Gout is a chronic disease that occurs due to metabolic disorders. This disease affects people who have high concentrations of uric acid in their blood. Gout is characterized by deposition of sodium loss in the joints, and in more complex stages of the disease in other vital organs. This substance is deposited in the joints in the form of small microcrystals, which, in fact, cause joint damage. For this reason, arthritis of this type is called microcrystalline.
In a complex stage of the disease, the joint may swell slightly, be hot to the touch, and redness may form. This disease is diagnosed very simply; for this it is necessary to do a blood test to determine the percentage of uric acid in it. Most people who have suffered from this disease claim that physical rehabilitation for gout can solve this problem in the bud.
Correct therapeutic prescriptions, diet, massage and exercise therapy in combination demonstrate excellent results in the treatment of gout, which suggests a favorable prognosis.
It is not without reason that doctors have high hopes for physical rehabilitation. Gymnastics, exercise therapy, dosed walking and other physical exercises have a beneficial effect on the condition of the patient and his affected joints. The main tasks set for physical rehabilitation are:
Therapeutic exercise is a set of special exercises for sore joints (a combination of active and passive loads), carried out in conjunction with general developmental and breathing exercises.
In this way, an improvement in general metabolism (including protein) is achieved, the functioning of the respiratory system and the functional state of the patient’s central nervous system are normalized. Exercise therapy is also recommended for the prevention of gout.
Research has confirmed that when performing various physical exercises, there is a significant decrease in the percentage of uric acid in tissues, which leads to a decrease in this active substance in the blood and urine. When performing active physical exercises, the process of joint destruction completely stops, while their structure and contracture are preserved. These physical therapeutic exercises can be prescribed both individually and in groups.
Patients with a chronic disease and normal condition of the cardiovascular system, without any pain in the joints, are allowed to participate in group classes. Individual physical rehabilitation for gout is prescribed to patients whose stage of the disease is in a subacute state, where joint pain is inherent and their deformation is visible.
For group classes, simple physical activities for gout are prescribed: exercise therapy, sports games, skating and skiing in winter, and swimming in summer. When conducting group physical exercises for gout, it is necessary to gradually increase the intensity and frequency of exercise, focusing on the general adaptation of the team to the load and the achieved effect of sports work.
Particular attention should be paid to breathing exercises. If a patient with gout does not have any heart problems, then it is necessary to prescribe applied and complex exercises. Those patients who are indicated for physical exercise for gout on an individual basis are prescribed special “joint exercises,” intense walking and breathing complex exercises. After such a patient begins to decrease pain in the joints, he may be allowed to do group exercises for gout.
For gout patients, comprehensive breathing exercises play a key role. When conducting such exercises, it is necessary to control breathing and its depth as accurately as possible.
The following basic physical exercises for gout should be noted:
Before starting physical rehabilitation, patients are recommended to undergo a comprehensive examination and tests. If the disease is of the nature of long-standing deformations, then additional x-rays are necessary.
After completing the rehabilitation course, patients are re-examined to assess the dynamics of recovery of the affected joints and the overall result achieved by physical exercise.
Gout is a chronic disease associated with the deposition of urate crystals (uric acid salts) in the joints and kidneys. The symptoms of gout are quite characteristic and manifest themselves in the form of recurrent attacks of arthritis, which have a progressive course and are accompanied by intense pain.
Also, during the development of the disease, gouty nodules appear. They lead to gradual deformation of the affected joints (tophi are formed). In the future, there is a risk of involvement of the kidneys in the process with the subsequent development of urolithiasis and renal failure. Diagnostic and therapeutic measures for gout are aimed at relieving all symptoms with further normalization of uric acid levels.
The basis for the development of gout are metabolic disorders. They are caused by disturbances in the regulation of purine metabolism in the body, which entails the accumulation of uric acid along with its derivatives - acid salts (urates). A decrease in acid excretion in the urine, coupled with increased synthesis, leads to its increased concentration in the blood (hyperuricemia).
If we talk about the reasons for the development of gout, it should be noted that all of them, to one degree or another, provoke a violation of the delicate balance between the synthesis of uric acid and the process of its elimination. On this basis, hyperuricemia in gout is divided into several main types:
An increase in the amount of urate in gout leads to the accumulation of urate crystals. This mainly occurs in the joint cavity, resulting in gouty inflammation. If accumulation occurs in the kidneys, nephropathy occurs. People over forty are most susceptible to gout. Men suffer from it about twenty times more often than young people, children or women.
The mechanism of gout development is quite simple and understandable. As long-term hyperuricemia develops, the body tries to eliminate it in different ways: accelerated release of uric acid by the kidneys occurs, and urate begins to be deposited in the tissues. This mainly affects joints, kidneys and skin. When deposited in tendons or under the skin, crystals form so-called “tophi” (rounded formations of different sizes).
As a result of the accumulation of uric acid in gout in the synovial fluid, its salts precipitate. These are crystals of sodium urate.
Gradually they begin to penetrate into the cartilage tissue and synovial membrane, forming defects. Through them, uric acid penetrates into the bone tissue, which leads to its destruction (marked on the x-ray as a symptom of a “punch”).
But a particular danger with gout is the accumulation of urate in the kidneys. This can lead not only to urolithiasis, but also to serious kidney failure. Coupled with high blood pressure and vascular pathologies, it leads to a several-fold increase in the risk of heart attacks and strokes. Therefore, it is so important to contact a medical facility at the first signs of illness.
The very first symptom of gout, or its clinical manifestation, is an acute attack of arthritis. Most often it manifests itself against the background of complete well-being, in the midst of absolute health. Only in a few cases can certain unpleasant sensations occur in one or another joint, nervousness and general malaise. Fever or chills, as well as insomnia, may sometimes occur.
Often the first gout attack is triggered by poor diet, which includes eating foods rich in purines (meat, fish, mushrooms or legumes), as well as alcohol abuse. In other cases, various injuries can become provoking factors. Various infections, physical or mental overloads can also serve as a kind of impetus.
A certain classic picture is very typical for an attack of gout: at night or early in the morning, very sharp pain suddenly appears in the area of one of the joints. Most often this is the joint of the big toe on one foot.
It begins to swell quickly, the skin over it turns red and becomes hot to the touch. Body temperature often rises to 40° C. The pain is so excruciating that even simply touching the joint becomes impossible.
After five or six days, all of the listed signs of gout begin to subside and gradually disappear by the tenth day. Over time, in the absence of timely therapy, the number and frequency of such attacks increases, and more and more joints are involved in the pathological process of gout.
Important! Currently, a classic attack of gout occurs in only 60% of all cases. In the remaining 40%, the clinical manifestations are somewhat blurred, and gouty arthritis has an atypical localization, affecting the small joints of the hands, knees or elbow joints.
Over time and in the absence of proper treatment, gout will lead to arthritis of several joints, damage to internal organs and the formation of tophi. In the first five years after the onset of the disease, attacks will recur at varying intervals. In this case, all manifestations will reverse, and the function of the joints will be completely restored.
Each new attack of gout will lead to the fact that over time other joints will be involved in the pathological process. The exception is the spine and hip joints, which are rarely affected by the disease. There may be damage to the tendon tissue. Most often this occurs in the heel joint area.
Attacks of the disease can range from a couple of months to several years. Between them, the symptoms of gout disappear completely, and overall health improves. But five or six years after the onset of the first gouty attack, in the absence of therapy, the interval between attacks decreases. And due to the destruction of articular tissues by urates, deformations occur in the area of the affected joints, causing stiffness of the latter.
Another characteristic sign of gout will be the appearance of tophi under the skin. They can have a wide variety of sizes - from a match head to a small apple. The main locations are the ears, heel tendons, small joints of the hands, the area of the big toe, knee joints or elbows. In severe cases, tophi can ulcerate with the formation of fistulas.
Important! There is such a thing as “gouty status,” which is characterized by the most severe course of gout. For several months, inflammation and attacks of arthritis are almost constantly observed, affecting one or several joints at once.
Gradually, gout leads to the development of secondary osteoarthritis. It not only increases the deformation of the joints, but also leads to a decrease in their mobility to an even greater extent. Also, at least 70% of patients with gout are affected by spondylosis deformans. Of particular danger is kidney damage associated with the formation of urate stones and tophi. With timely initiation of drug therapy, you can avoid such complications and continue to live and work fully.
Of great importance in the process of establishing the diagnosis of gout is a set of laboratory tests, which includes determination of the content of uric acid in blood serum and daily urine, as well as an analysis of uric acid clearance. Indicators of normal values do not exceed the following values:
In the acute attack period or with chronic arthropathy, these numbers are increased.
In gout, the most common type of hyperuricemia is the metabolic one. It is characterized by a high level of uric acid in the blood, normal clearance and good excretion in the urine. In second place is the mixed type, in which the acid levels in the blood will be the same or lower, and the clearance and daily urine data will be reduced. In the renal type, all indicators are significantly reduced.
During the period of acute gouty arthritis, a general blood test is characterized by an increase in leukocytes and ESR. Biochemical analysis shows an increase in C-reactive protein. Hypercholesterolemia and increased triglycerides are also often detected.
Gout is almost always characterized by the involvement of the kidneys in the pathological process, which is why the urine contains an insignificant content of albumin, leukocytes and even blood, and its density will be slightly reduced. A test for residual nitrogen and a Zimnitsky test for renal concentration function will help identify interstitial nephritis in cases where it is asymptomatic.
The study of synovial fluid in gout plays a huge role, since it serves as the leading method for the final diagnosis. Liquid is taken from the cavity of the affected joint.
A polarizing microscope for gout can detect thin needles of sodium urate crystals. The procedure for morphological examination of material taken from the subcutaneous tophi is of the same importance.
Important! X-rays of joints in the early stages of gout do not have much diagnostic value, since there are no characteristic changes yet. But at later stages, tophi and the so-called “punch” symptom are detected, which serves as one of the leading criteria for establishing disability in this disease.
The process of treating gout should be handled by a specialized specialist - a rheumatologist. The criteria for making a diagnosis are:
Two of the signs listed are sufficient for the diagnosis of gout to be established and treatment prescribed. It is often necessary to carry out a differential diagnosis of gout with arthritis of a rheumatoid or infectious nature.
Complex therapy for gout has the following main objectives: stopping acute attacks and preventing them, stopping the process of accumulation of urates in tissues and stimulating their resorption. In most patients with gout, these problems are solved successfully, provided they take appropriate medications for life.
In the absence of any symptoms characteristic of gout, therapy is prescribed only in cases where the uric acid level is more than 0.54 mmol/l, since there is a high risk of an acute gout attack. If the number is lower, then no treatment is required.
To suppress an acute attack of gout in medicine, the drug Colchicine is often prescribed, which has an effective effect on the processes of synthesis, excretion and solubility of urates. It should be taken before the onset of an attack, when discomfort in the joint begins to appear or a feeling of heaviness begins.
A day after taking the drug, inflammatory swelling and pain in the joint decrease, but you should continue to take the medicine for three or four days. You need to know that Colchicine can have a negative effect on the gastrointestinal tract, which sometimes requires an urgent dosage reduction or complete withdrawal.
Also, Butadione, Ketazone, Reopirin and Indocid have worked well for gout. They belong to a number of pyrazolone and indole drugs that have a pronounced anti-inflammatory effect, enhance the excretion of urate and have fewer side effects than Colchicine.
Doctors often prescribe corticosteroid drugs (Prednisolone) for gout, but the latter do not provide a lasting effect, and after their discontinuation there is a risk of resumption of arthritis symptoms. In addition to drug therapy, during an acute attack of gout, complete rest, abundant alkaline drinking and a proper diet are important.
Since gout is a chronic disease, it requires constant, almost lifelong therapy, the most important component of which is a special diet. It is necessary to exclude foods rich in purines, proteins and lipids from the diet.
Situational therapy problems with answers 1-10
Situational therapy task 1
A 57-year-old man was admitted to the clinic with complaints of cough with sputum, the presence of blood streaks, pain in the right side when inhaling, excessive sweating, weakness, and an increase in body temperature to 37.4 0 C.
From the anamnesis: 10 years ago he suffered from focal pulmonary tuberculosis and was removed from the register.
The condition is satisfactory. The skin is of normal color. On auscultation, harsh breathing, isolated dry rales and fine bubbling rales in the interscapular space after coughing are heard in both lungs. Blood test: e - 4.8x10 12, Hb - 142 g/l, l - 9.2x10 9, p - 2, s - 78, l - 12, m - 8, ESR - 25 mm/hour.
MBT was not detected in sputum by bacterioscopy.
1. Establish a preliminary diagnosis.
2. Outline a plan for additional examination.
4. Prescribe treatment.
1. Preliminary diagnosis: subacute disseminated pulmonary tuberculosis.
2. Additional examination plan: an. sputum and urine for MBT by culture, general urine analysis, consultation with an otolaryngologist, tomographic examination of the lungs, tuberculin tests, bronchoscopy.
3. In favor of the tuberculous etiology of the process is evidenced by: mild manifestations of clinical symptoms, a characteristic x-ray picture: the presence of polymorphic foci in both lungs, moderate changes in the blood picture.
4. The patient is indicated for treatment with antibacterial drugs: isoniazid, streptomycin, ethambutol, tizamide every other day.
Patient P., 35 years old, suffered exudative pleurisy at the age of 16, and 20 years later he was diagnosed with disseminated pulmonary tuberculosis in the decay phase. MBT +. He was treated for 14 months in a hospital and sanatorium. There was a cessation of bacterial excretion, resorption and thickening of lesions in the lungs, but a cavity with thick walls was formed on the right in the 2nd segment. The patient refused surgical treatment.
The condition is satisfactory. The skin is of normal color. Peripheral lymph nodes are not palpable. When percussing on the right above the right apex of the lung from behind, dullness of the pulmonary sound is determined: in the same area, when coughing, persistent moist rales of medium caliber are determined. Physical examination revealed no abnormalities in other systems and organs.
Blood test: er. - 4.5x10 9, Hb - 130 g/l, l - 8.0x10 9, p - 0, s/i - 75, lymph. - 20, m - 5, ESR - 12 mm/hour.
1. Make a clinical diagnosis and justify it.
2. Determine the tactics of the TB doctor after the patient refuses surgery.
3. Tactics of the local physician in relation to this patient.
1. First of all, in this situation, it is necessary to draw up a differential diagnostic series of the most common diseases. This should include: fibrous-cavernous pulmonary tuberculosis, chronic abscess, disintegrating lung cancer.
2. This patient has fibrous-cavernous pulmonary tuberculosis. This is evidenced by:
1) a history of exudative pleurisy and disseminated pulmonary tuberculosis with abacillation diagnosed 14 months ago;
2) the formation of the final process as a result of long-term ineffective treatment in hospitals and sanatoriums with AB drugs;
3) characteristic x-ray picture:
4) localization of the cavity in the 11th segment
5) the nature of the cavity - thick walls
6) the cavity is located against the background of fibrosis of the lung tissue
7) the presence of dense foci of bronchogenic dissemination
3. The patient will be observed at 1 A g. DU (BC+). He will continue the main course of treatment with two antibacterial drugs intermittently on an outpatient basis and undergo X-ray monitoring every 3 months.
4. The local general practitioner has information about the presence of a bacilli-transmitting patient in the area.
5. Considering the number of contacts in the epidemic. outbreak and when they go to the clinic, they show phthisiatric alertness.
6. Together with the epidemiologist and the phthisiologist, he visits the epidemiological site. the outbreak immediately after its detection and participates in drawing up a plan for its recovery.
Situational therapy task 3
Patient M., 27 years old, two weeks ago developed weakness, sweating, low-grade fever, shortness of breath, and chest pain on the left. She was treated with a diagnosis of acute respiratory infections without improvement. Shortness of breath increased, body temperature increased to 39.0 0 C, although the chest pain on the left decreased.
Objectively: the condition is satisfactory. The skin is moist and of normal color. The left half of the chest lags behind in the act of breathing. Percussion reveals dullness on the left below the 1st rib. Breathing in this area cannot be heard. The abdominal organs are not changed.
Blood test: er. - 4.2x10 12, Hb - 140 g/l, l - 12x10 9, p - 2, s - 80, l - 12, m - 6, ESR - 38 mm/hour.
MBT was not detected in sputum.
1. Establish a preliminary diagnosis taking into account the etiology of the disease.
2. Outline a plan for further examination indicating possible results.
Standard of answers to a situational therapy task
1. Preliminary diagnosis: left-sided exudative pleurisy of tuberculous etiology.
2. Examination plan:
1) pleural puncture; the cellular composition of the exudate can be lymphocytic, the protein content is more than 30 g/l;
2) tuberculin tests may show increased sensitivity to tuberculin;
3) X-ray tomography after evacuation of exudate;
4) pleuroscopy can reveal macroscopic and microscopic data in favor of a preliminary diagnosis.
3. Differential diagnosis is carried out with nonspecific pleurisy. In favor of tuberculosis etiology is evidenced by:
- gradual development of the disease with symptoms of tuberculosis intoxication;
- young age of the patient;
- lack of effect from nonspecific treatment;
4. Before receiving the first results of the examination, prescribe treatment with broad-spectrum antibiotics.
A 52-year-old patient complains of shortness of breath, cough with greenish sputum, weakness, and sweating. Considers himself sick for many years. The disease progressed in waves, initially with rare and then more frequent exacerbations. Recently, my appetite has worsened, I have noticed weight loss, and my shortness of breath has increased. On examination, a shortening of the percussion sound was noted at the apex of the right lung. Here, sharply weakened breathing with a bronchial hue and scanty dry wheezing can be heard. Above the lower parts of the lungs, breathing is weakened, inhalation is lengthened. The borders of the heart are not clearly defined due to the box-like tint.
Blood test: er. - 3.5x10 12, Hb - 100 g/l, l - 9.0x10 9, p/box - 2, s/box - 82, lymph. - 10, m - 6, ESR - 30 mm/hour.
Urinalysis: no pathology.
Sputum analysis shows a large number of leukocytes and elastic fibers. BC was detected once by the Ziehl-Nielson method.
Assignment for a situational therapy task
1. Create a differential diagnostic series.
2. Justify the preliminary diagnosis.
3. Draw up a plan for additional examination.
4. Determine treatment tactics.
1. Differential diagnostic series:
- chronic lung abscess
— fibrous-cavernous pulmonary tuberculosis.
2. Preliminary diagnosis: fibrous-cavernous pulmonary tuberculosis. This diagnosis is evidenced by:
- presence of MBT in sputum;
- absence of catarrhal phenomena in the lungs in the area of noticeable dullness of pulmonary sound and altered breathing;
- moderate changes in the general blood test, in particular moderate leukocytosis;
- X-ray picture - the upper lobe is reduced due to fibrosis, in the area of which ring-shaped shadows with thick walls are visible.
3. To clarify the diagnosis it is necessary:
examination of sputum for MBT by culture;
conduct diagnostic bronchoscopy with sampling of bronchial contents for bacteriological examination for MBT;
If possible, perform a computed tomography scan of the lungs.
4. Treatment tactics:
- the patient must be hospitalized in an inpatient TB dispensary;
- antibacterial therapy is required - at least 3 antibacterial drugs;
— in the absence of radiological dynamics after two months of conservative treatment, the patient must be offered surgical treatment - resection of the upper lobe of the right lung.
Situational therapy task 5
Patient K., 29 years old, works at YaMZ. Over the past three months, he began to notice periodic rises in temperature to 38.0 0 C, increasing weakness, drowsiness, weight loss, and increased sweating. The patient continued to work, but two days ago hemoptysis appeared, which forced him to consult a doctor.
Objectively: the patient’s condition is satisfactory. The skin is pale and moist. Peripheral lymph nodes are not enlarged. The right half of the chest lags behind in breathing. On percussion - dullness of sound in the upper lobe of the right lung. Breathing in this area is harsh; after coughing, fine moist rales are heard. Pulse - 92 per minute, rhythmic, satisfactory filling. Heart sounds are clear. The abdomen is painless on palpation. The liver is not enlarged.
Hemogram: e - 3.8x10 12, Hb - 134 g/l, l - 11.2x10 9, p - 2, s - 78, l - 16, m - 4, ESR - 28 mm/hour.
1. Make a preliminary diagnosis.
3. Conduct differential diagnostics.
1. Preliminary diagnosis: infiltrative tuberculosis of the upper lobe of the right lung.
1) analysis of sputum for MBT by bacterioscopy and culture
4) lateral radiograph and tomograms
5) tuberculin tests
6) in the absence of contraindications - bronchoscopy.
3. Differential diagnosis is carried out with pneumonia and central lung cancer. Tuberculosis is supported by the gradual development of the disease with symptoms of tuberculous localization, the nature of auscultatory data, x-ray patterns and hemograms.
4. Treatment: isoniazid, streptomycin, ethambutol, vitamin E. hemostatic therapy.
In a 40-year-old patient, when performing the clinical minimum, a rounded shadow with a bay-shaped disintegration in the center, measuring 3.5 cm in the third segment of the right lung, was revealed. The surrounding lung tissue is not changed.
I consulted a doctor due to a long-lasting, dry hacking cough, which has recently been accompanied by hemoptysis (blood streaks in the sputum), weight loss, weakness, and loss of appetite.
Single dry rales are heard over the lungs, and the heart sounds are clear and rhythmic. Pulse - 80 per minute, rhythmic. Blood pressure - 140/90 mm Hg. Art.
Blood analysis; Nb - 95 g/l, er. - 3.6x10 12 /l, l - 5.18x10 9 /l, ESR - 44 mm/hour.
1. Name and justify the preliminary diagnosis, having drawn up a preliminary differential diagnostic series.
2. Draw up an examination plan to verify the diagnosis.
3. Determine treatment tactics.
1. Preliminary diagnosis: in this clinical situation, it can be assumed that the patient has the following diseases:
- decaying lung cancer
- tuburculoma with decay
2. More evidence for the presence of a disintegrating tumor in the patient (primary cavitary cancer). This diagnosis is evidenced by:
- presence of a long, dry, hacking cough
- hemoptysis (streaks of blood in the sputum)
- presence of asthenic syndrome
- the presence of a rounded shadow with a bay-shaped decay in the center
— location of the formation in the third segment.
3. Examination plan: to verify the diagnosis it is necessary to carry out:
— fibrobronchoscopy with biopsy in the presence of pathology in B 3 and sampling of bronchial contents for atypical cells and MBT
— catheterization biopsy with histological and bacterioscopic examination of the material
- subcutaneous test with tuberculin (Koch).
4. Treatment tactics: to confirm the diagnosis of the tumor, an urgent radical operation is necessary - removal (resection) of the upper lobe on the right with revision of regional lymph nodes.
Situational therapy task 7
An 18-year-old patient undergoing fluorography (he had not been examined for many years before) was called in for further examination. It turned out that in childhood (6 years old) he had contact with his older brother, who had tuberculosis. Starting from this age, Mantoux tests became positive (previously negative): 5 mm, 9 mm, 12 mm, 11 mm.
He received one course of chemoprophylaxis, then the family moved to another city and the boy was not registered (his brother lived separately). There were no noticeable deviations in health.
Examination of sputum for CD revealed pinkish “rods” on a blue background in the Ziehl-Nielson smear; subsequent treatment with 96 0 alcohol led to the disappearance of the rods.
Koch test - for subcutaneous administration of 50 I.E. - no local, general or focal reactions were noted.
1. Make a clinical diagnosis.
2. Reasons for the one-time detection of rods in sputum.
3. Determine the dispensary registration group.
1. Clinical diagnosis: primary tuberculosis complex in the petrification phase.
2. Saprophyte sticks
Dispensary registration group Y11-B
The patient is 51 years old. After suffering from the flu, a low-grade fever persists for 3 weeks. I went to the clinic again. She complains of weakness, loss of strength, cough with scanty sputum, shortness of breath at rest. On auscultation on the right in the upper part of the lung, weakened breathing is heard.
Blood test: er. - 4.1x10 12 /l, hemoglobin - 112 g/l, leukemia. - 3.8x10 9 /l, ESR - 40 mm/hour.
1. Your preliminary diagnosis.
2. What additional studies should be used for differential diagnosis.
3. What treatment methods are indicated to verify the diagnosis.
1. Preliminary diagnosis: cancer of the upper lobe bronchus on the right.
2. The first task is to confirm or rule out cancer. Required: a complete clinical examination, bronchoscopy with collection of material for morphological examination, tomography of the lungs, ultrasound of the abdominal organs.
3. During morphological verification of the diagnosis, local (localization, histological characteristics of the tumor, anatomical type of growth, stage of the disease) and general (functional state of respiratory and cardiovascular activity and other concomitant diseases, immune status) criteria of the disease are determined.
Based on the data obtained, a treatment method is chosen:
1) radical - surgery (lobectomy, pneumonectomy), combined (surgery + radiation therapy), chemotherapy, complex (removal of the primary lesion + chemotherapy).
Situational therapy task 9
A 57-year-old patient came to you (at an outpatient appointment) with complaints of chest pain, an annoying dry cough, and shortness of breath. Sputum is separated rarely, with difficulty, scanty. Sometimes there are streaks of blood in the sputum. There was a history of acute respiratory infections and influenza, as a rule, carried on the legs. He has been working as a builder in Yaroslavl for 8 years; before that, he built industrial facilities in the Semipalatinsk region for 26 years. Sick for 2 months. During this time, he notes rapid fatigue and increasing weakness. The temperature was elevated only in the first week of the disease. During the examination, the temperature was normal. On auscultation in the lungs, breathing is vesicular, somewhat harsher on the right. Peripheral nodes are not enlarged.
1. What disease can you think about?
2. Name the list of differentiated diseases.
3. What additional research data will help clarify the diagnosis.
4. If cancer is detected, determine the clinical group.
5. What documents should be filled out.
1. Preliminary diagnosis: lung cancer.
2. Differentiable diseases: lung cancer, tuberculosis, bronchitis, pneumonia.
3. Additional examination: plain radiography in 2 projections, tomography of the chest, tracheobronchoscopy with biopsy, general blood test, tuberculin tests, ultrasound of the abdominal organs, neck lymph nodes.
4. 2nd clinical group in the absence of distant metastases.
Control card of dispensary observation (onco), form 030-6/у. “Medical card of an outpatient” - 025-6/у. A notification for a newly identified patient with a malignant tumor (F. 090/u) is sent within three days to the oncology clinic, oncology department at the patient’s place of residence
Patient G., 61 years old, is in the clinic for examination. General condition is satisfactory. A dense formation is palpated in the epigastrium, moderately painful. FGS did not reveal any pathology in the esophagus, stomach or duodenum. Laparoscopy revealed a single tumor node measuring 5 x 6 cm in the left lobe of the liver, protruding 2 cm above the liver capsule.
1. Your recommendations for further examination.
2. Once the diagnosis is established, determine the clinical group.
Standard answers to the therapy task
1. It is necessary to do: a complete clinical examination, ultrasound of the abdominal organs, including the uterus and appendages, fibrocolonoscopy, x-ray examination of the chest.
2. After detecting the primary tumor focus, determine local and general criteria for the disease. In case of resectability of the tumor with a single distant metastasis, the second clinical group.
3. Treatment plan: surgical removal of the primary tumor, resection of the left lobe of the liver (combined operation), subsequent chemotherapy if the tumor is sensitive to cytostatics. If multiple distant metastases are detected, treatment is palliative.
An increase in the rate of synthesis of ketone bodies sharply increases their content in the blood - ketonemia and the development of metabolic acidosis. Its symptoms include fatigue, irritability, stomach pain, and nausea.
Rice. 39 Changes in the rate of metabolic processes in adipose tissue with low insulin secretion
Rice. 40 Synthesis of ketone bodies in the liver
19. Lipid anabolism. Biochemistry of atherosclerosis. vitamins Sufficient intake of ascorbic acid from food is extremely important to combat atherosclerosis. Thus, in guinea pigs whose diet did not contain this vitamin, hypercholesterolemia and atherosclerosis were observed.
Explain the effect of vitamin C deficiency on atherogenesis. What other symptoms are observed with a lack of vitamin C in food?
a) explain why guinea pigs were chosen for the described experiment rather than laboratory mice;
b) describe the pathways of formation of reactive oxygen species and their role in LPO and the consequences of LPO from fatty acid radicals of phospholipids, triacylglycerols, cholesterol esters in LDL; name vitamins that have antioxidant properties and prevent this process;
c) write the reactions of bile acid synthesis; indicate the role of vitamin C in this process, explain how its deficiency will affect the level of cholesterol in the blood.
a) A characteristic feature of the metabolism of primates (including humans) and guinea pigs is the absence of the possibility of endogenous synthesis of vitamin C, therefore for these animals ascorbic acid is a necessary component of food.
b) The source of reactive oxygen species in the cell can be the leak of electrons from the CPE, enzymes of redox reactions (ORR), which directly reduce oxygen, as well as the action of ionizing radiation and some chemicals. Oxygen radicals are capable of starting a chain of free radical reactions. Such reactions disrupt the properties of membranes and form covalent cross-links between proteins and lipids. In lipoproteins (LP), changes are observed in the structure of apoproteins and lipids, which disrupts their binding to receptors and causes phagocytosis by macrophages using scavenger receptors.
Antioxidant vitamins (C and E) protect cells from lipid peroxidation. Moreover, vitamin E, being a lipophilic compound, is located in cell membranes and serves as the main reducer of free radicals of fatty acids. Vitamin C inactivates hydrophilic (superoxide anion, hydroxyl radical and hydrogen peroxide) free radicals in the cytosol and restores the oxidized form of vitamin E, thus maintaining the required concentration of the latter in cell membranes.
c) In the reactions of bile acid synthesis, vitamin C is a coenzyme of hydroxylases (they serve as isoforms of cytochrome P-450), which introduce an OH group into the 7th and 12th positions. With a lack of vitamin C, the formation of bile acids at the stage of 7?-hydroxylation is inhibited, blocking the main pathway for the removal of cholesterol from the body, which leads to hypercholesterolemia and an increased risk of atherosclerosis. In addition, the likelihood of gallstone formation increases.
Rice. 41 Synthesis of bile acids in the liver
21. VITAMINS. Metabolism of proteins and amino acids. Specific metabolic pathways for some amino acids. NUCLEOPROTEID EXCHANGE. A woman consulted a dentist about frequent inflammations and ulcers in the gum area. The woman carefully observed oral hygiene and had no signs of caries. The doctor associated the occurrence of stomatitis with a lack of vitamin B 2 and advised the patient to consume more dairy products - the main sources of riboflavin. After some time, the patient again consulted the doctor with a complaint of increased exacerbations of stomatitis, although she followed all the doctor’s recommendations. During a conversation with the patient, the doctor learned that she suffered from insomnia and used barbiturates. The patient's blood test showed a high level of homocysteine. The doctor prescribed the patient a drug containing folic acid (FA) and B 12 , because came to the conclusion that the cause of frequent exacerbations of stomatitis in the patient may be the use of barbiturates, which reduce the absorption and metabolism of folates in the body. Why does an increase in homocysteine in the patient’s blood and a lack of folic acid lead to stomatitis?
a) describe the metabolism of folic acid in the human body;
b) present a diagram of homocysteine metabolism, indicate the rate of which of the reactions decreases with a lack of FA;
c) explain why a lack of FA disrupts metabolism in oral epithelial cells;
d) name other possible disorders caused by folic acid deficiency in the body.
a) In the liver, folic acid is converted into coenzyme H 4 -folate, which is involved in the transformation of serine and glycine. During these reactions, methylene-H 4 -folate is formed, which can be converted into other one-carbon groups: methenyl, formyl, methyl. These one-carbon fragments are used to synthesize purine and pyrimidine (dTTP) nucleotides, which are essential for cell division and tissue growth.
With a lack of folic acid, methionine regeneration decreases, because The donor of the methyl group in this reaction is B 12 (-CH 3 ), which is formed by transferring the methyl group from H 4 F (-CH 3 ) to B 12 .
c) Epithelial cells have high mitotic activity, so they constantly need the presence of nucleotides for the synthesis of nucleic acids. Lack of folate disrupts the synthesis of DNA and RNA, which is manifested by damage to the gastrointestinal mucosa.
d) As is known, phenobarbital is a widely used sleeping pill, an antagonist of folic acid, the lack of which in the body causes disorders, in particular inflammation of the digestive system. Folic acid deficiency during pregnancy significantly increases the risk of birth defects in the child associated with neural tube defects, and can also lead to malnutrition and prematurity. The most dangerous are leukocyto- and thrombocytopenia.
22. Metabolism of proteins and amino acids. Specific metabolic pathways for some amino acids. Hartnup disease is a hereditary enzymopathy of tryptophan metabolism. The disease is caused by a defect in the structure of the amino acid transporter of the brush border of the jejunum and a violation of the reabsorption of tryptophan and its metabolic products in the kidneys. The pathology is manifested by cerebellar ataxia, pellagra-like skin changes, aminoaciduria, increased levels of indican and indole compounds in the urine. The patient experiences a lack of tryptophan in the body and the formation of a biogenic amine and one of the vitamins from it is disrupted.
Rice. 45 Formation of some biologically active substances from tryptophan
What vital processes are disrupted in this disease?
a) write a diagram of the synthesis of serotonin and indicate which hormone it is considered to be a precursor;
b) name the vitamin that is formed from tryptophan;
c) remember which coenzyme it is part of;
d) give an example of enzymes that require this coenzyme to function.
a) Serotonin is a biologically active substance with a wide spectrum of action. It stimulates the contraction of smooth muscles, has a vasoconstrictor effect, regulates blood pressure, body temperature, respiration, and has an antidepressant effect. Melatonin is a hormone that regulates daily seasonal changes in the body's metabolism and is involved in the regulation of reproductive function; regulates sleep/wakefulness states.
Rice. 46 Formation of serotonin and melatonin from tryptophan
b) Nicotinic acid (vitamin PP) is synthesized from tryptophan;
c) NAD + is formed from this vitamin. To synthesize it, enzymes located in the cytosol use nicotinic acid according to the following scheme: nicotinate -> nicotinate mononucleotide (NMN) -> desamido-NAD + -> NAD +;
Last night, tired after a long day of work, you lay in bed... drifted off to sleep... and suddenly it started. You woke up with excruciating pain in your big toe. When you turned on the light, you found that it was red, swollen, and hot to the touch. No matter what you did, the pain did not subside.
When you finally got to the doctor, a blood test was done and a diagnosis of gout was made. After thinking, you remembered that you had seen this disease mentioned somewhere in books.
The term gout was introduced in the thirteenth century, but the disease itself was described long before that by Hippocrates.
The classic symptom of gout is pain in the joint at the base of the big toe. Gout (gouty polyarthritis) affects not only the joints of the feet and wrists, but also the knees, shoulders and elbows. Sometimes you feel hot or cold due to inflammation. Gout begins suddenly, is accompanied by severe pain, and without treatment usually lasts 3–5 days. But the disease will recur again and last much longer. Many patients complain of aching pain, accompanied by a feeling of pressure and compression in the affected area. The pain is like a dislocation, and it also feels as if this part of the body has been doused with cold water.
There are several conditions that lead to gout, but the main one is high levels of uric acid in the blood, either because the body produces too much of it or it is poorly excreted from the body. Uric acid is waste waste from cell activity. When the level of uric acid in the blood increases, sodium salts begin to be deposited in the tissues. Salt deposition is not yet a symptom of gout. Now, when salts begin to accumulate in the joints and arthritis begins, these are already classic signs of gout.
High blood pressure and obesity also trigger gout. Diseases that destroy tissue, such as cancer, lymphoma, psoriasis, and anemia, cause uric acid levels in the blood to rise and stimulate gout attacks.
Gout is more common in men than in women because women are better able to eliminate uric acid through the kidneys. Gout is a common disease in men over middle age, especially those who drink and are obese. But it can also begin in relatively healthy people. Severe dehydration can cause a gout attack.
It is not gout itself that is dangerous, but the reasons underlying it. So if you have gout, you must undergo a medical examination and course of treatment. Besides visiting your doctor, there are some things you can do yourself.
If you develop gout, there are some things you can do to prevent attacks. Take the medications your doctor prescribes first. The following recommendations will also help, regardless of whether you are taking medication or not.
Keep your weight normal. Since obesity provokes the development of gout, it is recommended to reduce weight. It is better not to do this with a strict diet that will quickly shed pounds. You need to lose weight with a well-balanced diet, which gradually reduces weight. A diet with moderate protein and low fat is recommended. To develop such a diet, talk to your doctor or nutritionist.
Don't drink alcohol. Wine, beer and ale are especially bad, as they provoke gout attacks. Alcohol only makes the problem worse because it interferes with the excretion of uric acid salts.
Do not take diuretics. Diuretics prevent the natural elimination of uric acid salts, which accumulate in the body and cause gout attacks. If your doctor prescribes diuretics for high blood pressure, tell him that you are prone to gout.
Drink at least two liters of fluid per day. In addition to gout, high concentrations of uric acid salts in the blood serum can lead to the deposition of kidney stones. Increasing fluid intake prevents crystallization and reduces the risk of stones.
Wear comfortable shoes. Properly selected shoes reduce pain during gout attacks and do not stimulate their occurrence.
Follow your diet... and anything can happen. A low urea diet has been recommended in the past for the treatment of gout. Judging by theoretical studies, excluding foods high in urea from food is a panacea for all diseases. The problem is that switching from a regular diet to a urea-free diet reduces serum and uric acid levels in the blood quite slightly. Urea is found mainly in meat. Anchovies, sardines, legumes and poultry also have high urea content. If you want, try a low urea diet. It won't hurt you. But don't expect much.