virus infection

Section 1 Viral hepatitis

1. Clinical significance of hepatitis B triple antigen antibody system.

2.HBV DNA polymerase is located in the core of HBV, which is a direct indicator of HBV replication ability and the most direct, specific and sensitive indicator of HBV infection.

3.3 detection. HCV RNA in serum indicates the existence of HCV in blood, which is the direct evidence of infectivity.

4. Fecal transmission is found in hepatitis A and E, and body fluid transmission is the main transmission route of HBV, hepatitis D and hepatitis C..

5. Acute hepatitis can be divided into three stages: pre-jaundice, jaundice and recovery.

6. Chronic hepatitis is only found in hepatitis B, hepatitis C and hepatitis D..

7. Jaundice hepatitis needs to be differentiated from hemolytic jaundice and extrahepatic obstructive jaundice.

8. Antiviral treatment of hepatitis and prevention and treatment of hepatic encephalopathy caused by severe hepatitis.

Section 2 Epidemic hemorrhagic fever

1. The main pathogens of epidemic hemorrhagic fever are Apodemus agrarius and Rattus norvegicus.

2. Pathogenesis of shock, hemorrhage and acute renal failure.

3. Typical cases in five stages, including fever stage, hypotension shock stage, oliguria stage, polyuria stage and recovery stage. Clinical manifestations of fever.

4. The treatment principle of epidemic hemorrhagic fever is "three mornings and early mornings".

Section 3 AIDS

1. The pathogen is HIV, which mainly infects CD4+T lymphocytes.

2. The main route of transmission is body fluid transmission, among which sexual contact transmission is the main route of transmission.

3. The ways and manifestations of CD4+T lymphocyte injury.

4. The clinical course of AIDS is divided into four stages, and the main manifestations of each stage.

5. The possibility of AIDS should be considered in the following six clinical manifestations: weight loss 10% or more; Chronic cough or diarrhea exceeds 1 month; Fever exceeds 1 month; Systemic lymphadenopathy; Recurrent herpes zoster or chronic disseminated herpes; Oral candida infection.

6. The HIV-1antibody positive standard for two consecutive times was ELISA, which was confirmed by western blot.

Section IV Japanese Encephalitis

1. Japanese encephalitis virus belongs to arbovirus group B.

2. Pigs are the main source of infection, and Culex tritaeniorhynchus is the main vector.

3. Typical clinical course (three phases) and clinical types of Japanese encephalitis.

4. The specific antibody IgM for early etiological diagnosis was positive.

5. Treatment should focus on three levels, namely, high fever, convulsion and respiratory failure.

bacteria contamination

The first section frostbite

1. To clarify the epidemiological characteristics of typhoid fever.

2. In the third week of typhoid fever, necrotic tissue falls off to form ulcers, which easily leads to intestinal bleeding and intestinal perforation.

3. Four clinical manifestations and main complications of typical typhoid fever: intestinal bleeding and intestinal perforation.

4. Clinical significance of typhoid Bacillus culture.

5. typhoid antigen-antibody system and its diagnostic significance.

6. Quinolones are the first choice for typhoid treatment.

The second quarter bacillary dysentery

1. Shigella dysenteriae belongs to the genus Shigella, including Shigella dysenteriae, Shigella flexneri, Shigella baumannii and Shigella sonnei.

2. The epidemiology of bacillary dysentery, the main route of transmission is through the digestive tract.

3. The basic pathological features of bacillary dysentery are in colon. The acute stage is diffuse exudative inflammation of fibrin, and the chronic stage is intestinal mucosal edema and intestinal wall thickening.

4. Clinical manifestations of common bacillary dysentery and toxic bacillary dysentery.

5. Bacillary dysentery can be divided into shock type, brain type and mixed type.

6. Acute common bacillary dysentery needs to be differentiated from acute amoebiasis and bacterial gastrointestinal food poisoning.

7. The shock type of toxic bacillary dysentery should be differentiated from fulminant epidemic cerebrospinal meningitis, and the brain type should be differentiated from epidemic Japanese encephalitis.

8. Treatment principles: anti-infection (quinolones), fluid replacement, anti-shock, symptomatic treatment and strengthening support.

Cholera in the third quarter

1. The pathogen of cholera is Vibrio cholerae.

2. Patients and carriers are the main sources of infection of Vibrio cholerae.

3. The pathogenesis of cholera is mainly the action of cholera toxin, and the main pathological change is severe dehydration caused by severe diarrhea.

4. The clinical manifestations of typical cholera cases can be divided into three stages: vomiting and diarrhea, dehydration collapse and recovery.

5. The diagnosis of cholera includes epidemic history, clinical manifestations, positive stool culture or the increase of serum antibody titer by more than 4 times.

6. Treatment principle of cholera: isolate according to intestinal infectious diseases, replenish water to correct electrolyte disorder, and support treatment according to symptoms.

The fourth quarter meningitis

1. Meningococcus is the pathogen of epidemic cerebrospinal meningitis, which is mainly transmitted through respiratory tract.

2. Meningitis diplococcus can cause septicemia, bacteria invade skin vascular endothelial cells, rapidly multiply and release endotoxin, causing local bleeding, necrosis, cell infiltration and embolism, which is the cause of skin mucosal petechiae.

3. Clinical manifestations of common epidemic cerebrospinal meningitis: prodromal stage, septicemia stage, meningitis stage and recovery stage.

4. Cerebrospinal fluid examination is an important method for diagnosis.

5. Antibacterial therapy is the main treatment, and penicillin is often used. Chloramphenicol easily passes through the blood-brain barrier, and cephalosporin is suitable for patients who are not suitable for penicillin and chloramphenicol.

Section 5 Septic shock

1. The pathogenesis of septic shock is mainly microcirculation disturbance theory, including ischemia and hypoxia, congestion and hypoxia and microcirculation failure.

2. Pay attention to the identification of early clinical manifestations of shock.

3. Anti-shock treatment principle: replenish blood volume, correct acidosis, use vasoactive drugs, maintain the function of important organs, and use heparin early to block the vicious circle of shock.

Leptospirosis

1. Leptospira is the main pathogen. The storm flood type in China is mainly Pamona group, and the paddy field type is mainly jaundice bleeding group.

2. The main sources of infection are pigs and wild rats. It spreads through skin and mucous membrane contact.

3. The clinical manifestations are complex and diverse, which are divided into influenza typhoid type, jaundice bleeding type, pulmonary bleeding type, renal failure type and meningoencephalitis type.

4. Laboratory examination: commonly used auxiliary coagulation test.

5. Penicillin is the first choice for treatment; After the first dose of penicillin, some patients have hershey reaction, so it is suggested that the first dose of penicillin should be small. Gentamicin and tetracycline also have good curative effects.

protozoan infection

Section 1 Enteroamebiasis

1. The pathogen is Entamoeba histolytica, the big trophozoite is histopathogenic trophozoite, and the small trophozoite is intestinal cavity trophozoite, and the cyst is infected with Entamoeba histolytica.

2. The large trophozoite invades the intestinal mucosa, causing ulcers at the bottom of the small mouth. The normal intestinal mucosa between the ulcers is the characteristic intestinal lesion of amoebiasis.

3. The common clinical manifestations of intestinal amebiasis are slow onset, abdominal pain, diarrhea, smelly jam-like mucus and bloody stool; The main complications were liver abscess, intestinal bleeding, intestinal perforation and colon granuloma.

4. Metronidazole or tinidazole is the first choice for treatment.

Section 2 Malaria

1. Etiology: There are four kinds of plasmodium vivax, Plasmodium falciparum and Plasmodium ovale infected by human beings.

2. During the development of plasmodium in human body, the sporozoites of plasmodium develop into merozoites in the liver, and the merozoites release a large number of merozoites from the liver into the blood circulation, causing typical clinical attacks, and some merozoites invade red blood cells to form periodic attacks.

3. Malaria epidemiology: malaria patients and people with plasmodium are the sources of infection, and the bite of Anopheles is the main route of transmission, which is frequent in summer and autumn.

4. Clinical manifestations of typical vivax malaria: sudden chills, high fever and sweating, accompanied by general pain and fatigue, lasting for 2-6 hours, and then entering an intermittent period.

5. Treatment: chloroquine, mefloquine, artemisinin derivatives, etc. It can quickly kill the merozoite in red blood cells and control the onset of clinical symptoms; Primaquine can kill sporozoites in hepatic red blood cells, which is mainly used to control recurrence and prevent transmission. Pyrimethamine can kill all kinds of merozoites and can be used as a preventive medicine.

Worm infection

Section 1 Schistosomiasis japonica

Overview of test sites

1. The pathogen is Schistosoma japonicum, human is the ultimate host, and Oncomelania hupensis the only intermediate host.

2. The source of infection is patients and pest control hosts (pigs, cattle, sheep, dogs and other domestic animals and rats).

3. Transmission route: feces enter the water, eggs hatch into cercaria, and develop into cercaria in snails. After people come into contact with infected water, cercariae enter the body through the skin mucosa and become infected.

4. Clinically, it can be divided into acute, chronic and advanced schistosomiasis and heterotopic damage of lung and brain.

5. Treatment: Praziquantel is a broad-spectrum, high-efficiency, low-toxicity and convenient drug for oral administration.

Cysticercosis in the second quarter

1. Taenia solium patients are the only source of infection of this disease.

2. The clinical manifestations are complex and diverse: cerebral cysticercosis, subcutaneous and muscular cysticercosis, and ocular cysticercosis.

3. Pathogen treatment: albendazole (enterotoxin) and praziquantel are the first choice; Symptomatic treatment. neurology

Introduction to neurology

Motor neurons on 1. originate from pyramidal cells in the motor area of the anterior central gyrus of the brain, and their axons form corticospinal tract and corticospinal tract. Most of the fibers of the corticospinal tract cross to the opposite side at the medullary cone, forming a lateral corticospinal tract, which ends at the anterior horn of the spinal cord in all planes. The cortical brainstem bundle crosses to the opposite side on the plane of each motor nucleus of the brain and ends at each motor nucleus of the brain. It should be noted that, except for the submandibular nucleus and hypoglossal nerve nucleus, all other brain stem motor nuclei are innervated by bilateral branch brain stem bundles.

2. Characteristics of upper motor neuron paralysis: high muscle tension, hyperreflexia of tendon, disappearance of shallow reflex, pathological reflex, no atrophy of paralyzed muscle, normal nerve conduction, and no loss of nerve potential in electromyography.

3. Upper motor neuron paralysis can be divided into cortical type (monoplegia), internal capsule type (triad), brain stem type (cross paralysis) and spinal cord type (paraplegia or quadriplegia).

4. Lower motor neurons include anterior horn cells of spinal cord, motor nuclei of cranial nerves and their axons.

5. The characteristics of lower motor neuron paralysis: the muscle tension of paralyzed muscles is reduced, the tendon reflex is weakened or disappeared, the paralyzed muscles are atrophied, and there is no pathological reflex. EMG showed abnormal nerve conduction and denervation potential.

6. Localization diagnosis of lower motor neuron paralysis: the anterior horn cells of spinal cord cause flaccid paralysis, and its distribution is segmental without sensory disturbance; Anterior root, its distribution is also segmental, without sensory disturbance; Nerve plexus, its damage is mostly single limb motor, sensory and autonomic nerve dysfunction; The distribution of peripheral nerves, paralysis and sensory disturbance is the same as that of peripheral nerves.

7. The main component of extrapyramidal system is basal ganglia, also known as striatum system, including caudate nucleus, putamen and globus pallidus. Its main function is to maintain muscle tension, body posture and coordinated movement.

8. The most common symptoms of cerebellar lesions are ataxia and balance disorder. Acute minor brain injury is characterized by decreased muscle tone, dysarthria and intentional tremor.

9. Anatomy and physiology of sensory system: The primary neurons of pain and warmth sensation are located in the root ganglion of spinal nerve, ending in the posterior horn and exchange neurons, and the secondary neurons cross the contralateral spinal cord through the anterior commissure of spinal cord, forming the lateral bundle of spinal cord and thalamus, ascending to the ventrolateral thalamic nucleus (tertiary neuron) and ending in the sensory area of the central posterior gyrus; The primary tactile neurons are located in the root ganglion of spinal nerve, ending in the posterior horn and exchanging neurons. The secondary neurons cross to the opposite side through the anterior commissure of spinal cord, forming the anterior bundle of spinal cord and thalamus, ascending to the ventrolateral thalamic nucleus (tertiary neurons) and ending in the sensory area of parietal cortex. The primary sensory neurons are located in the root ganglion of spinal nerve, and the central process enters the posterior cord of spinal cord to form thin bundle and wedge bundle, ending in thin bundle and wedge bundle nucleus. The fibers emitted by the secondary neurons cross to the opposite side to form the medial colliculus, stop at the ventrolateral thalamic nucleus, and then send fibers to the central posterior gyrus of the cerebral cortex through the tertiary neurons.

10. The clinical manifestations of sensory disorders can be divided into inhibitory symptoms (sensory loss and hypoesthesia) and irritating symptoms. Stimulating symptoms include sensory inversion, allergy, hypersensitivity, paresthesia and pain.

1 1. Location diagnosis of sensory disturbance: peripheral nerve type, segmental type, conduction bundle type, cross type, lateral type and single limb type.

12. Optic nerve: Optic nerve originates from the ganglion cell layer of retina. After chiasma, the nerve fibers in the nasal part of the retina combine with the fibers in the temporal part of the retina of the contralateral eyeball to form the optic tract and reach the lateral geniculate body. After transposition, the fiber emits visual radiation and ends in the center of occipital visual cortex.

13. Different parts of optic nerve injury have different clinical manifestations.

14. oculomotor nerve paralysis: ptosis, exotropia, diplopia, dilated pupils, disappearance of light reflex and limited eye movement.

15. Clinical manifestations of peripheral facial paralysis: shallow nasolabial groove, drooping corners of the mouth, shallow or disappearing forehead lines, large eye fissure, sloping corners of the mouth to the healthy side, wrinkled forehead, closed eyes, raised cheeks and toothless.

16. Common deep reflexes include biceps brachii reflex, triceps brachii reflex, radial reflex, knee reflex and ankle reflex; Common superficial reflexes include abdominal wall reflex, testicle-lifting reflex and anal reflex.

17. indications and contraindications of lumbar puncture.

Peripheral neuropathy

Neuritis of the first face

1. Clinical manifestations of facial neuritis: acute onset, the main symptoms are paralysis of facial expression muscles on one side, disappearance of forehead lines, eyes not closed, bell phenomenon when trying to close eyes, shallow nasolabial groove on the affected side, drooping mouth and air leakage when whistling.

2. Treatment of facial neuritis: glucocorticoid is used to relieve nerve edema in acute stage, and acyclovir is taken orally if it is caused by herpes zoster virus; Vitamin B drugs and physical therapy also played a role.

The second quarter trigeminal neuralgia

1. Trigeminal neuralgia is a kind of transient, recurrent and paroxysmal severe pain with unknown reasons in the distribution area of trigeminal nerve, which lasts for several seconds to 2 minutes, stops suddenly, and the condition gets worse gradually, and the remission period can reach several days to several years; However, the physical examination did not show any positive signs.

2. Trigeminal neuralgia should be differentiated from secondary trigeminal neuralgia, toothache, sinusitis and temporomandibular joint diseases.

3. The therapeutic drugs for trigeminal neuralgia are: carbamazepine, phenytoin sodium and clonazepam are the first choice; Radio frequency ablation selectively destroys the pain fibers of trigeminal nerve, with simple operation, few complications and low recurrence rate, which is especially suitable for elderly patients who are not suitable for surgery.

Section 3 Acute inflammatory demyelinating polyneuropathy

1. Acute inflammatory demyelinating polyneuropathy is an autoimmune disease characterized by demyelination of peripheral nerves and nerve roots and inflammatory reaction of lymphocytes and macrophages around small blood vessels. Its pathogenesis is generally considered as delayed hypersensitivity autoimmune disease.

2. More than half of acute inflammatory demyelinating polyneuropathy had a history of upper respiratory tract or digestive tract infection before the onset, which was characterized by symmetrical weakness of limbs with sensory disturbance; Bilateral facial paralysis is common in cranial nerves and may have autonomic nerve dysfunction; The typical change of cerebrospinal fluid is the increase of protein content and normal cell number, which is called protein-cell separation. The conduction velocity of motor nerve gradually slows down, the latency is prolonged and the amplitude of action potential is reduced.

3. Acute inflammatory demyelinating polyneuropathy should be differentiated from acute poliomyelitis, myasthenia gravis and periodic paralysis.

4. The treatment of acute inflammatory demyelinating polyneuropathy respiratory muscle paralysis includes symptomatic support and etiological treatment, but the application of hormones is still controversial. Observe the vital signs closely, keep the respiratory tract unobstructed, and use the ventilator as soon as possible when there are indications.

myeleterosis

The first section of spinal cord compression

1. Spinal cord compression is a major disease caused by space-occupying lesions in the spinal canal. The progressive development of the lesion eventually leads to different degrees of spinal cord transection injury and spinal canal obstruction; Spinal cord compression can be caused by pathological changes of spine, spinal cord membrane, spinal cord and nerve roots.

2. Acute spinal cord compression is mostly manifested as transverse spinal cord injury, often accompanied by spinal cord shock; Symptoms of chronic spinal cord compression are progressive, which are usually divided into stimulation period, partial spinal cord compression period and completely transected spinal cord injury period, and can be manifested as nerve root symptoms, sensory disturbance, motor disturbance, abnormal reflex and autonomic nerve dysfunction. Pay attention to distinguish between extramedullary compression and intramedullary compression.

The second quarter myelitis

1. Acute myelitis is an acute transverse injury of the spinal cord caused by demyelination or necrosis of the white matter of the spinal cord, which leads to motor, sensory and autonomic nerve dysfunction of both lower limbs or limbs.

2. Clinical manifestations of acute myelitis: acute onset, backache, abdominal pain, or belching sensation in the waist, often accompanied by paralysis of lower limbs, hypotonia, disappearance of tendon reflex, sensory disturbance of conduction bundle, and recovery after 4 weeks.

3. Glucocorticoid therapy is the main treatment in acute stage, and vitamin B group is helpful to the recovery of neurological function; Strengthen physical exercise in recovery period and promote the recovery of muscle strength.

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