the lesion.

Hereditary polyneuropathies

This is a heterogeneous group of diseases inherited in autosomal dominant, autosomal recessive and X-linked sex types.

1. Hereditary sensorimotor PSP(Charcot-Marie-Tooth disease).
There are two options of this disease:
1) Type I (demyelinating) occurs in 66.2% of patients
2) Type II (axonal) – in 23% of all cases

Clinically both options are similar and differ in ENMG results.
The disease begins at 10-16 years of age and is characterized by triad of symptoms:
1. atrophy of the hands and feet
2.disorder of superficial types of sensitivity
3.hypo- or areflexia

Patients often develop foot deformities (Friedreich's, hollow, equinovarus). Some patients experience a moderately progressive, ascending course. The arms are involved later and are less affected. Pronounced interfamilial and intrafamilial polymorphism is characteristic.

2. Dejerine-Sotta disease (type III) and Refsum disease (type IV) begin in the first years of life and are manifested by motor disorders in the limbs in combination with hypertrophy of peripheral nerves and ichthyosis.

3. Hereditary PSP with a tendency to pressure paralysis is a kind of recurrent focal PSP, inherited in an autosomal dominant manner. Begins at the age of 20-30 years with equal frequency in men and women.

Clinical picture is associated with the formation of painless acute mononeuropathies or multiple mononeuropathies with motor and sensory disorders in the extremities.

Nerves are most often affected in the areas of their most typical compression. after minor injuries and compressions:
fibular (35%)
elbow (20%)
radial (9%)

Neurological symptoms last from several days to several weeks. As the disease progresses, regression slows down with the formation of amyotrophies of the limbs.
ENMG reveals the demyelinating nature of the lesion.
Most patients have a favorable prognosis.

Toxic polyneuropathies develop due to:
taking a number of medications (vincristine, cisplatin, ethambutol, etc.)
intoxication with household or industrial poisons, such as lead, arsenic, thallium, carbon disulfide, nitric oxide, and manifest themselves as purely motor (for example, lead) or sensory (carbon disulfide, etc.) PNP

PSP caused by exposure to physical factors develops when:
general or local vibration
after frostbite, burns, electrical injuries
They are characterized mainly by sensory disorders in the extremities.

The term "PUP"

POP is the abbreviated name for the bottomhole formation zone. The bottomhole formation zone is a section of the formation that is adjacent to the wellbore and within which the filtration properties of the productive formation change during construction, operation and repair of the well. The reasons that lead to changes in the characteristics of the bottomhole zone of the formation include the following: redistribution of stress in the near-wellbore part, various physical and chemical effects of various process fluids, as well as various processes, which are caused by modes and operating conditions. The dimensions, configuration, as well as the hydrochemical properties of the bottomhole zone of the formation change during the entire period of the well's existence. They affect the hydraulic connection of the well with the EOR and very often affect its productivity.

The configuration of the formation zone with changed characteristics in the near-wellbore part does not have any geometric shape. Its morphology is very diverse and complex, especially for fractured-pore and fractured reservoirs. Thanks to hydrodynamic studies of wells, it is possible to obtain a quantitative and qualitative assessment of the properties of the bottomhole formation zone, as well as determine hydraulic resistance. In the course of such studies, data is obtained on the size of the equivalent, rather than actual, circular zone. Thus, the dimensions of the formation zone are measured from fractions to several tens of meters. Sometimes you can observe the separation of the formation and the well, both during construction, as well as during repairs and operation. As a result, when tested, such objects may not produce products. To prevent a reduction in the filtration properties of the bottomhole formation zone, a number of measures are carried out that reduce the pressure on the formation during drilling, as well as during well casing and repair. Process fluids or compositions that are compatible with the formation rock or fluids saturating it can also be used. When influencing the bottom-hole zone, various methods increase or restore its filtration properties. The maximum effect can be achieved with a complex effect on PNP.

The success of the user experience largely depends on how well the external and internal devices. For best work equipment, you need good, proven drivers. Today, and over several topics later, we will discuss the basic issues of working with drivers for various devices.

Today's post will be a concentration of definitions related to the topic of computer hardware. This record is needed so that you can easily refer to it if a question arises regarding any definition. Having once explained what is what, I will deprive myself of the need to repeat definitions again and again. Go.

What is a device driver?

What is a device driver? A device driver is software package, which specifies the rules of use of this device. A driver is a transition layer between the operating system and computer hardware. By using operating system we give a signal, for example, to turn on the web camera. To physically turn on the web camera, you need to transmit some signal to it. The device driver acts as a software signal transmitter to the physical device and back. Without drivers, we would not be able to work on the computer, since the operating system cannot directly access the device. This is precisely what explains the possibility in which it is no longer possible to return the operating system to life.

Plug and Play technology

Plug and Play technology (plug and play, PnP) is a technology Microsoft, thanks to which it is possible automatic detection and setting up the connected device. In other words, plug in the device and use it. That is why the technology was called Plug and Play. This technology eliminates the need for the user to search manually. For example, most computer mice and keyboards are ready for use immediately after the first connection. But you haven’t even installed the driver for this device!

What is a PnP device?

A PnP device is one that supports Plug and Play technology. This means that thanks to the work of several subsystems, the driver for this device will be found and installed automatically, without user intervention. Therefore, on the product packaging they try to indicate that the device is a Plug and Play device - after all, this deprives the user of doubts about whether he can install the device himself.

Where can I find Device Manager in Windows?

Device Manager is an MMC console snap-in that specializes in managing computer hardware. Here you can get acquainted with full list all devices installed on the computer. But since the main task for the operating system in terms of devices, this is theirs correct work and the only way to manage this is to manage their drivers, then the main functionality of the Device Manager is associated with this. Here you can view full information about the driver of a device, and much more.

What is DirectX?

DirectX is API set. And API is an application programming interface. The API contains a set of already ready-made templates for application programming. DirectX is an example of an API. And it was created by Microsoft Corporation. Naturally, for your own purposes. DirectX is a set of APIs for programming under Windows. Mostly used to create and support games.

What is driver signature?

Device driver signature. Each person has their own signature. And each person has his own first and last name. Drivers should have the same unique information. Drivers are mainly created by device developers themselves. And having created the driver, they must provide it with a unique signature, which indicates the developer, information about the driver, and so on. The presence of a driver signature indicates that the driver was created by this particular developer and that no changes were made to it. And this leads to the idea that unsigned drivers can be dangerous.

What is the Driver Store?

Driver storage is a protected area on the computer's hard drive in which all installed drivers. Also, there may be device drivers that are on this moment not used by the system. But all of them can be used at any time. You can also do it manually.

Understanding these concepts is quite important to understand the subsequent topics about hardware and their drivers. See you.

A PNP transistor is an electronic device, in a certain sense the inverse of an NPN transistor. In this type of transistor design, its PN junctions are opened by voltages of reverse polarity with respect to the NPN type. In the symbol of the device, the arrow, which also determines the emitter output, this time points inside the transistor symbol.

Device design

The design circuit of a PNP-type transistor consists of two regions of p-type semiconductor material on either side of a region of n-type material, as shown in the figure below.

The arrow identifies the emitter and the generally accepted direction of its current ("inward" for a PNP transistor).

The PNP transistor has very similar characteristics to its NPN bipolar counterpart, except that the directions of currents and voltage polarities in it are reversed for any of the possible three connection schemes: common base, common emitter and common collector.

The main differences between the two types of bipolar transistors

The main difference between them is that holes are the main current carriers for PNP transistors, NPN transistors have electrons in this capacity. Therefore, the polarities of the voltages supplying the transistor are reversed, and its input current flows from the base. In contrast, with an NPN transistor, the base current flows into it, as shown below in the circuit diagram for connecting both types of devices with a common base and a common emitter.

The operating principle of a PNP-type transistor is based on the use of a small (like the NPN-type) base current and a negative (unlike the NPN-type) base bias voltage to control a much larger emitter-collector current. In other words, for a PNP transistor, the emitter is more positive with respect to the base and also with respect to the collector.

Let's look at the differences between the PNP type in the connection diagram with a common base

Indeed, it can be seen that the collector current IC (in the case of an NPN transistor) flows from the positive terminal of battery B2, passes through the collector terminal, penetrates into it and must then exit through the base terminal to return to the negative terminal of the battery. In the same way, looking at the emitter circuit, you can see how its current from the positive terminal of battery B1 enters the transistor through the base terminal and then penetrates into the emitter.

Thus, both the collector current I C and the emitter current I E pass through the base terminal. Since they circulate along their circuits in opposite directions, the resulting base current is equal to their difference and is very small, since IC is slightly less than I E. But since the latter is still larger, the direction of flow of the difference current (base current) coincides with I E, and therefore a PNP-type bipolar transistor has a current flowing out of the base, and an NPN-type one has an inflowing current.

Differences between PNP type using the example of a connection circuit with a common emitter

In this new scheme The base-emitter PN junction is biased by battery voltage B1, and the collector-base junction is reverse biased by battery voltage B2. The emitter terminal is thus common to the base and collector circuits.

The total emitter current is given by the sum of two currents I C and I B; passing through the emitter terminal in one direction. Thus, we have I E = I C + I B.

In this circuit, the base current I B simply “branches off” from the emitter current I E, also coinciding with it in direction. In this case, a PNP-type transistor still has a current flowing from the base I B, and an NPN-type transistor has an inflowing current.

In the third of the known transistor switching circuits, with a common collector, the situation is exactly the same. Therefore, we do not present it in order to save space and time for readers.

PNP transistor: connecting voltage sources

The base-to-emitter voltage source (V BE) is connected negative to the base and positive to the emitter because the PNP transistor operates when the base is biased negatively relative to the emitter.

The emitter supply voltage is also positive with respect to the collector (V CE). Thus, with a PNP-type transistor, the emitter terminal is always more positive in relation to both the base and collector.

The voltage sources are connected to the PNP transistor as shown in the figure below.

This time the collector is connected to the supply voltage VCC through a load resistor, R L, which limits the maximum current flowing through the device. A base voltage VB, which biases it negatively relative to the emitter, is applied to it through a resistor RB, which again is used to limit the maximum base current.

Operation of a PNP transistor stage

So, to cause base current to flow in a PNP transistor, the base must be more negative than the emitter (current must leave the base) by about 0.7 volts for a silicon device or 0.3 volts for a germanium device. The formulas used to calculate base resistor, base current or collector current are the same as those used for an equivalent NPN transistor and are presented below.

We see that the fundamental difference between an NPN and a PNP transistor is the correct biasing of the pn junctions, since the directions of the currents and the polarities of the voltages in them are always opposite. Thus, for the above circuit: I C = I E - I B, since the current must flow from the base.

Generally, a PNP transistor can be replaced with an NPN one in most electronic circuits, the only difference is the polarity of the voltage and the direction of the current. Such transistors can also be used as switching devices, and an example of a PNP transistor switch is shown below.

Transistor characteristics

The output characteristics of a PNP transistor are very similar to those of an equivalent NPN transistor, except that they are rotated 180° to allow for reverse polarity of voltages and currents (the base and collector currents of a PNP transistor are negative). Similarly, to find the operating points of a PNP transistor, its dynamic load line can be depicted in the third quarter of the Cartesian coordinate system.

Typical characteristics of the 2N3906 PNP transistor are shown in the figure below.

Transistor pairs in amplifier stages

You may be wondering what is the reason to use PNP transistors when there are many NPN transistors available that can be used as amplifiers or solid state switches? However, the presence of two various types transistors - NPN and PNP - provides great advantages when designing power amplifier circuits. These amplifiers use “complementary” or “matched” pairs of transistors (representing one PNP transistor and one NPN transistor connected together, as shown in the figure below) in the output stage.

Two corresponding NPN and PNP transistors with similar characteristics, identical to each other, are called complementary. For example, TIP3055 (NPN type) and TIP2955 (PNP type) are good example complementary silicon power transistors. They both have gain direct currentβ=I C /I B consistent within 10% and high current collectors are around 15A, making them ideal for motor control or robotic applications.

In addition, class B amplifiers use matched pairs of transistors in their output power stages. In them, the NPN transistor conducts only the positive half-wave of the signal, and the PNP transistor only conducts its negative half.

This allows the amplifier to pass the required power through the speaker in both directions at a given power rating and impedance. As a result, the output current, which is usually on the order of several amperes, is evenly distributed between the two complementary transistors.

Transistor pairs in electric motor control circuits

They are also used in H-bridge control circuits for reversible DC motors, which make it possible to regulate the current through the motor evenly in both directions of its rotation.

The H-bridge circuit above is so called because the basic configuration of its four transistor switches resembles the letter "H" with the motor located on the cross line. The transistor H-bridge is probably one of the most commonly used types of reversible DC motor control circuit. It uses “complementary” pairs of NPN and PNP transistors in each branch to act as switches to control the motor.

Control input A allows the motor to run in one direction, while input B is used for reverse rotation.

For example, when transistor TR1 is on and TR2 is off, input A is connected to the supply voltage (+Vcc), and if transistor TR3 is off and TR4 is on, then input B is connected to 0 volts (GND). Therefore, the motor will rotate in one direction, corresponding to the positive potential of input A and the negative potential of input B.

If the switch states are changed so that TR1 is off, TR2 is on, TR3 is on, and TR4 is off, the motor current will flow in the opposite direction, causing it to reverse.

By using opposite logic levels "1" or "0" on inputs A and B, you can control the direction of rotation of the motor.

Determining the type of transistors

Any bipolar transistors can be thought of as consisting essentially of two diodes connected together back to back.

We can use this analogy to determine whether a transistor is a PNP or NPN type by testing its resistance between its three terminals. Testing each pair of them in both directions using a multimeter, after six measurements we get the following result:

1. Emitter - Base. These leads should act like a normal diode and only conduct current in one direction.

2.Collector - Base. These leads should also act like a normal diode and only conduct current in one direction.

3. Emitter - Collector. These conclusions should not be drawn in any direction.

Transition resistance values ​​of transistors of both types

Then we can determine the PNP transistor to be healthy and closed. A small output current and negative voltage at its base (B) relative to its emitter (E) will open it and allow much more emitter-collector current to flow. PNP transistors conduct at a positive emitter potential. In other words, a PNP bipolar transistor will conduct only if the base and collector terminals are negative with respect to the emitter.