Cardiology

Case 1 AG

Duration -5 minutes

You are a local therapist at the Central District Hospital. You are approached by a 55-year-old man, an accountant,
with complaintsfor headaches, nausea, flies before the eyes.
Previously, he did not go to the doctors, did not measure blood pressure. Deterioration of the general condition notes
within 3 days. He took aspirin, citramon - without effect. On the second day of illness, the doctor of the ambulance
team recordedrise in blood pressure to 165/100 mm Hg, and after taking 1 tablet of captopril 25 mg, blood pressure
decreased to 140/90 mm Hg. On the third day, due to an increase in blood pressure to 175/110 mm Hg, he went to
the emergency room of the Central District Hospital.
From the anamnesis: Works as an accountant, work is associated with constant stress. Smokes a lot.
Indulges in salty foods. She has been suffering from diabetes for a year. Takes 1 diabeton tablet in the morning. The
mother suffered from arterial hypertension for many years.
Objectively: height 178 cm, weight 99 kg. BMI 32. OT-102cm. Restless, can answer questions. The face is
hyperemic. There are no peripheral edema. Vesicular breathing in the lungs, no wheezing. NPV 20 times per minute.
The left border of relative cardiac dullness was expanded by 2-2.5 cm. Heart sounds are muffled, the rhythm is
correct. Pulse 96 per minute. BP 175/105 mmHg The liver is not enlarged.
Research:
General blood analysis:Hb - 145 g / l, erythrocytes - 4.8x1012 / l, leukocytes - 5.6x109, stab neutrophils - 2%,
segmented neutrophils - 67%, eosinophils - 2%, basophils - 1%, monocytes - 5%, lymphocytes - 25%, ESR - 10
mm/h.
Blood chemistry:creatinine - 59 µmol/l, glucose - 5.3 mmol/l, total cholesterol - 6.6 mmol/l, HDL 0.8 mmol/l, LDL 3.53
mmol/l, TG 2.0 mmol/l, ALT - 16 IU. ECG:

Give answers to the following questions:

1. Determine the degree of hypertension, risk factors.

AH 2 degree FC 4, signs of damage, target organssigns of left ventricular hypertrophy
- concomitant diabetes mellitus;
- absence of peripheral edema and liver enlargement;
Risk factors in this patient:
● Potentially avoidable factors: smoking, obesity (grade 1 according to BMI = 32), stress, elevated cholesterol
levels (dyslipidemia, increased LPNP) and eating a lot of salty foods;
● Fatal factors: age, gender (men older than 55 years are predisposed), hereditary predisposition (in the mother
of AH).

2. Interpret laboratory data.

General blood analysiswithin the normal range.(Hb 130-160 er 4-5.1 lei 4-9 p / i 1-6% s / i 47-72% e 0-5% b 0-1% m
2-9% lim 18-40% ESR 1-10)
TANK:creatinine - 59 µmol/l (normal 45-97 µmol/l), glucose - 5.3 mmol/l (normal 3.3-5.5), total cholesterol - 6.6 mmol/l
(increased, normal 3 ,1-5.2), HDL 0.8 mmol/l (dyslipidemia decreased, normally more than 1.45 mmol/l), LDL 3.53
mmol/l (increased, normally less than 3.37 sol/l) , TG 2.0 mmol / l (normal up to 2.25), ALT - 16 IU (normal up to 30
IU).
● hypercholesterolemia
● dyslipidemia:
● LDL increased - increased atherogenic index

3. Interpret the ECG

1) RR intervals of the same duration indicate the correct heart rhythm.
The presence of P waves before each QRS complex tells us about sinus rhythm.
HR: 60/R-Rx T(25mm=0.04s, 50mm=0.02s)= 60/24x0.04=(62)60 bpm
2) Axis of the heart R2>R1>R3 (normal axis of the heart)
3) The P wave is the same, In AVR (and 3) -, in the rest +, lasting up to 0.1 s, up to 2.5 mm high
PQ interval duration up to 0.2s
4) the QRS complex is the same, lasting up to 0.1 s (from V1 to V4 progression of the R wave, V4 max to V6
regression of the R wave)
5) QT interval up to 0.44 sec
the T wave in aVR lead is negative; in 1.2, aVF, V2-V6 positive; in 3,V1, aVL can be +,- or biphasic
Normal ST-T wave complexes with no evidence of repolarization disturbances or LA overload.
Conclusion: correct sinus rhythm, normal ECG.

4. Formulate a clinical diagnosis

Hypertensive crisis, II degree arterial hypertension, risk 4 (very high risk)

Diabetes mellitus type 2, subcompensation.
(Uncomplicated hypertensive crisis of the neurovegetative form (hyperemia of the face + sweat))
The diagnosis was made on the basis of:
- the level of maximum increase in blood pressure in 3 episodes is not more than 176/110;
- the presence of risk factors (smoking, obesity, stress, dyslipidemia - high cholesterol and eating a lot of salty foods;
age, gender, hereditary predisposition);
- signs of damage to target organs (signs of left ventricular hypertrophy during an objective examination);
- concomitant diabetes mellitus;
- absence of peripheral edema and liver enlargement.

5. Provide first aid and further tactics

Primary Care:
● Lay in a comfortable semi-sitting position, ensure peace, access to fresh air (unbutton the shirt collar, ventilate
the room, etc.).
● It is necessary to take the antihypertensive drug captopril sublingually 1 tab. 25-50 mg.
● Heart rate + tachycardia metoprolol or propranolol (betta blocker) IV bolus slowly at 0.05-0.1 mg/kg up to 3
times a day or orally at 0.5-1 mg/kg
● Record heart rate and blood pressure every 15 minutes
Non-drug treatment:
1. Correction of all modifiable risk factors (smoking cessation, correction of dyslipidemia, hyperglycemia with diet No.
9, obesity with exercise therapy and walking, salt restriction to 6g / day, restriction of carbohydrates and fats).
2. Achievement of the target level of blood pressure <135/85 mm. rt. Art. (in the absence of diabetes mellitus BP
<140/90 mm Hg)
3. Preventive measures that slow down the rate of progression of damage to target organs.
Medical treatment:
1. development and appointmentbasicantihypertensive therapy, taking into account concomitant disease (diabetes
mellitus)
a. Diuretics:hypothiazide (12.5), indapamide (2.5);
b. Beta blockers:metoprolol (50-200), bisoprolol (5), carvedilol (12.5-50);
c. ACE inhibitors:captopril (25-100), enalapril (5-20);
d. calcium antagonists:nifedipine(40), amlodipine(5-10), verapamil(120-240).
Angiotensin II receptor antagonists: losartan (25-100), eprosartan (600)
2. treatment of diabetes
Daily monitoring of blood pressure (not higher than 130/80 mm Hg), pulse.
Initially, monotherapy (3 months) if bitherapy (diuretic + any, calcium antagonist + beta block or ACE inhibitor) does
not help, if triple therapy (beta blocker + ACE inhibitor or calcium antagonist + thiazide diuretic) does not help.
 Case 2 ACS, MI

Clinical Details: You- Clinical doctor. A 57-year-old man came to your appointment with intense pain behind the
sternum.
Complaints: burning pain behind the sternum, a feeling of lack of air, increased sweating, weakness. Pain appeared
after exercise, lasting about one hour. I took nitroglycerin tablets under the tongue twice, the condition was somewhat
relieved, but the pain did not go away. The last time I took nitroglycerin was 5 minutes ago.
History:Consists on "D" accounting with coronary artery disease and currents of 5 years. Periodically takes
bisoprolol 5 mg, cardiomagnyl 75 mg. Consists on the D account with AG. The maximum increase in blood pressure
is up to 160\100mm. Hg Regularly takes antihypertensive drugs. He smokes 1 pack of cigarettes a day.
Mom suffered from coronary artery disease and died at the age of 65 from a heart attack. This deterioration was
about 1 hour when the above complaints appeared.
Objectively:The skin is pale, covered with cold sticky sweat. There are no peripheral edema. Vesicular
breathing in the lungs, no wheezing. NPV 20 per minute. The heart sounds are muffled, the rhythm is correct. BP
140/90 mmHg Art. Heart rate 92 beats per minute.
On the ECG

1) Formulate a diagnosis and justify

ACS (acute coronary syndrome) MI with ST segment elevation. Absence of pathological Q wave. AH grade 2,
transmural damage
The diagnosis was established on the basis of: typical localization of pain behind the sternum, feelings of lack of air,
fear, sweating, provoked by stress, lack of effect from nitrates; burdened heredity, the presence of coronary artery
disease in history andaggravatingcoronary tachycardia syndrome (pulse 92 beats per minute).
It is necessary to measure blood pressure, pulse, conduct auscultation of the heart and lungs, take an ECG.

2) Interpret the ECG

one.The rhythm is sinus, because there are P waves
Hwrong, because different distance between RR
HR: 60/R-Rx T(25mm=0.04s, 50mm=0.02s)=Heart rate 92 beats per minute.
2. The axis of the heart R1>R2>R3 (the axis of the heart is shifted to the left) - LV hypertrophy
3. The P wave is the same, in AVR -, in the rest +, up to 0.1 s long, up to 2.5 mm high
PQ interval duration up to 0.2s
4. QRS complex is the same, lasting up to 0.1 s (from V1 to V4 progression of the R wave)
5.QT interval up to 0.44sec
7. The rise of the ST segment in the chest leads in the form of a "cat's back" with the absence of a pathological Q
wave.
T wave in aVR -; in 1.2, aVF, V2-V6+; in 3,V1, aVL +
Front side and bottom walls
ECG picture in acute pericarditis:Simultaneous ST segment elevation of varying severity in all ECG leads (except
aVR). Depression of the PQ segment is detected (better seen in V2-V4), which is a specific, but optional sign of acute
pericarditis.
The second complex in the standard leads and the third complex in the chest leads is the supraventricular
extrasystole.
The ECG picture of the acute phase of myocardial infarction is characterized by ST segment elevation only in part of
the ECG leads, while it is accompanied by ST segment depression (reciprocal changes) in the leads opposite to the
zone of myocardial ischemia.

3) Provide emergency care to the patient

five.Gave nitroglycerin sublingual tablet 0.5 mg or aerosol nitroglycerin 0.5 mg/dose under BP control.
6.Provided access to fresh air and carried out oxygen inhalation (oxygen mask)
7.Dal acetylsalicylic acid at a dose of 250 mg (½ tablet) to chew, drink water.
eight.Took the ECG results from the table, interpreted, explaining to the patient that the elevation of the ST segment in
the chest leads confirms the preliminary diagnosis of acute coronary syndrome
nine.Gave clopidogrel 300 mg (4 tablets) vnugr
10.Established venous access to the cubital vein connected a ready-made dropper with saline
eleven.Explained to the patient that he would take an anesthetic
12.Conducted anesthesia with morphine 1% -1.0 in a solution of sodium chloride 0.9% to 20.0 in fractional 3 mg
solution (in rubber | adapter to the dropper needle). During the administration of morphine, he periodically asked about
the nature of the pain syndrome, stopped the administration of the drug after the pain disappeared.
13.Determined troponin T using a rapid test, the result is negative.
fourteen.Taking into account the rapid pulse, he introduced metoprolol 0.1% -5.0 in / in a bolus (into the rubber
adapter to the dropper needle) /
fifteen.Determined further tactics:
Hospitalization in the nearest cardiology department or hospital; With fibrinolytic therapy. transport more than 30
minutes is shown to thrombolysis. Clarified by asking the patient about the presence of a history of stroke, injuries,
operations, peptic ulcer. hemorrhagic syndrome, the presence of contraindications for taking anticoagulants,
hemorrhagic syndrome, a history of stroke, FM trauma, liver failure) - if there are no contraindications, we perform
thrombolysis (alteplase or tenecteplase IV), if there are contraindications, see next paragraph
17.Introduced heparin 5000 IU IV bolus, or fondaparinux - 2.5 mg s / c, or enoxaparin - IV bolus 30 mg;
eighteen.Measured BP. When blood pressure is not lower than 90 mm Hg. Art. I connected dinitrate (isoket) 0.1% -
10.0 ml previously diluted with a solution of sodium chloride 0.9% - 100.0 into the system for i.v. administration of
isosorbide with an initial speed of 3-4 drops per minute.
nineteen.Conducted a control study of cardiac activity, stated an improvement in the state of pain relief, stable blood
pressure, a decrease in heart rate to 76 in 1 min.
twenty.Determined further treatment tactics:
-Emergency hospitalization in a medical institution, which has the conditions for performing coronary angiography and
blood pressure. Heart rate and rhythm of PCI
Transport in the supine position with a raised head end under the control of blood pressure. Heart rate and rhythm.
Through the dispatcher, informed the staff of the admission department by radio or telephone about the delivery of the
patient

4) Determine the tactics of conducting

1. emergency hospitalization in a medical institution, which has the conditions for performing percutaneous coronary
revascularization (PCI);
List of essential medicines:
1. Oxygen for inhalation (medical gas)
2. Metoprolol tartrate (ampoules 1% 5.0 ml; tablet 50 mg)
3. Nitroglycerin* (solution 0.1% for injection in 10 ml ampoules; tablet 0.0005 g or aerosol). 4. Morphine (solution for
injection in ampoules 1%, 1.0 ml)
5. Acetylsalicylic acid (tablet, 500 mg)
6. Ticagrelor (tablet, 90 mg)
7. Clopidogrel (tablet, 75 mg)
8. Fondaparinux (syringe 0.5 ml 2.5 mg)
9. Enoxaparin sodium (syringe 0.2 and 0.4 ml)
10. UFH (5000 IU, vials)
11. Physiological solution (0.9% 200 ml, vial)
2. transport in the supine position with an elevated head end under the control of blood pressure, heart rate and
rhythm;
3. explain to the dispatcher to inform the staff of the admission department about the delivery of a patient with ACS.
4. In the presence of contraindications to fibrinolytic therapy and the impossibility of performing PCI, the appointment
of direct anticoagulants:
5. Monitoring the patient's condition
 Case 3
Transmural anterior-septal apical myocardial infarction with transition to the lateral wall of the left ventricle

Case Study: You are a therapist. A 65-year-old man had an ECG.

Interpret the ECG and write a conclusion.

Final result:

1) Conducting ECG interpretations

The rhythm is sinus (because there is a P wave before each QRS)
The rhythm is regular and correct (the duration of RR=0.76 sec is the same)
Atrial conduction: duration P = 0.08 s in standard lead 2 (normal up to 0.10 sec)
HR=60/0.76=79 bpm (normal)
AV conduction, assessment of conduction in the ventricles and el systole (OT): PQ=0.16s (normal 0.12-.018s)
Ventricular conduction: QRS=0.08s (normal up to 0.10s)
Electrical systole: QT=0.38s (normal)
EOS: RII>RIII>RI, RI>SI (EOS vertical position)
The P wave is normal (negative in AVR, height up to 1.5 mm)
QRS in the form of QS in V1-V4,
The ST segment in I, V1, V6 is above the isoline and merges with the T wave (T negative in AVR; positive in other
leads, TV4>TV6 biphasic)

2) Formation of an ECG conclusion.

Transmural anterior-septal apical myocardial infarction with transition to lateralwall of the left ventricle
 Case 4
Atrial fibrillation - arrhythmia

Situational task:You are a therapist. A 55-year-old man came to the appointment with a diagnosis of CRHD. Taken an
ECG.
Interpret the ECG and write a conclusion.

Final result:

1) Carrying out the interpretation of the ECG

The rhythm is not sinus because there is no P wave before each QRS complex.
Irregular RR intervals indicate arrhythmia (irregularity) of the rhythm.
Instead of the P wave, flickering (fibrillation) waves with different amplitudes and shapes are recorded, which are most
clearly visualized in V1 and V2 leads.

Wave flicker frequency 450-600 min.

HANDC min 120 max 200 per min.
The electrical axis of the heart is located inhorizontalposition.
The ventricular QRS complex is not changed, the shape is normal, the width does not exceed 0.12 sec.
QT interval up to 0.44 sec

2) Formation of an ECG conclusion

Atrial fibrillation.The electrical axis of the heart is located inhorizontalposition. HANDFrom 120-200 min. (arrhythmia,
non-sinus rhythm)
 GIT
Case 5 GERD

Woman, 35 years old.

Complaints:for heartburn, belching, aggravated by taking spicy and fatty foods, black bread, carbonated drinks.
Heartburn is aggravated in the supine position, when the torso is bent forward, sometimes it feels the return of food
eaten into the oral cavity, an unpleasant smell and taste in the mouth, and the feeling of a lump behind the sternum
when eating is also disturbing.
From the anamnesisdiseases:
Heartburn and belching have been bothering me for 1.5 years, heartburn is aggravated in the supine position, when
the torso is leaning forward. Often there is an eructation of food eaten and a feeling of a coma behind the sternum
when eating. She did not go to the doctor, these symptoms disappeared after dieting.
From the history of life:
Chronic diseases of the gastrointestinal tract, liver denies.
Dietary history: Likes chocolate, fatty meat, plov, manti, hamburgers, fried potatoes, fish. Bad habits: denies. Abuses
strong coffee, daily drinks Coca-Cola. According to the patient often takes aspirin.
Objectively:
The condition is relatively satisfactory. Increased nutrition. Height 170 cm, weight 92 kg. BMI31.83 kg/m2(obesity 1
degree). The skin is clean, of normal color. NPV 16 in 1 min.Heart sounds are muffled, rhythmic, heart rate is 80
beats. in min. BP 120/80 mm Hg The tongue is hyperemic, wet. There are 5 carious teeth. The abdomen is soft and
painless. The liver and spleen are not enlarged. The chair is regular, 1 time per day, decorated. Urination free,
painless. There are no edema.
Laboratory test data:
1. UAC:erythrocytes 4.1x1012/l, hemoglobin 128 g/l, leukocytes 8.2x109/l, s/i 62%, p/i 2%, eosinophils 3%,
lymphocytes 28%, monocytes 5%, platelets 234x109/l, ESR 8 mm/h.
2. TANK:total protein 68 g/l, glucose 4.5 mmol/l, ALT - 23 U/l, AST - 21 U/l, total bilirubin 12.7 µmol/l, cholesterol 4.8
mmol/l.
3. EFGDS:The esophagus is freely passable, the mucous membrane in the lower third for 7 mm is sharply hyperemic,
edematous, loosened. In the distal esophagus, there are single small-pointed erosions covered with fibrin. The cardiac
sphincter is hyperemic, edematous, gaping. The gastric folds expand freely during insufflation. The mucous
membrane of the antrum of the stomach is pale orange in color, edematous.
4. Urease test:negative.

The task:

1) Interpret the data of the laboratory-instrumental examination

1. UAC:
erythrocytes 4.1x1012 / l - a normal indicator
hemoglobin 128 g / l - a normal indicator
leukocytes 8.2x109 / l s / i 62%, p / i 2%, eosinophils 3% - - normal
lymphocytes 28% - normal
monocytes 5% - normal
platelets 234x109 / l - a normal indicator
ESR 8 mm / h - - normal
Interpretation:All parameters of the general blood test were within the normal range.
2. TANK:
total protein 68 g / l - a normal indicator
glucose 4.5 mmol / l - a normal indicator
ALT - 23 U / l - normal
AST - 21 U / l - normal
total bilirubin 12.7 µmol/l - normal
cholesterol 4.8 mmol / l - a normal indicator
Interpretation:All parameters of the biochemical blood test were within the normal range.

3. EFGDS:The esophagus is freely passable, the mucous membrane in the lower third for 7 mm is sharply hyperemic,
edematous, loosened. In the distal esophagus, there are single small-pointed erosions covered with fibrin. The cardiac
sphincter is hyperemic, edematous, gaping. The gastric folds open freely during insufflation. The mucous membrane
of the antrum of the stomach is pale orange in color, edematous.
Interpretation:
"GASTROESOPHAGEAL REFLUX DISEASE, B (Classification of reflux - esophagitis (Los Angeles, 1994because
there are mucosal defects (one or more) limited to one SOP fold, larger than 5 mm;)) (1 degree according to Savary
Miller classification)Reflux esophagitis, exacerbation
Urease testH. pylori - negative

2) Formulate and justify the diagnosis

"Gastroesophageal reflux disease, erosive form,onedegree (like), stage of exacerbation(the diagnosis was
substantiated taking into account the main pain syndromes, objective examination, and the conclusion of EFGDS).
The diagnosis was made on the basis of:
1. Patient complaints:dyspeptic syndrome, soreness, heartburn, belching, aggravated by the intake of spicy and
fatty foods, black bread, carbonated drinks. Heartburn is aggravated in the supine position, when the torso is
bent forward, sometimes it feels the return of food eaten into the oral cavity, an unpleasant smell and taste in
the mouth, and the feeling of a lump behind the sternum when eating is also disturbing.
2. Anamnesis:heartburn and belching have been disturbing for 1.5 years, heartburn is aggravated in the supine
position, when the torso is leaning forward. Often there is an eructation of food eaten and a feeling of a coma
behind the sternum when eating.
● He abuses strong coffee, drinks Coca-Cola daily - these are risk factors. Carbonated drinks are a risk factor for
heartburn during sleep in patients with GERD
The role of coffee as a risk factor for GERD is unclear; coffee may exacerbate heartburn in some
patients [18], but the mechanism for this is unknown and may be due to caffeine rather than coffee
per se. Coffee is not a dominant risk factor.
● Frequently taking aspirin, according to the patient, can damage the upper GI mucosa and exacerbate reflux-like
symptoms and damage caused by reflux.
3. Objective research: obesity of the 1st degree is a risk factor.
4. Conclusion on EFGDS: the mucous membrane in the lower third for 7 mm is sharply hyperemic, edematous,
loosened. In the distal esophagus, there are single small-point erosions covered with fibrin. The cardiac
sphincter is hyperemic, edematous, gaping.

3) Principles of treatment.

Non-drug treatment:
Mode: I, II, III.
Table number 2-3 (restriction of animal fats, chocolate, mint, spices, onions, coffee, tomatoes, citrus fruits, alcohol
- they all relax the lower esophageal sphincter)
● Controlled weight loss in overweight and obese individuals is an important part of the long-term management of
GERD and should not be ignored as a therapeutic measure.
● Lifestyle - light meals, avoiding late meals, avoiding triggers, using a sleep pillow (raised head end of the bed),
after eating, avoid bending forward and do not lie down, do not wear tight clothing
● Over-the-counter drugs (antacids or alginate-antacids) provide the most immediate, but usually transient, relief
of symptoms and can be taken as needed.

Medical treatment
Medicines with gastroprotective action:
Proton pump inhibitors:
● omeprazole 20-40 mg, by mouth, before meals once a day for 7 to 30 days (4-8 weeks)
● rabeprazole (in the absence of omeprazole), 20–40 mg, by mouth, once a day (7–30 days)
Prokinetics:Itopride hydrochloride 50 mg 1 cap x 3 times a day 20 minutes before meals (up to 4 weeks).
H2-histamine receptor blockers:
● ranitidine, 150 mg, 300 mg, 25 mg/ml; in / in, in / m, 1 time per day for 10 days
● famotidine (in the absence of ranitidine), 10 mg, 20 mg, 40 mg, im, once a day in
within 10 days
Antiemetics:
● ondansetron 4mg/2ml, 8mg/4ml, IM, 1x, with vomiting
● promethazine (in the absence of ondasterone), 50 mg / 2 ml; 25 mg, i.m., 1-fold, with
vomiting
 Case 6

Stomach ulcer
Patient A., 44 years old, a leading engineer of the mine, complains of periodic pain in the epigastric proper, more on
the right, which occurs 20-30 minutes after eating, and significantly decreases or disappears after 1.5-2 hours. He
notes heartburn, sometimes bitterness in the mouth, appetite is preserved, stools are normal 1 time per day.
Anamnesis of the disease: for several years he noted discomfort in the epigastric proper after sour, smoked, salty
foods. He took enzymes, these phenomena disappeared. In recent months, he experienced overload at work (night
shifts), stress (pre-accident situations at the mine). He began to notice pains at first dull moderate, which were
removed by Almagel, milk. In the future, the pain intensified, especially after eating, regardless of its quality. There
was heartburn, which was often accompanied by bitterness in the mouth. He reduced the amount of food he took, but
the pain progressed, he was hospitalized in the department. He smoked ½ pack a day, has not smoked for the last 5
years.
Objectively:skin of normal color, turgor preserved. Peripheral lymph nodes are not palpable. The borders of the heart
are normal. Heart rate - 70 beats per minute, blood pressure - 130/70 mm Hg. Art. The tongue is coated with white.
The abdomen is involved in breathing. On palpation notes a slight soreness in the epigastrium. On palpation of the
intestines, pain, volumetric formations were not detected. The liver is along the edge of the costal arch, cystic
symptoms (Kera, Murphy, Ortner) are negative. The spleen is not palpable.
Data from laboratory and instrumental studies:Complete blood count: hemoglobin - 148 g/l, ESR - 4 mm/h,
erythrocytes - 5.2×1012/l, leukocytes - 7.6×109/l, eosinophils - 2%, stab neutrophils - 5%, segmented neutrophils -
56%, lymphocytes - 37%. Biochemical blood test: total protein - 82 g / l, total bilirubin - 16.4 (direct - 3.1; free - 13.3)
mmol / l, cholesterol - 3.9 mmol / l, potassium - 4.4 mmol / l, sodium - 142 mmol / l, glucose - 4.5 mmol / l.
FGDS:we pass the esophagus, the rosette of the cardia closes tightly. The mucosa in the esophagus is unchanged. In
the middle third of the stomach along the lesser curvature there is an ulcerative wall defect(mucous and submucosal)
up to 1.2 cm, the bottom of the defect is filled with fibrin, the edges of the defect are raised, edematous. On the rest of
the stomach there is a focus of dim hyperemia. DPC unchanged. 4 pieces of material were taken for biopsy. When
taking a biopsy from the edges of the ulcer, moderate neutrophilic infiltration and edema are noted.
The task:

1) Interpret the data of the laboratory and instrumental examination Make and justify a plan for additional examination
of the patient.
General blood analysis:
hemoglobin - 148 g / l - within the normal range (130-160 g / l)
ESR - 4 mm/hour - norm (1-10 mm/hour)
erythrocytes - 5.2 × 1012 / l - norm
leukocytes - 7.6 × 109 / l - normal
eosinophils - 2% - normal
stab neutrophils - 5% - normal
segmented neutrophils - 56% - normal
lymphocytes - 37% - normal
Conclusion: in the UAC, all indicators are within the normal range.

Blood chemistry:
total protein - 82 g / l - norm (64-83)
total bilirubin - 16.4 (direct - 3.1; free - 13.3) mmol / l - norm (total is normal 3.4 - 17.1)
cholesterol - 3.9 mmol / l - norm
potassium - 4.4 mmol / l - norm (3.5-5.5)
sodium - 142 mmol / l - norm (135-145)
glucose - 4.5 mmol / l - norm
Conclusion: In the biochemical blood test, all indicators are within the normal range.
The patient is advised to additionally undergo:
- research on H. p. (helicobacter pylori): sampling for cytological examination with FEGDS;
-determination of antigen H.r. ELISA method (determination of N.R. is essential, since up to 80% of gastric ulcers and
90% of duodenal ulcers are N.R. - associated).
- Ultrasound of the abdominal organs to exclude other pathologies of the abdominal organs.
-Feces for occult blood to exclude microbleeding from the ulcer. (Hemocult test, Gregersen reaction- a fecal
examination aimed at detecting asymptomatic bleeding of the digestive system.)

2) Formulate the main and concomitant diagnoses

Main diagnosis: Peptic ulcer of the stomach, first detected severe, with localization of the ulcer in the middle third of
the stomach along the lesser curvature.
Associated diagnoses:Chronic antral active gastritis,
The diagnosis of gastric ulcer was made on the basis ofthe presence of early, within 20-30 minutes after eating pain,
relieved by almagel and dairy food; dyspeptic phenomena: bitterness in the mouth, heartburn. The presence of a
peptic ulcer in the stomach, an ulcer localized in the middle third of the stomach along the lesser curvature indicate a
long-term course of peptic ulcer, but it has only been detected at the present time, therefore it is encrypted as first
detected.
There are also signs of chronic active gastritis.- foci of edema and dim hyperemia, (as well as duodenitis - foci of
hyperemia, infiltration. DPC seems to be normal. xs why it is written like that)

3) Principles of treatment

-Non-drug treatment. (For everyone)

Diet:
• diet No. 1A for 5-7 days: milk (if tolerated), fresh cottage cheese, jelly,
jelly, slimy and pureed soups from cereals and milk, fish soufflé, limited
salt.
• diet No. 1B for 14 days: with the expansion of the diet - crackers, meat, fish, cereals
pureed, soups from cereals in milk, salt in moderation.
• diet number 1: in compliance with the principle of mechanical and chemical sparing.
The duration of a sparing diet depends on the effectiveness of therapy, with
improvement of the state, the diet is expanded, alternations of table No. 1 with
diet expansion, you can use table number 5.
When taking bismuth preparations, a dairy-free diet is prescribed (diet No. 4).
Spicy seasonings, pickled and smoked foods are excluded. Nutrition
fractional, 5-6 times a day.
Optimization of the regime of the day and loads.
- Medical treatment
1) For ulcer healing therapyshould be prescribed - PPI (proton pump inhibitor) --- (Esomeprazole, Rabeprazole,
Omeprazole). PPIs in a standard dose are prescribed until the ulcer is completely healed (4-6 weeks), it should be
borne in mind that the ulcer heals first with a red scar, which is unstable and can collapse when anti-acid therapy is
stopped. When the ulcer heals with a red scar, maintenance therapy is prescribed - PPI in half of the therapeutic dose
for 1-2 months (the time of formation of a white scar, devoid of blood vessels).
2) Prokinetics(in order to normalize the motor function of the duodenum, biliary tract):
• domperidone 0.25-1.0 mg/kg 3-4 times a day for 20-30 minutes. before meals,
duration of treatment for at least 2 weeks.
3) Given the severity of the disease, the most effective drugs should be prescribed - (Nexium 20 mg 2 times, Pariet 20
mg 2 times, Losek maps 20 mg 2 times).
4) In cases where nocturnal symptoms on the background of PPI persist,should be connected for several days - H2-
histamine blockers - Famotidine 40 mg at night.
5) ANTIBIOTIC THERAPYif H.R. associated - Clarithromycin - 500 mg; Amoxicillin - 1000 mg - 2 times a day - 10-14
days.
4) What recommendations should be given to the patient to prevent exacerbation of the disease?
Primary Prevention:regimen and clinical nutrition, rejection of bad habits, examination for helminthiases, sanitation of
the oral cavity.
Secondary preventionprovides anti-relapse therapy.
It is carried out in periods preceding the expected exacerbation and includes dietary nutrition in accordance with the
clinical and endoscopic stage of gastric ulcer and duodenal ulcer, physiotherapy exercises, water procedures,
increased physical activity, hardening, improvement of the situation, which has a beneficial effect on the psyche.
Drug - continuous therapy with antisecretory drugs (famotidine, omeprazole)
 Case 7 HBV

Situational task:You are a local doctor in a polyclinic. A 42-year-old woman came to you with complaints of weakness,
bitterness in the mouth, and occasional pain in the right hypochondrium. History of chronic cholecystitis for more than
5 years. An examination has been carried out.
The task:interpret laboratory tests and make a diagnosis.
General blood analysis
Hemoglobin 132 g/l - normal
Erythrocytes 4.59×1012/l — normal
CPC 0.84 - lower limit of normal
Platelets 150×109/l - thrombocytopenia
Leukocytes 3.0×109/l - leukocytopenia
Neutrophils 49% - normal
Monocytes 3% - normal
Lymphocytes 36% - normal
ESR 8 mm/h - normal
OAM:
Amount of urine - 100 ml
Color - light yellow
Transparency - transparent
Relative density - 1020 is normal (1010-1030)
pH - 6.0 normal (5-7) slightly acidic
LEU-neg
NIT - neg
PRO-neg
GLU-norm
KET-neg
UBG–neg
BIL–norm
ERI - neg
indicators are normal

Blood chemistry
Components Result Units
Iron 17.69 (N20-30) µmol/l norm
ALT 140.60 (N 19-79) U/l increased
AST 88.20 (N to 31) U/L increased
Bilirubin (total) 25.0 (N 3-17) U/L increased
GGTP(gammaglutamylt 58.00 (N 6-42) U/L increased
ranspeptidase)
AP 138.00 (N to 240) U/L norm
Syndrome of cytolysis and cholestasis
ELISA for SH markers
OPK OPP
HBsAg positive 0.240 3.124
aHBs negative
aHBcor IgG positive
HBe Ag positive
aHBe negative
aHCV total negative
aHDV IgG negative
HbsAg-primary screening marker for hepatitis B virus
aHBcor IgG- found in people who have had contact with the virus, indicate either a past illness or a chronic infection.
HBeAg-viral replication marker, present in almost all DNA-positive patients
everything else is negative

PCR result - research

Infection Result
HBV DNA (qualitative) positively
HBV DNA (quantitative) 4.2×105 IU/ml
HBV DNA (qualitative) - inviral hepatitis B (HBV) is an infectious liver disease caused by the DNA-containing hepatitis
B virus (HBV). Thanks to a qualitative method, the presence of the hepatitis B virus in the body and its active
reproduction are confirmed. Qualitative detection of viral DNA plays an important role in the early detection of hepatitis
B in people at high risk of infection. The genetic material of the virus is found in the blood several weeks earlier than
HBsAg. A positive PCR result for more than 6 months indicates chronic infection.
HBV DNA (quantitative).Quantification of the viral load allows you to assess the intensity of the disease, the
effectiveness of the therapy or the development of resistance to antiviral drugs. The effectiveness of antiviral therapy
is assessed by reducing the amount of virus DNA in the blood. 3-6 months after the start of treatment, the viral load
with an adequate therapeutic response should decrease by 1-2 orders of magnitude. The absence of a decrease in
the amount of the virus or its increase against the background of ongoing treatment requires a review and change in
therapy.
● "Not detected" – hepatitis B virus DNA was not detected or the value is below the sensitivity limit of the
method (50 IU/ml);
● < 75 IU/mL - Hepatitis B virus DNA detected at a concentration below the linear concentration range;
● from 75 to 1.2 * 10^5 IU / ml - DNA of the hepatitis B virus was detected, low viremia;
● from 1.2*10^5 to 1.2*10^6 IU/ml – hepatitis B virus DNA detected, medium viremia;
● more than 1.2 * 10 ^ 6 IU / ml - DNA of the hepatitis B virus was detected, high viremia;
● > 1*10^8 IU/mL - Hepatitis B virus DNA detected at a concentration above the linear concentration range.

Elastometry of the liver

The principle of the method is to measure the stiffness of the liver parenchyma (LPP)by the propagation velocity in it
of an elastic shear wave generated by a mechanical wave. During the UTE of the liver, digital stiffness values in

kilopascals (kPa) are obtained, by which the degree of fibrosis can be determined:
2.0-5.8 kPa corresponds to the F0 stage of fibrosis (normal), 5.9-7.2 kPa - F1st,7.3-9.2kPa - F2st, 9.3-12.9kPa - F3st,
more than 13.0kPa - F4st (cirrhosis).

Diagnosis:
Chronic viral hepatitis B, HbeAg-positive, moderate viremia, moderate ALT activity, fibrosis stage F2
Additional diagnostic testscarried out at the stationary level: Biochemical profile: urea, potassium, sodium, gamma
globulins, total cholesterol, triglycerides, glucose, serum iron, ferritin, ammonia;
HBsAg (quantitative test);
anti-HAV; ceruloplasmin;
IgG; ANA: A.M.A.;
Functional tests of the thyroid gland: TSH, T4 free, Ab to TPO;
Pregnancy test; Ultrasound of the vessels of the liver and spleen; EGDS;
CT scan of the abdominal organs (with suspicion of volumetric formations and thrombosis - with intravenous
contrasting);
MRI of the abdominal organs (if volumetric formations and thrombosis are suspected - with intravenous contrast;)
MRCP; eye examination.

Non-drug treatment:
General measures:
Protective mode: avoid insolation, overheating of the body, in the advanced stages of the disease and portal
hypertension - limiting physical activity, facilitating the mode of work;
Barrier contraception during sexual intercourse with unvaccinated partners
Hepatitis vaccination
Vaccination of sexual partners against hepatitis B
Individual use of personal hygiene products
Minimization of risk factors for progression: exclusion of alcohol, tobacco, marijuana, hepatotoxic drugs, including
dietary supplements, normalization body weight, etc.

Medical treatment:
The basis of the treatment of chronic hepatitis B is antiviral therapy.
Fixed course of therapy with Peg-IFN (pegylated interferon) and, in some cases, AN
Long-term treatment with nucleotide/nucleoside analogues
 Case 8 XP Pancreatitis

Patient K., 45 years old, turned to a general practitioner with complaints of pressing pains in the epigastric region,
periodically girdle pains, occur 40 minutes after eating fatty and fried foods, accompanied by bloating; on vomiting that
does not bring relief, on eructation of air.
Disease history:considers himself ill for about two years, when there was pain in the left hypochondrium after eating
fatty and fried foods. He did not seek medical help. 3 days ago, after an error in the diet, the pains resumed, bloating
appeared, belching with air, nausea, and vomiting that did not bring relief.
Objectively:condition is relatively satisfactory, consciousness is clear. Skin of normal color. In the lungs, vesicular
breathing, no wheezing. NPV - 18 per minute. Heart sounds are clear, rhythmic. Heart rate - 72 beats per minute.
Tongue wet, lined with white-yellow coating. The abdomen is soft on palpation, painful in the epigastrium and left
hypochondrium. The liver is not palpable, the dimensions according to Kurlov are 9×8×7 cm, the symptom of
effleurage is negative bilaterally.
General blood analysis: erythrocytes - 4.3 × 1012 / l, hemoglobin - 136 g / l, color index - 1.0; ESR - 18 mm/h,
platelets - 320×109 /l, leukocytes - 10.3×109 /l, eosinophils - 3%, stab neutrophils - 4%, segmented neutrophils - 51%,
lymphocytes - 32%, monocytes - 10 %.
General analysis of urine: light yellow, transparent, acidic, specific gravity - 1016, leukocytes - 1-2 in the field of view,
epithelium - 1-2 in the field of view, oxalates - a small amount.
Biochemical blood test:AST - 30 U / l; ALT - 38 U / l; cholesterol - 3.5 mmol / l; total bilirubin - 19.0 µmol/l; direct - 3.9
µmol/l; amylase - 250 units/l; creatinine - 85 mmol / l; total protein - 75 g / l.
Coprogram:color - grayish-white, consistency - dense, smell - specific, muscle fibers +++, neutral fat +++, fatty acids
and soaps +++, starch ++, connective tissue - no, mucus - no. Urease test for the presence of H. pylori is positive.
FGDS:esophagus and cardia of the stomach without features. The stomach is of normal shape and size. Mucous pink,
hyperemic. The folds are well defined. Bulb of the duodenum without features.
Ultrasound of the abdominal organs: the liver is of normal size, the structure is homogeneous, normal echogenicity,
the ducts are not dilated, the common bile duct is 6 mm, the gallbladder is of normal size, the wall is 2 mm, stones are
not visualized. The pancreas of increased echogenicity, heterogeneous, duct - 2 mm, the head is enlarged in volume
(33 mm), heterogeneous, increased echogenicity.
The task:

1) Highlight the main syndromes

Pain syndromeincludes the presence of pressing pains in the epigastric region, periodically - girdle. Pain
occurs 40 minutes after eating fatty and fried foods.
to dyspeptic syndromeinclude belching with air, nausea, which are associated with dyskinesia of the
descending duodenum and duodenostasis.

2) Interpret the data of the laboratory-instrumental examination.

Evaluate the coprogram data.

In the UACerythrocytopenia; leukocytosis, due to an increase in the number of monocytes, acceleration of

ESR (signs of inflammation).
in OAMthere is a small amount of oxalates.
In a biochemical blood testincreased content of total bilirubin due to its direct fraction; increased activity of
amylase (a sign of inflammation in the pancreas).
In the coprogramfeces are not a characteristic grayish-white color, because undigested food accumulates in
the stool due to pancreatic enzyme deficiency. In addition, there is a creatorrhea, steatorrhea, amylorrhea
(signs of severe pancreatic insufficiency).
Ultrasound of the pancreasincreased echogenicity, heterogeneous, duct - 2 mm, the head is enlarged in
volume (33 mm), which indicates the presence of chronic inflammation.

3) Formulate the main and concomitant diagnoses

Clinical diagnosis-chronic pancreatitis in stage C2, recurrent, exacerbation phase, hypersecretory
- C1(patients with endocrine disorder);
- C2(presence of exocrine disorders);
- C3(presence of exo- or endocrine disorders and/or complications.
The diagnosis was established on the basiscomplaints of the patient on pressing pains in the epigastric
region, periodically - girdle, arising 40 minutes after eating fatty and fried foods, on belching with air. Appeared
flatulence, belching, nausea, episodic vomiting occur as a result of exocrine pancreatic insufficiency.
According to the anamnesis, previously there were recurring symptoms of acute pancreatitis, but now, there
was an exacerbation of already chronic pancreatitis. The aggravation occurred due to errors in nutrition. In
addition, on physical examination, pain in the epigastrium and left hypochondrium is observed. Laboratory and
instrumental data confirm the diagnosis of chronic pancreatitis, changes in the general and biochemical blood
tests indicate an exacerbation of the process, changes in the coprogram indicate severe pancreatic
insufficiency. The criteria identified by ultrasound also confirm the presence of chronic inflammation.
Concomitant diagnosis-chronic gastritis (in the acute stage), Helicobacter-positive, without atrophy of the
glands, without metaplasiain favor of which is evidenced by the presence of a white-yellow coating on the
 tongue during physical examination, a positive urease test, hyperemia of the gastric mucosa during EGD. So,
during the period of exacerbation of chronic pancreatitis, in Helicobacter-positive patients, inflammatory
changes in the gastric mucosa with thickening, swelling of the folds, hyperemia of the membrane
predominate.

4)What additional studies should be prescribed to the patient

duodenal sounding(hypersocretory type of sap secretion in the initial stages of chronic pancreatitis,
hyposecretory - with the development of fibrosis of the gland).
Plain radiography of the OBP(calcifications in the pancreas tissue). X-ray of the stomach and duodenum with
contrast (dyskinesia, duodenostasis, changes in the position and shape of the duodenum).Duodenography in
conditions of hypotension(enlargement of the head of the pancreas).
CT, gland biopsy, vascular angiography(volumetric formations).
Endoscopic retrograde cholangiopancreatography(alternating expansions and narrowings of the large
pancreatic duct, tortuosity and unevenness of the walls, deformation of the lateral branches).

5) Principles of treatment

Non-drug treatment of CP includes:

Stop drinking alcohol
smoking cessation: effectively reduces the frequency of pain attacks in chronic pancreatitis, is the
prevention of pain syndrome, primary pancreatic cancer
adherence to the principles of rational nutrition, with sufficient intake of foods containing calcium, fat-soluble
vitamins
fat restriction is not recommended
fractional meals (up to 6 or more times)

Enzyme replacement therapy for CP

appointed after the relief of the acute phase of pancreatitis;
preparations based on pancreatic enzymes with enteric-soluble minimicrospheres with a high content of
lipase, sensitive to changes in pH, should be prescribed;
The recommended minimum dose is 40,000-50,000 units of lipase for the main meal, half the dose (20,000-
25,000 units of lipase) for snacks;
the drug is recommended to be taken with meals, with a large dose of ZFF it is possible to divide the dose
into two doses: the beginning and the end of a meal;
term of taking the drug - lifelong;

antisecretory therapy.
PPI: Esomeprazole 20 mg twice a day, 40 minutes before meals
Pantoprazole 40 mg 2 times a day, 40 minutes before meals
Rabeprazole 20 mg x 2 times a day, 40 minutes before meals
Lansoprazole 30 mg x 2 times a day, 40 minutes before meals
Omeprazole 20 mg x 2 times a day, 40 minutes before meals
H2 blockers: Famotidine 40-60 mg 2 times a day, 40 minutes before meals
Ranitidine 150 mg 2 times a day, 40 minutes before meals

Therapy of pain syndrome CP.

NSAIDs. Paracetamol 500 mg: single dose 500 mg; the maximum daily dose is 2000 mg, in the absence of
liver pathology;
Ibuprofen 200 mg: single dose 200-400 mg; daily dose of 1200 mg;
 Hematology
Case 9 IDA
Situational task:You are a local doctor in a polyclinic. A 38-year-old woman came to you with complaints of severe
weakness, dizziness, and palpitations. Sick for the last 2 months. History of childbirth 5 months ago.
History:Works as a technician in an office center (3-4 hours a day). The rest of the time is busy with the children at
home. She had never been ill before and had not gone to the doctor. I noticed that for the last 2-3 months weakness
has appeared and is growing, it has become difficult to work - “no strength”, dizzy, it is difficult to breathe during
exercise and the heart beats often. I noticed that sometimes I want to eat chalk. He notes that his nails have become
brittle, his hair falls out. The parents are healthy. Hereditary diseases are denied.
Objectively:pale skin, dull and brittle hair, brittleness and change in the configuration of the nails (spoon-shaped
depression of the nail), "geographic tongue", seizures in the corners of the mouth. Vesicular breathing in the lungs, no
wheezing. On auscultation of the heart at the apex of the heart, there is a systolic murmur that does not radiate to the
axillary region and does not change during exercise. BP 100/60 mm Hg Heart rate 98 bpm. On palpation, the
abdomen is painless. The liver and spleen are not enlarged. Stool and diuresis are normal.
UAC: TANK:serum iron - 6.5 µmol / l,
HGB - 49g/L total iron-binding capacity of serum - 98 µmol / l,
WBC - 4.0 x 109 /L total bilirubin - 18.2 µmol / l
HT-18% creatinine 83 µmol/l
RBC - 2, 9 x 1012 / L urea 4.2 mmol/
LYM - 39% ALT 18 U/l
MCV - 63.1 fl AST 22 U/l
MID - 6%
MCH - 16.7 pg
GRA - 56%
MCHC - 265g\L
PLT - 354 x 109 /L
CPU-0.5
ESR - 12 mm / h.
Microscopy: Hypochromia +++, anisocytosis +++,
poikilocytosis ++.

OAM:
Amount of urine - 100 ml
Color - light yellow
Transparency - transparent
Relative density - 1020
pH - 6.0
LEU-neg
NIT - neg
PRO-neg
GLU-norm
KET-neg
UBG–neg
BIL–norm
ERI - neg

1) Make a preliminary diagnosis, justify it

From the above complaints, anamnesis of the disease and life, we can distinguish:
- General anemic syndrome:weakness, fatigue, dizziness, headaches, palpitations,
- Sideropenic syndrome:changes in the skin and its appendages (dryness, peeling, easy cracking, pallor). Hair is dull,
brittle, falls out intensely, changes in nails: thinning, brittleness, and changes in the configuration of nails (spoon-
shaped depression of the nail). Changes in the mucous membranes ("geographical tongue", seizures in the corners of
the mouth) Predilection for unusual odors. Taste perversion. It is expressed in the desire to eat something little edible.
Sideropenic myocardial dystrophy - a tendency to tachycardia, hypotension.
Provisional diagnosis:Iron deficiency anemia, 3 degrees of severity (hemoglobin-49g / l), due to the loss of a large
amount of blood during uterine bleeding after childbirth.
Rationale: the presence of a general anemic(weakness, fatigue, dizziness, headaches) and sideropenic (taste
perversion of syndromes, the skin is dry to the touch, the visible mucous membranes are pale, the tongue is unevenly
furred (“geographical tongue”), there are cracks in the corners of the mouth, dry hair, thinning nails, fragility, and
change in the configuration of the nails (spoon-shaped depression of the nail).

2) Interpret laboratory tests

HGB (hemoglobin) - 49 g/L reduced 120-140 130-160
WBC (leukocytes) - 4.0 x 109 / L norm
HT (hematocrit) -18% lowered 36-46 40-48
RBC (erythrocytes) - 2.9 x 1012 /L reduced 3.7-4.7 4-5.1
LYM (lymphocytes) - 39% normal 18-40
MCV (mean red blood cell volume) - 63.1 fl reduced (81-100)
MID(the content of a mixture of monocytes, eosinophils, basophils and immature cells)– 6% norm 3-7
MCH (mean hemoglobin content in 1 erythrocyte) - 16.7 pg reduced (27-31)
GRA (granulocytes) - 56% normal 50-75
MCHC (mean concentration of hemoglobin in erythrocytes) - 265 g \ L lowered (300-380)
PLT (platelets) - 354 x 109 /L increased 180-320
CPU-0.5 lowered 0.85-1.05
ESR - 12 mm / h. Norm 2-15 1-10
Microscopy: Hypochromia +++, anisocytosis +++, poikilocytosis ++.
Conclusion:microcytic hyporegenerative hypochromic anemia, low hematocrit (18%), MCV (average er volume) - low
(normal-81-100), anisocytosis, poikilocytosis
TANK:serum iron - 6.5 µmol/l reduced (9-27),
total iron-binding capacity of serum - 98 µmol / l increased (46-90),
total bilirubin - 18.2 µmol / l norm 8-20
creatinine 83 µmol/l norm 44-106
urea 4.2 mmol / l norm 2.4-6.4
ALT 18 U/l norm up to 45
AST 22 U/l norm up to 47
Conclusion:decrease in serum iron (9-27), TIBC-increased (46-90),
OAM:
Amount of urine - 100 ml
Color - light yellow
Transparency - transparent
Relative density - 1020
pH - 6.0
LEU-neg
NIT - neg
PRO-neg
GLU-norm
KET-neg
UBG–neg
BIL–norm
ERI - neg
Conclusion: no change

3) Make a clinical diagnosis, justify it

Microcytic hyporegenerative, hypochromicIron deficiency anemia, severe(hemoglobin-49g / l), due to the loss of a
large amount of blood during uterine bleeding after childbirth
Based
complaints: severe weakness, dizziness, palpitations. Sick for the last 2 months
history: childbirth 5 months ago, for the last 2-3 months, weakness has appeared and is growing, it has become
difficult to work - “no strength”, dizzy, it is difficult to breathe during exercise and the heart beats often. I noticed that
sometimes I want to eat chalk. He notes that his nails have become brittle, his hair falls out.
objective research:pale skin, dull and brittle hair, brittleness and change in the configuration of the nails (spoon-
shaped impression of the nail), "geographic tongue", seizures in the corners of the mouth At auscultation of the heart
at the apex of the heart, systolic murmur, heart rate 98
laboratory research:in the general blood test: hypochromic anemia, poikilocytosis, anisocytosis; in a bc blood test: a
decrease in serum iron, an increase in TI

4) Assign a treatment

1) non-drug treatment
- A diet rich in iron is indicated. The patient is recommended foods containing iron: beef, fish, liver, eggs, greens,
vegetables, oatmeal, buckwheat, wheat, beans, chocolate, fruits, raisins, prunes, etc.
2) drug treatment
It is carried out only with Fe preparations, mainly oral, less often parenteral, for a long time, under the control of a
detailed blood test. Oral preparations of ferrous sulfate are usually taken. With intolerance to ferrous sulfate, iron
gluconate and fumarate preparations are taken. Dosage: for adults 200 mg, for children 1.5-2 mg/kg. Additionally,
ascorbic acid is prescribed (200 mg for every 30 mg of iron), and succinic acid (185 mg per 37 mg of iron) for better
absorption of iron.
Treatment result: Restoration of iron stores in the depot occurs no earlier than 3 months from the start of treatment.
The criterion for the effectiveness of treatment with iron preparations is an increase in reticulocytes (reticulocyte crisis)
by 3–5 times on the 7–10th day from the start of therapy (with a single control, it is not always recorded).
Prevention of IDAshould be carried out in the presence of hidden signs of Fe deficiency or risk factors for its
development. The study of Hb, serum Fe should be performed at least once a year, and in the presence of clinical
manifestations as needed in patients: donors; pregnant women, women with prolonged (more than 5 days) and heavy
bleeding, premature babies and children born from multiple pregnancies; patients with constant and difficult to
eliminate blood loss; long-term NSAIDs
 Case 10 V12-def

Situational task:You are a local doctor in a polyclinic. A 67-year-old man was admitted with complaints
ofshortness of breath when walkingdizziness, impaired concentration, loss of appetite, weight loss, epigastric discomfort,
pain and burning sensation in the tongue, periodically loosening of the stool; pain and numbness in the lower extremities,
muscle weakness ("wadded legs").
History: Sick for about 2 months, when fatigue, severe dizziness, impaired concentration appeared. Gradually joined
by shortness of breath when walking, weakness, tingling in the limbs, legs "wadded" - it is difficult to walk; loss of
appetite, weight loss. Recently, these complaints have intensified. I did not go to the doctor for the entire time of the
illness. 2 years ago, during the examination, gastritis and pancreatitis were exposed, but he did not receive treatment.
In the last week he has noticed a sharp deterioration, in connection with which he consulted a doctor.
Objectively: The skin is pale with an icteric tint, the sclera are subicteric. The muscles of the extremities are
atrophied, the muscle tone is reduced. Neurological status: The gait is unsteady, uncertain, movements are
uncoordinated. BP 95/60 mm Hg Heart rate 100 bpm. The tongue is moist, bright red in color, smooth - "varnished"
(due to the pronounced smoothness of the papillae), there are single aphthae on the buccal mucosa. The liver
protrudes 2.0 cm from under the edge of the costal arch, the surface is smooth, the consistency is pasty, the spleen is
not enlarged.
UAC: TANK:
HGB - 74 g/L reduced 120-140 130-160 creatinine 83 µmol/l norm 44-106
WBC(leukocytes)– 3.0 x 109 /L reduced 4-9 urea 4.2 mmol / l norm 2.4-6.4
RBC(erythrocytes)– 2, 8 x 1012 /L reduced 3.7- ALT 18 U/l norm up to 45
4.7 4-5.1 AST 22 U/l norm up to 47
LYM - 30% norm 18-40 Total bilirubin: 44.0 µmol/l increased 8-20
MID(monocytes, eosinophils, basophils and Indirect bilirubin: 40.0 µmol/l increased to 13
immature cells)– 6% norm 3-7 The content of vit. Serum B12 -
GRA - 60% norm 50-75 70 pg/ml reduced (160-950 pg/ml).
MCHC(mid.conc hemoglobin in erythrocytes)– serum iron: 15.6 µmol/l normal (9-27)
265 g\L reduced (300-380) EFGDS + biopsy:atrophic changes in the mucous
PLT (platelets) - 185 x 109 / L norm 180-320 membrane of the digestive tract. Atrophy of parietal
CPU-1.3 increased 0.85-1.05 and chief cells. Atypical cells were not found.
Microscopy: hyperchromia of erythrocytes,
anisocytosis (macrocytes, megalocytes),
poikilocytosis, Jolly bodies, Cabot rings,
hypersegmentation of neutrophil nuclei, ESR -
35 mm/h increased 2-15 1-10.
OAM:
Amount of urine - 100 ml
Color - light yellow
Transparency - transparent
Relative density - 1020
pH - 6.0
LEU-neg
NIT-neg
PRO-neg
GLU-norm
KET-neg
UBG–neg
BIL–norm
ERI-neg
no changes

1) Preliminary diagnosis:Hyperchromic anemia of the 2nd degree of severity. B12 deficiency anemia.
Rationale:the patient shows all the symptoms of B12-deficiency anemia, which are indicated by the patient's
complaints, such as shortness of breath when walking (hypoxemia), dizziness, impaired concentration (due to
impaired myelination of neurons due to impaired formation of methionine components), decreased appetite, weight
loss ( the patient associates food intake with pain, so he tries to eat less, and this can also be caused by a lack of
important elements that are poorly absorbed due to atrophic gastritis), pain and burning in the tongue, periodically
loosening of the stool; paresthesia, epigastric pain
At the same time, it is known from the anamnesis of the disease that he has chronic diseases, such as gastritis and
pancreatitis. In turn, it was gastritis that led to impaired absorption of vitamin B12 and the development of B12-
deficiency anemia.
The development of B12-deficiency anemia is also indicated by physical examination data, such as pallor of the skin
with an icteric tint, subicteric sclera, muscles are atrophied, a shaky gait, uncoordinated movements, a “lacquered”
tongue, single aphthae, hepatomegaly are determined.
2) Interpretation of laboratory and instrumental data
UAC:
● Decreased hemoglobin level (norm for men 130-160 g/l)
● Decrease in the level of erythrocytes (the norm for men is 3.7-4.7 * 10 ^ 12 / l)
● Decrease in the level of leukocytes (norm 4-9 * 10 ^ 9 / l)
● Platelets are normal (180-320*10^9/l)
● Lymphocytes are normal (18-40%)
● Monocytes are normal (2-9%)
● Granulocytes are normal (50-70%)
● The average concentration of hemoglobin in the blood is normal (260-340 g / l)
● CPU boost (normal 0.85-1.15)
● Microscopy revealed hyperchromia of erythrocytes (normochromia), anisocytosis, poikilocytosis, Jolly bodies,
Kebot rings, hyperpigmentation of neutrophil nuclei (all these blood microscopy data are characteristic of B12-
deficiency anemia and should not be normal)
● ESR acceleration (norm 2-15 mm/h)
microcytic, hyperchromic, hyporegenerative anemia

TANK:
● The level of creatinine is normal (62-106 µmol/l)
● The level of urea is normal (2.8-7.2 µmol/l)
● ALT/AST normal (up to 45 U/l/up to 41 U/l)
● Increase in the level of total bilirubin (norm 8.5-20.5 µmol / l)
● Increasing the level of indirect bilirubin (normal 1-8 µmol / l)
● Decreases in serum vitamin B12 levels (normal 160-950 pg/ml)
● Serum iron level is normal (12-29 µmol/l)

OAM:
● Bilirubin in urine (normally absent)
EFGDS + biopsy:
● EFGDS revealed atrophic changes in the mucous membrane of the digestive tract and atrophy of the parietal
and chief cells, which also indicates the presence of B12-deficiency anemia and the development of its complication -
atrophic gastritis.

3) Clinical diagnosis:Megaloblastic hyperchromic B12 deficiency anemia, moderate severity.

Rationale for the diagnosis:The following data indicate the diagnosis of megaloblastic hyperchromic B12-deficiency
anemia, of moderate severity:
● Complaints :shortness of breath when walking (hypoxemia), dizziness, impaired concentration (due to
impaired myelination of neurons due to impaired formation of methionine components), decreased appetite,
weight loss (the patient associates food intake with pain, so he tries to eat less, and this can also be caused
by a lack important elements that are poorly absorbed due to atrophic gastritis), pain and burning in the
tongue, periodically loosening of the stool; paresthesia, epigastric pain.
● Disease history:Ill for about 2 months, when increased fatigue, severe dizziness, impaired concentration
appeared. Gradually joined by shortness of breath when walking, weakness, tingling in the limbs, legs
"wadded" - it is difficult to walk; loss of appetite, weight loss. Recently, these complaints have intensified. I did
not go to the doctor for the entire time of the illness. 2 years ago, during the examination, gastritis and
pancreatitis were exposed, but he did not receive treatment.
● Physical examination data:pallor of the skin with an icteric tinge, subicteric sclera, atrophied muscles, shaky
gait, uncoordinated movements, "lacquered" tongue, single aphthae, hepatomegaly.
● Laboratory examination data:decrease in hemoglobin level (norm for men 130-160 g / l), decrease in the level
of erythrocytes (norm for men 3.7-4.7 * 10^12 / l), decrease in the level of leukocytes (norm 4-9 * 10^9 / l), an
increase in the level of CP (normal 0.85-1.15), microscopy revealed hyperchromia of erythrocytes
(normochromia), anisocytosis, poikilocytosis, Jolly bodies, Cabot rings, hyperpigmentation of neutrophil nuclei
(all these blood microscopy data are characteristic of B12-deficient anemia and should not be normal),
accelerated ESR (normal 2-15 mm / h), increased total bilirubin (normal 8.5-20.5 µmol / l), increased indirect
bilirubin (normal 1-8 µmol / l), a decrease in the level of vitamin B12 in serum (normal 160-950 pg / ml),
bilirubin in the urine (normally absent)
● Instrumental study data:EFGDS revealed atrophic changes in the mucous membrane of the digestive tract
and atrophy of the parietal and chief cells, which also indicates the presence of B12-deficiency anemia and
the development of its complication - atrophic gastritis.

4) Treatment:

Non-drug:
● Quitting smoking and drinking alcohol
 ● Balanced diet, with a high content of vitamin B12 in foods (beef, pork and chicken liver, mackerel, rabbit meat,
beef, sea bass, pork, cod, carp, chicken egg, sour cream)
Medical:
● 3. Pathogenetic therapy Cyanocobalamin 200-500 mcg, 1r/day s/c for 4-6 weeks. After normalization of the
blood composition (after about 1.5-2 months), 1 r / week is administered for 2-3 months, then 2 r / month for
six months. 6 injections per course)
● Etiotropic therapy Treatment of atrophic gastritis with replacement therapy (only during an exacerbation)
betaine + pepsin.
● Phytotherapy of atrophic gastritis: infusion of plantain leaves, chamomile, mint, St. 3-4 weeks
● Vitamins B1, B2, folic acid
● If H.pylori is detected, eradication therapy is carried out

2. Treatment of gastritis, deworming, correction of the diet, etc.

Given the activation of cell proliferation during cyanocobalamin therapy, it is possible to add folate and iron deficiency,
therefore, after 7-10 days from the start of cyanocobalamin therapy, it is necessary to additionally prescribe:
folic acid, and with a decrease in the color index, iron preparations.
 Rheumatology
Case 11
Gout

Male R., 45 years old, complains of swelling and sharp pain in the first toe of the right foot, restriction of movement,
headaches.

From history:He fell ill acutely 2 days ago: after visiting the sauna and a plentiful feast at night, there was a very strong
pain in the first toe of the right foot. In the morning the patient noticed swelling of the first toe of the right foot and
purple coloration of the skin above it. Body temperature increased to 37.8 °C, and therefore applied to the clinic at the
place of residence.

From the history of life:over the past 3 years, rises in blood pressure up to 160/100 mm Hg have been observed
occasionally, and he has not received constant antihypertensive therapy.

Objectively:In the lungs, vesicular breathing, no wheezing. Respiratory rate - 18 per minute. Heart sounds are slightly
muffled, the rhythm is correct. Heart rate - 84 per minute. BP - 150/105 mm Hg. The abdomen is soft and painless.
The liver and spleen are not enlarged. The area of the kidneys is not visually changed. The symptom of tapping is
negative on both sides. There are no peripheral edema.

1) Interpret the data of complaints and anamnesis

Articular syndrome in the form of monoarthritis; unilateral lesion of the first metatarsophalangeal joint, which reached
its maximum on the 1st day; a trigger factor for the development of acute arthritis is a stay in the sauna followed by a
plentiful feast.

2) Conduct an examination of the joints

Examination of the joints (examination, determination of the color of the skin, local temperature over the joint, pain,
range of motion in the joint): The affected joint is the first metatarsophalangeal joint of the right foot, edematous,
hyperemia and hyperthermia are determined above it, the range of motion in the joint is sharply limited due to pain
and edema. Other joints are not changed, their palpation is painless, movements are in full.

3) Preliminary diagnosis

Main diagnosis: Gout: acute gouty arthritis of the first metatarsophalangeal joint on the right. Concomitant disease:
arterial hypertension II degree.

4) Draw up a survey plan indicating the expected changes

-General blood analysis(leukocytosis, increased ESR),

-General urine analysis(urates),

-Blood chemistry: uric acid (hyperuricemia), increased C reactive protein

-X-ray of feet- without pathological changes (since the patient has the first attack of gouty arthritis; subcortical cysts
without erosion are possible),

-Examination of synovial fluid (detection of sodium monourates)

5) Make a treatment plan

 - Non-drug treatment:

For the period of acute arthritis, rest and cold are needed on the area of the affected joint.

Teaching the patient the right way of life (reducing body weight with obesity, diet, reducing alcohol intake, especially
beer).

Elimination of risk factors for exacerbation of arthritis, revision of the drugs used in the treatment of concomitant
diseases that cause hyperuricemia in this category of patients (primarily diuretics, acetylsalicylic acid).

Identification and correction of the treatment of concomitant diseases.

Mode: II DIET (table No. 6). Restriction of purines (shellfish, anchovies, red meat, offal), low-calorie diet, abundant
alkaline drinking up to 2-3 l / day, exclusion of ethanol-containing drinks, especially beer, restriction of carbohydrates
and the inclusion of polyunsaturated fatty acids in the diet are shown.

- Medical treatment:

List of essential medicines:

Non-steroidal anti-inflammatory drugs: (ibuprofen, naproxen) Diclofenac; Meloxicam.

Glucocorticosteroid therapy: Methylprednisolone; Methylprednisolone acetate; Methylprednisolone sodium succinate;

Prednisolone; Prednisolone hemisuccinate.

Antihyperuricemic therapy: Colchicine; Allopurinol (xanthine oxidase inhibitor); Febuxostat.

List of additional medicines: Benzbromarone; Losartan (angiotensin 2 receptor antagonist for hypertension);
Fenofibrate; Omeprazole.

− Other types of treatment:

Plasmapheresis (with a severe course of the disease resistant to therapy)

 Case 12 ORL

Male, 18 years old, student

Complaints.Pain and swelling in the knee joint, shortness of breath with moderate exercise. Unpleasant sensations in
the region of the heart, changes in heart rhythm, subfebrile rate up to 37.5, general weakness and rapid fatigue
From history.3 weeks ago I had a sore throat. At that time there was a sore throat, the pace was up to 39, he took
paracetamol and rinsed his mouth with soda. The condition improved, but a week later the pace again rose to
subfebrile, there was pain and swelling in the knees, a rash and general weakness appeared on the body. Used
NSAID ointment, but there was no effect. 2-3 days ago I felt discomfort in the heart and palpitations and shortness of
breath.

1) Interpretation of complaints and anamnesis

Complaints: pain, swelling of the knee joints - symptoms of arthritis. Symptoms of shortness of breath with moderate
exercise, discomfort in the heart, arrhythmias, subfebrile condition, general weakness, increased fatigue. From the
anamnesis: 3 weeks ago he fell ill with typhoid fever (?)

2) Interpretation of objective examination

Big Criteria:
joint syndrome -knee joints - arthritis (monoarthritis)

skin syndrome -erythema ring rash

cardiac syndrome-carditis - pain, shortness of breath, tachycardia

Small Criteria :
fever, arthralgia

3) Preliminary diagnosis:ARF with manifestations of carditis, monoarthritis

4) Diagnosis plan

complete blood count (CBC): increased ESR, possibly leukocytosis with a shift of the leukoformula to the left;

blood chemistry(AlT, AST, total protein and fractions, glucose, creatinine, urea, cholesterol);

coagulogram;

immunological blood test:C reactive protein (CRP) (positive), Rheumatoid factor (RF) negative, Antistreptolysin-O
(ASL-O) elevated or, more importantly, titers increasing in dynamics;

bacteriological examination: throat swab for the determination of B-hemolytic streptococcus group A (BSHA) -
detection of GABHS in a throat swab, can be both with active infection and with carriage.

ECG:clarification of the nature of cardiac arrhythmias and conduction disorders (with concomitant myocarditis);

Chest X-ray: for diagnostic purposes. (Possible signs of rheumatic pneumonitis)

echocardiography: necessary for the diagnosis of valvular pathology of the heart and the detection of pericarditis. In
the absence of valvulitis, the rheumatic nature of myocarditis or pericarditis should be interpreted with great caution.

x-ray of joints for differential diagnosis with other arthritis.·

CT scanhigh resolution in special cases, to detect signs of rheumatic pneumonitis, thromboembolism in small
branches of the pulmonary artery.

5) Treatment tactics

Non-drug treatment:

Non-drug treatment:

Bed rest for 2-3 weeks (for the period of disease activity);

Diet number 10.

− Medical treatment:

ARF treatment includes etiotropic antibiotic therapy, anti-inflammatory therapy

Medical

Etiotropic - AB - benzylpenicillin, macrolides, lincosamides can be

Pathogenetic - GCS - methylprednisolone and prednisolone, NSAIDs (diclofenac, aceclofenac)

Potassium and magnesium asparaginate, inosine, nandrolone

Symptomatic– antiplatelet agents, anticoagulants – warfarin, ACE inhibition (captopril, enalapril), calcium antagonist –
diltiazem, verapamil, beta-blockers – metoprolol, bisoprolol, ARBs, cardiac glycosides – digoxin, diuretics

List of essential medicines:

benzylpenicillin sodium salt; cefuroxime; azithromycin; diclofenac; aceclofenac; etoricoxib; prednisolone;

methylprednisolone.
 Case 13

Rheumatoid arthritis

Woman, 28 years old, teacher

Complaints: pain and swelling in the interphalangeal joints of the hand, carpal and elbow joints, morning stiffness lasts
2 hours.
From the anamnesis: pain and swelling in the interphalangeal joints of the hand appeared after childbirth 2 months
ago, after which pain, swelling in the carpal and elbow joints were added. With a general blood test: COE-40 mm / h
Objectively: he cannot clench the hand into a fist, the strength of the hand is reduced, active and passive movements
are limited in the joints.

Ayel 28 zhasta, teacher

Shagymdary:kol basynyn sausak aralyk buyndarynda, bilezik zhane shyntak buyndarynda aura sezimі men іsіnu,
tanertengilik құrysu 2 sagatka sozylada.
Anamnesis:kol basynyn sausak aralyk buyndarynda aura of the season2 ai bұryn bosangannan son paida boldy, ari
karaybilezik zhane shyntak buyndarynda auyrsynu, іsіnuler kosyldy. Zhalpy can anlize: ETZH-40mm\sag
Objectives:kol basyn kysa almaydy, kol basynyn kushi azaygan, belsendi zhane passivti kozgalistary buyndarynda
shektelgen.

1) Interpretation of anamnesis and complaints

Symmetrical pains in symmetrical joints, morning stiffness, kobinese kishi metacarpophalangeal (proximal) buyndar
zardap shegedi, aura of azanga uakytta mazalaida, inflammatory aura, Basque organdardan kobinese kozdi
(conjunctivitis), Ulnar deviation, Rheumatoid nodules.

2) Interpretation of objective examination

- pain (on palpation, on movement), Decrease in the force of compression of the hand.

- Symmetrical swelling

- morning stiffness

Ulnar deviation, "swan neck" (overextension in the proximal interphalangeal joints).

3) Preliminary diagnosis

Rheumatoid arthritis, symmetrical, very early stage up to 6 months,

(early 6 months-1 year, deployed more than 1 year, late 2 years or more)

Functional class (FC):

· I class - completely preserved opportunities for self-service, non-professional and professional activities.

· Class II - retained the possibility of self-service, non-professional activities, limited opportunities for professional
activities.

· Class III - self-service opportunities are preserved, opportunities for non-professional and professional activities are
limited.

· IV class - limited opportunities for self-service, non-professional and professional activities.

4) Survey plan

- UAC(hypochrom anemia, Increased ESR, hypergammaglobulinemia, decreased concentration of complement

system proteins

- BH analysis(thyroid increase, transaminases, ALS, AST, protein, glucose, creatinine, cholesterol)

- Immunological characteristics (CRP -on, RF -on, antibodies to the cyclic citrullinated peptide ACCP)

- analysis of synovial fluid– help-reduce viscosity, loose mucin clot, leukocytosis

- RadiographyI of the hands and feet (periarticular osteoporosis, blurring of the contours of the joints., erosion on the
joint surfaces, narrowing of the joint cracks, ankylosis)

X-ray stage (according to Steinbroker):

I - periarticular osteoporosis;

II - periarticular osteoporosis + narrowing of the joint space, there may be single erosions;

III - signs of the previous stage + multiple erosions + subluxations in the joints;

IV - signs of previous stages + bone ankylosis.

Arthroscopy with biopsy

Bone densitometry

- Ultrasound (Buyndardyn), MRI of the hands

- ECG

- echocardiography

- Radiography of the lungs in two projections.

5) Treatment tactics

-Non-drug treatment: Avoid factors that can potentially provoke an exacerbation of the disease (intercurrent infections,
stress, etc.);

Quitting smoking and drinking alcohol; · Smoking may play a role in the development and progression of RA. An
association was found between the number of cigarettes smoked and RF positivity, erosive changes in the joints and
the appearance of rheumatoid nodules, as well as lung damage (in men);

Maintaining an ideal body weight; A balanced diet that includes foods high in polyunsaturated fatty acids (fish oil, olive
oil, etc.), fruits, vegetables, potentially suppresses inflammation, reduces the risk of cardiovascular complications;

Patient education (changing the stereotype of motor activity, etc.); Physiotherapy exercises (1-2 times a week);

Physiotherapy: thermal or cold procedures, ultrasound, acupuncture, laser therapy; Orthopedic benefits (prevention
and correction of typical joint deformities and instability of the cervical spine, orthoses, insoles, orthopedic shoes);
Sanatorium-and-spa treatment is indicated only for patients in remission; During the course of the disease, active
prevention and treatment of concomitant diseases are necessary.

- Medical treatment

Basic anti-inflammatory drugs (DMARDs):

TNFa inhibitors (Infliximab, Adalimumab, Golimumab),

GIBP with another mechanism (Rituximab, Abatacept, Tocilizumab)

- Cytostatic therapy– Methotrexate (antimetabolite) initial dose 10-15 mg/week, Sulfasalazine

- Glucocorticosteroid therapy (bridge therapy)– Methylprednisolone, Prednisolone

- Nonsteroidal Anti-Inflammatory Drugs– Diclofenac, Nimesulide

- Calcium preparations - Calcium carbonates

- Opioid analgesic – Tramadol

- Vitamin therapy - Folic acid

PROBLEM RA
Woman 34 years old, accountant
Complaints: pain and swelling in the carpal and elbow, metacarpophalangeal and proximal interdigital joints of the
hand, morning stiffness, which lasts up to 12 hours, in the evening - low-grade fever.
Anamnesis: ill for the last 3 years. She took NSAIDs (ketonal), currently taking ketonal as an injection, the effect is
negligible.
Objectively:
 Case 14

OSTEOARTHROSIS
50 year old woman....
Woman, 58 years old, pensioner
Complaints: pain that occurs when walking in the knee joints and disappears at rest. Morning stiffness lasts 30
minutes, limitation of movements in the knee joints, especially in the right knee (extension and flexion, squatting is
limited)
From the anamnesis: pain in the knee joints has been disturbing for the last 5 years. Physiotherapy, with severe pain,
he independently took non-steroidal anti-inflammatory drugs (diclofenac, ketonal), the effect was temporary. Over the
past month, the disease worsened, swelling appeared in the right knee joint.
Objective:

1) Interpretation of complaints and anamnesis

Complaints:pain in the area of the affected joint(s); Increasing pain when standing or during exercise.
Anamnesis:pain occurs during exercise or at rest; · By the end of the day after exercise, the pain intensifies, after rest
the pain decreases · the presence of "starting pain"; · whether there is a slight morning stiffness and stiffness, ·
whether there is a limitation in the function of the joint.

2) Interpretation of the physical examination

crepitus

An increase in the volume of the joint often occurs due to proliferative changes (osteophytes), but may also be the
result of edema of the periarticular tissues.

The formation of nodules in the distal (Heberden's nodes) and proximal (Bouchard's nodes) interphalangeal joints of
the hands.

Severe swelling and local temperature increase over the joints is rare, but may occur with the development of
secondary synovitis.

Varus deformity of the knee joints, "square" hand, Heberden's and Bouchard's nodes, respectively, in the distal and
proximal interphalangeal joints of the hands.

3) Preliminary diagnosis– OSTEOARTHRISIS, GONATHROSIS, idiopathic

VI - Functional ability of the joints (FNS):

0 - saved (FTS 0).

1 - functional ability is limited (FTS 1).

2 - lost ability to work (FTS 2).

3 - needs outside care (FTS 3).

4) Survey plan

Laboratory studies [1-4.7-10.12]:

KLA in the presence of synovitis, acceleration of ESR;
BAC (total protein, urea, creatinine, ALT, AST, total bilirubin, thymol test, cholesterol, glucose, CRP);
RF (for differential diagnosis with rheumatoid arthritis);
- Synovial fluid - turbidity, increased viscosity, Leukocytes

Instrumental research[1-6,14]:

List of main diagnostic measures:

1. X-ray examination of the joint.
2. Computed tomography of the joints.
3. Nuclear magnetic resonance of the joints.
4. Ultrasound of internal organs.

X-ray of the affected joints; knee joints - uneven narrowing of the joint space, osteophytes, signs of osteosclerosis
Ultrasound of the joints in the presence of synovitis;
MRI of knee jointsfor differential diagnosis.

IV. X-ray stage:

0 - no changes.
I - doubtful radiological signs.
II - minimal changes (slight narrowing of the joint space, single osteophytes).
III - moderate manifestations (moderate narrowing of the joint space, multiple osteophytes).
IV - pronounced changes (articular space is almost not traced, coarse osteophytes).
V - Synovitis: present; · absent.

5) Treatment tactics

Non-drug treatment[1-4,9]:

Non-drug treatment

Mode: II, free; · Table number 15.

- physiotherapy (thermal procedures, hydrotherapy);

- physiotherapy exercises (the main task is to reduce the load on the joint and strengthen the muscles): correction of
posture and length of the lower limbs, exercises with isometric load, exercises for individual muscle groups;

- local analgesics and NSAIDs (ointment, gel, cream).

Drug treatment [3-6,10]:

X-ray stage I non-drug treatment and NSAIDs;

X-ray stage II non-drug treatment, NSAIDs, intravenous administration of artificial synovial fluid preparations in
courses;

X-ray stage III non-drug treatment, NSAIDs, antidepressants and intravenous administration of artificial synovial fluid
preparations in courses;

X-ray stage IV arthroplasty of the affected joint.

ANALGESICS-paracetamol,

NSAIDs- diclofenac,

CHONDROPROTECTORS- chondroitin sulfate, glucosamine sulfate,

Narcotic analg– tramadol, derivatives of hyaluronic acid,

GK-triamcinolone, methylprednisolone, betamethasone

List of essential medicines:

1. *Ibuprofen 200 mg, 400 mg tab.

2. * Diclofenac sodium 25 mg, 100 mg, 150 mg tab.

3. Diclofenac sodium, emulgel 1% for external use

4. Diclofenac potassium 12.5 mg tab.

5. Ketoprofen injection 100 mg/2 ml, amp.

6. Lornoxicam 4 mg, 8 mg tab.

7. Celecoxib 100 mg, 200 mg caps.

8. Naproxen 250 mg tab.

9. Piroxicam 10 mg tab.

10. Chondroitin sulfate 5%, ointment

11. Phosfaden 0.05 g tab., 2% solution for injection, amp.

12. Pentoxifylline 100 mg, dragee, injection 100 mg/5 ml amp.

13. *Nadroparin calcium - injection in pre-filled syringes 2850 IU anti-Xa / 0.3 ml; 3800 IU anti-Xa/0.4 ml; 5700 IU anti-
Xa/0.6 ml; 7600 IU anti-Xa/0.8 ml, 9500 IU anti-Xa/1.0 ml
 Case 15
HRBS

Man, 37 years old

Complaints: a burning sensation in the region of the heart, shortness of breath with minor physical exertion,
palpitations, weakness.
From the anamnesis: ill since the age of 10, is registered at the dispensary, takes anti-relapse treatment. Hemoptysis
occurred 1 week ago after exercise
Objectively: the skin is pale, the face is "reddened", cyanosis of the lips. In the lungs, dull moist rales at the bottom.
In the region of the heart - "bend of the heart."
Auscultatory: I tone is reinforced, clapping, the rhythm is wrong, the sound of a click of the mitral valve at the apex of
the heart, diastolic murmur, the epicenter of which is located at the apex of the heart. The liver is not enlarged.

1) Symptoms of CRPS

Mitral insufficiency: long-term patients do not complain, the defect can be detected during an accidental medical
examination. With the progression of the disease appear: shortness of breath during exercise, and then at rest, cough,
asthma attacks at night; acrocyanosis; cough with a small amount of sputum; pain in the right hypochondrium due to
an increase in the size of the liver; swelling of the legs and feet. Auscultatory-systolic murmur, reflecting mitral
regurgitation, has the following characteristics: long, intense, blowing; has a different duration and intensity, especially
in the early stages of the disease; does not change significantly when changing the position of the body and the phase
of breathing; associated with tone I and occupies most of the systole, and is optimally auscultated at the apex of the
heart, carried out in the left axillary region.

Mitral stenosis(narrowing of the left atrioventricular opening): cyanotic flush of the cheeks; heartbeat; swelling; pain in
the chest; general weakness, increased fatigue; asthma attacks at night; cough with sputum, sometimes streaked with
blood. Auscultatory-loud I tone of mitral valve opening, "quail rhythm", diastolic murmur in the apex of the heart.

Aortic valve insufficiency: pulsation on the carotid artery, in the region of the heart, a heartbeat noticeable to the eye;
pallor, dizziness, fainting; pain in the region of the heart that occurs during physical exertion; dyspnea; general
weakness, fatigue. Auscultatory sign: protodiastolic murmur at Botkin's point. Blood pressure: high - systolic, low -
diastolic.

Aortic stenosischaracterized by pain behind the sternum, which occurs during physical exertion; headache; dizziness;
dyspnea; increased fatigue; pallor of the skin; symptom of systolic "cat's purr". Arterial pressure is reduced to 100/60
mm Hg. and below.

2) Survey plan

·ECG - prolongation of the P-Q interval.

• EchoCG - signs of damage to the heart valves (more often mitral insufficiency, less often aortic insufficiency, mitral
stenosis and concomitant defect).

• RoentgenGK - cardiomegaly and signs of damage to the heart valves.

Inflammatory activity of the blood: increased ESR and positive CRP.

• bacteriological examination: detection of GABHS in a throat swab.

• serological studies: elevated or increasing in dynamics titers of antistreptolysin-O, antistreptohyaluronidase and

antideoxyribonuclease-B

3) Preliminary diagnosis: CRPS Mitral stenosis maybe?

4) Treatment tactics

Non-drug treatment:

Mode 2; Diet No. 10;

Sanitation of tonsils.

Medical treatment

List of essential medicines:

benzylpenicillin sodium salt; cefuroxime; azithromycin; benzathine benzylpenicillin; bicillin-5; diclofenac; aceclofenac;
etoricoxib; prednisolone; methylprednisolone

♦ Diuretics:loop - furosemide; thiazide and thiazide-like -

hydrochlorothiazide, indapamide; potassium-sparing - spironolactone,

triamterene.

♦ Calcium channel blockersfrom the group of long-term dihydropyridines

action (amlodipine).

♦ B-adreioblockers(carvedilol, metoprolol, bisoprolol).

♦ Cardiac glycosides(digoxin). Doses and schemes of application

the above drugs are similar to those in the treatment of congestive heart

insufficiency of a different etiology.

♦ Application of nitratesin the complex treatment of congestive heart failure in patients

NSAIDs and ACE inhibitors can lead to a weakening of the vasodilating effect of the latter.

In particular, with the development of cardiac decompensation as a consequence of acute valvulitis (which usually
occurs only in children), the use of cardiotonic drugs is inappropriate, since in these cases a clear therapeutic effect
can be achieved using high doses of prednisolone (40-60 mg per day) .

In patients with sluggish carditis against the background of RPS (rheumatic heart disease), when choosing drugs used
in the treatment of congestive heart failure, their possible interaction with anti-inflammatory drugs should be taken into
account.
osteoarthritis

Woman, 65 years old, pensioner

Complaints: pain in the knee joints that occurs when walking and disappears at rest. Morning stiffness lasts 10-15
minutes, with movements there is a crunch in the knee joints, limitation of movements in the knee joints (limited in the
prone and sitting position), going down the stairs is also difficult

From the anamnesis: pains in the knee joints have been disturbing for 10 years. She independently took non-steroidal
anti-inflammatory drugs (diclofenac) and treated her knee joints with salt, later painless nodes appeared in the distal
and proximal joints of the fingers. During the last 3 months, the pain in the joints, the crunching increased, and the
movements were also somewhat limited.

1. Interpretation of complaints and anamnesis

2. Interpretation of objective examination
3. Diagnosis
4. What changes in analyzes and examination plan
5. Treatment

1. The patient complains of pain in the knee joints that occurs when walking and disappears at rest. There is also
morning stiffness lasting 10-15 minutes, with a crunch in the knee joints upon movement and limitation of movements
in the knee joints (especially in the prone and sitting position). Going down stairs is also difficult. These symptoms
have been present for 10 years, and the patient has self-medicated with non-steroidal anti-inflammatory drugs
(diclofenac) and treated her knee joints with salt. Painless nodes appeared in the distal and proximal joints of the
fingers, and over the last 3 months, the pain, crunching, and limited mobility have worsened.

2. The objective examination may reveal signs of joint inflammation, such as swelling, warmth, and tenderness in the
knee joints. There may also be crepitus (a crunching sensation) upon movement of the knee joint and limited range of
motion, particularly in flexion or extension. A physical exam of the fingers may also be warranted to evaluate for any
nodules or joint deformities.

3. The patient's symptoms and examination findings suggest a diagnosis of osteoarthritis (OA) of the knee joints. OA
is a degenerative joint disease characterized by progressive loss of cartilage in the joint, leading to pain, stiffness, and
limited range of motion. The development of nodes in the fingers is also a common feature of OA.
4. Additional tests that may be helpful in confirming the diagnosis and assessing disease severity include:

- X-rays of the knee joints to evaluate for joint space narrowing, bone spurs, and other signs of OA

- Blood tests to rule out other causes of joint pain, such as rheumatoid arthritis or gout.

5. Treatment for OA may include a combination of non-pharmacologic and pharmacologic interventions. Non-
pharmacologic treatments may include weight loss (if applicable), physical therapy, and assistive devices (e.g. knee
braces or shoe inserts). Pharmacologic treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs),
acetaminophen, or intra-articular corticosteroid injections. In severe cases, joint replacement surgery may be
recommended. Treatment should be tailored to the individual patient's needs and preferences, with the goal of
improving pain and function and preserving joint mobility.
№8 – AS

Man, 54 years old

Complaints: pain in the cervical, thoracic and lumbar vertebrae, reduction of pain in a calm position and when moving,
morning stiffness that lasts until noon, limitation of spinal movement, change in posture, fatigue.
From the anamnesis: considers himself ill for 25 years. At first, the disease began with pain in the lower back, the pain
occurs at rest and in the second half of the night, with movement, the pain subsides. Independently took diclofenac,
there was an effect. Subsequently, pain and stiffness in all parts of the spine are disturbing. Gradually, there was a
restriction of movement of the spine, a change in posture. Repeatedly underwent treatment by an ophthalmologist for
bilateral recurrent uveitis.
Objectively: the musculoskeletal system: the spine is a flattened lumbar lordosis. The rectus dorsi muscles are tense.
Pain on palpation in the area of the ileosacral ligament. Head rotation and forward tilt are limited. The inclination of the
body to the lateral edge is limited. Thomayer's sign 40 cm. Ott's sign 2 cm, Schober's sign 1 cm.

1. Interpretation of complaints and anamnesis

2. Interpretation of objective examination
3. Diagnosis
4. What changes in analyzes and examination plan
5. Treatment

1. The patient complains of pain in the cervical, thoracic, and lumbar vertebrae, morning stiffness that lasts until noon,
limitation of spinal movement, change in posture, and fatigue. These symptoms have been present for 25 years, and
the patient initially experienced pain in the lower back that occurred at rest and in the second half of the night, with
relief upon movement. The patient self-medicated with diclofenac, which had a positive effect. Over time, the pain and
stiffness spread to all parts of the spine, and there was a restriction of spinal movement and a change in posture. The
patient also had bilateral recurrent uveitis, for which they received treatment from an ophthalmologist.

2. The objective examination shows a flattened lumbar lordosis, tense rectus dorsi muscles, and pain on palpation in
the area of the ileosacral ligament. There is limited head rotation and forward tilt, limited inclination of the body to the
lateral edge, Thomayer's sign is 40 cm, Ott's sign is 2 cm, and Schober's sign is 1 cm.

3. The patient's symptoms and examination findings suggest a diagnosis of Ankylosing Spondylitis (AS), a type of
inflammatory arthritis that primarily affects the spine. AS is characterized by morning stiffness and pain that improves
with movement, spinal fusion leading to a loss of spinal mobility, and changes in posture. Recurrent uveitis is a
common extra-articular manifestation of AS.

4. Additional tests that may be helpful in confirming the diagnosis and assessing disease activity include:

- Blood tests to measure levels of inflammation (e.g. C-reactive protein, erythrocyte sedimentation rate)

- HLA-B27 genetic testing

- Imaging studies, such as X-rays, magnetic resonance imaging (MRI), or computed tomography (CT) scans to assess
for evidence of spinal inflammation or fusion.

5. Treatment for AS typically involves a combination of medication, exercise, and lifestyle modifications. Medications
may include nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation, disease-modifying
antirheumatic drugs (DMARDs) to slow disease progression, and biologic agents (e.g. TNF inhibitors) to target
specific inflammatory pathways. Exercise programs, such as physical therapy or yoga, can help improve spinal
mobility and posture. Lifestyle modifications may include avoiding smoking and maintaining a healthy weight.
Treatment should be tailored to the individual patient's needs and may require a multidisciplinary approach involving
rheumatologists, ophthalmologists, and other healthcare providers.
Clinical zhagday №9
SLE
The receptionist is a 19 year old girl.
Complaints: fatigue, weakness, pain in the knee, shoulder joints, rashes on the face, rash, sores in the hard palate of
the oral cavity, hair loss, fever up to 38.0 0C, weight loss of 2.5 kg of body weight per 2.5 weeks
From the anamnesis: according to the patient, they rested on Issyk-Kul (rested 20 days ago), rashes appeared on the
face, body temperature rose to 38 C, paracetamol, local Advantan ointment (containing methylprednisolone) were
used, there was a slight effect, then there were pains in knee and shoulder joints, ulcerative lesion of the hard palate
in the oral cavity, hair loss, weakness, fatigue, was at the therapist, during the examination: KLA: leukocytes - 3.0 x
109 / l, platelets - 170 x10 9 / l, erythr - 3.1 x10 12/l, HB-98 g/l, ESR 30 mm/h.
Objective:

Vesicular breathing in the lungs, no wheezing. RR 16 times min. The heart sounds are muffled, the rhythm is correct,
the pulse is 84 beats/min. BP 110 / 70 mmHg the tongue is moist and clean. The abdomen is soft and painless. Liver
in the right costal arch. The spleen is not enlarged. The symptom of effleurage is negative on both sides. Urination is
free, without pain.
Objectives:

1. Interpretation of complaints and anamnesis

2. Interpretation of objective examination
3. Diagnosis
4. What changes in analyzes and examination plan
5. Treatment

1. The patient complains of fatigue, weakness, pain in the knee and shoulder joints, rashes on the face and body,
sores in the hard palate of the oral cavity, hair loss, fever, and weight loss. According to the anamnesis, the symptoms
started after a trip to Issyk-Kul, where rashes appeared on the face and a high fever followed. Treatment with
paracetamol and topical methylprednisolone had a slight effect. Subsequently, joint pain, oral ulcers, hair loss,
weakness, and fatigue developed.

2. On objective examination, the patient has vesicular breathing in the lungs without wheezing, a muffled heart sound
with a correct rhythm and a pulse of 84 beats/min, and a blood pressure of 110/70 mmHg. The tongue is moist and
clean, and the abdomen is soft and painless. The liver is palpable in the right costal arch, and the spleen is not
enlarged. The symptom of effleurage is negative on both sides, and urination is free without pain.

3. The patient's symptoms and laboratory findings suggest a systemic autoimmune disease, such as systemic lupus
erythematosus (SLE) or mixed connective tissue disease (MCTD). The presence of rashes, joint pain, oral ulcers, and
hair loss are all common symptoms of these diseases. The low leukocyte count and anemia seen on laboratory tests
may also be indicative of autoimmune disease.
4. Further laboratory testing may include antinuclear antibody (ANA) testing, anti-dsDNA, and anti-Sm antibody testing
to help confirm a diagnosis of SLE or MCTD. Additional imaging studies, such as X-rays or MRI, may be performed to
evaluate joint involvement.

5. Treatment will depend on the specific diagnosis, but may include nonsteroidal anti-inflammatory drugs (NSAIDs)
and corticosteroids to manage symptoms such as joint pain and inflammation. Immunomodulatory drugs, such as
hydroxychloroquine or methotrexate, may also be used to manage disease activity. Topical and systemic treatments
may be used for skin and oral involvement, and regular monitoring by a rheumatologist is important to ensure effective
disease management.
Clinical №10
scleroderma

Woman 40 years old

Complaints: frostbite, numbness, whitening and cyanosis of the fingers after stress and hypothermia, pain and
swelling of the small joints of the hands, the appearance of vascular patterns on the face, hair loss, weakness, fatigue.
From the anamnesis: for a long time (about 10 years), frostbite, numbness of the hands, whitening of the fingers when
washing hands in cold water or after stress were observed. Over the past 1.5-2 years, I noticed the appearance of
expanded vascular patterns on the face and back, when pressed, no traces remain, there are pains in the fingers, hair
loss, weakness. She turned to a general practitioner in a polyclinic, during the examination, an increase in CRP and
an acceleration of ESR up to 30 mm / h were revealed. The patient was referred for a consultation with a
rheumatologist.

Objective:

1. Interpretation of complaints and anamnesis

2. Interpretation of objective examination
3. Diagnosis
4. What changes in analyzes and examination plan
5. Treatment

1. The patient has a history of frostbite and numbness in the hands, which can indicate poor blood circulation in the
fingers. The appearance of vascular patterns on the face and back, pain and swelling of the small joints of the hands,
hair loss, weakness and fatigue can be signs of an autoimmune disease. An increase in CRP and ESR levels in the
blood test further suggest an inflammatory process.

2. The objective examination reveals no additional information to aid in the interpretation of the patient's symptoms
and history.

3. The diagnosis is systemic sclerosis (scleroderma), an autoimmune connective tissue disease characterized by the
hardening and tightening of the skin and connective tissues, as well as the malfunctioning of blood vessels and
internal organs.

4. Additional tests such as ANA (antinuclear antibodies) and anti-Scl-70 (anti-topoisomerase) antibody tests can
confirm the diagnosis of scleroderma. Imaging studies such as chest x-ray, echocardiogram, or pulmonary function
tests may be ordered to assess the involvement of internal organs.

5. Treatment for scleroderma aims to manage symptoms, slow down the progression of the disease, and prevent
complications. Medications such as immunosuppressants, vasodilators, and pain relievers may be prescribed.
Physical therapy and occupational therapy can help improve mobility and function. Additionally, lifestyle modifications
such as avoiding cold temperatures and quitting smoking can also help manage symptoms.