Internal Medicine 1 Step 2 (All Subjects)

Translated from Russian to English - www.onlinedoctranslator.
com
“S.Zh. ASFENDIYAROV ATYNDAGY KAZAKH ULTTYK MEDICINE UNIVERSITY» KEAK

NJSC "KAZAKH NATIONAL MEDICAL UNIVERSITY NAMED AFTER S.D. ASFENDIYAROV"
Department of Internal Medicine Relief of the crisis Revision: 1
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Cardiology
Rear1 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:
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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.
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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).
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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.
Zad2 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
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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.
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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
Ass3
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.
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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
Ass4
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.
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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
Back5 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.
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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
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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
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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
Ass6
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
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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.
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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)
Ass7 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)
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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(gammaglutam 58.00 (N 6-42) U/L increased
yltranspeptidase)
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
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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);
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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
Peg-IFN alfa-2a (Pegylated interferon alfa-2a - immunomodulator) Interferons. Solution for injection 180
mcg/0.5 ml 180 mcg weekly subcutaneously
Lamivudine Nucleosides - reverse transcriptase inhibitors 100 mg per day orally
Rear8 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
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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).
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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
Rear9 IDA
Page19from50
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
WBC - 4.0 x 109 /L / l,
HT-18% total bilirubin - 18.2 µmol / l
RBC - 2, 9 x 1012 / L creatinine 83 µmol/l
LYM - 39% urea 4.2 mmol/
MCV - 63.1 fl ALT 18 U/l
MID - 6% AST 22 U/l
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:
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:
Page20from50
- 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:
Page21from50
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
Page22from50
Rear10 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 ALT 18 U/l norm up to 45
3.7-4.7 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 serum iron: 15.6 µmol/l normal (9-27)
erythrocytes)– 265 g\L reduced (300-380) EFGDS + biopsy:atrophic changes in the
PLT (platelets) - 185 x 109 / L norm 180- mucous membrane of the digestive tract.
320 Atrophy of parietal and chief cells. Atypical
CPU-1.3 increased 0.85-1.05 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:
pH - 6.0
LEU-neg
NIT-neg
PRO-neg
GLU-norm
KET-neg
Page23from50
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)
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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
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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
Ass11
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

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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:
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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)

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Rear12 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

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

methylprednisolone.
Ass13
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.
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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
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- 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

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- ECG
- echocardiography
- Radiography of the lungs in two projections.
-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

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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:
Ass14
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:
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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.
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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.
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,

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Narcotic analg– tramadol, derivatives of hyaluronic acid,
GK-triamcinolone, methylprednisolone, betamethasone
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
Ass15
HRBS
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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,
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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?
Non-drug treatment:
Mode 2; Diet No. 10;
Sanitation of tonsils.
Medical treatment
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.
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♦ 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.
CHALLENGE - 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.
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1. Interpretation of complaints and anamnesis

2. Interpretation of objective examination
3. Diagnosis
4. What changes in analyzes and examination plan
5. Treatment
Klinilyk zhagday №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.
Tapsyrma:
1. Shagymdary men anamnesis malimetterin interpretationlau
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Buyndyk syndrome of oxyalda körenisteri - moiyn, keude zhane bel omyrtkasynyn

auyrsynuy, omyrtka kozgalysynyn shekteluine
tanertengi kurysu tuke deyin sozylady
Anamnesis: 25zhyl auyrady, Algashky kezde aura arkanyn tömengi bөlіgіnіn auruymen
bastalgan, қozғalys kezinde auyrsynu basylody. Diclofenac
Tirek qimyl apparar thousand:
Birneshe ret ophthalmologist darigerinen ekіzhakty relapse uveitis boyinsha em kabyldagan.
2. Objectives karap texeru malimetterin interpretationlau

Omyrtka -tegistelgen bel lordosis
Ileosacraldy baylam aimagynda palpation of barysynda auyrsynady
Basty bұru zhane alga karay enkeyu shektelgen.
Thomayer symptoms 40 cm. Ott symptoms 2 cm, Schober

symptoms 1 cm.
Schober symptomaticazayuyna (standard 15 cm), bel bөlіminіn zaқymdalu kөrsetkіshі
bolyp kөrsetіledі
Thomayer symptomaticzhogarylauynan (kalyptyda 10-ғa deyin), omyrtka iіlgіshtigіninіn,
қozғаlysynyң shekteluіne baylanists.
Otta symptomaticazayuyna (kalyptyda 5-ten artyk) baylanists, keude bolіminіn
zaқymdaluy.
3. Berilgen klinikalyk zhagdayda kanday bolzham diagnosis boluy mүmkin?

Naukastyn shagymdaryna karap - Omyrtkanyn moiyn, keude, bel aimagyndagy aur
sezimi men қimyl қozғalystyn
Tuske deyin sozylatyn tangy kurysuga
Sol kozdіn koruinіn tөmendeuimen қyzaryp auruyna - Uveit
Anamnesis: aura
Objectives karau kezinde - Buyndyk syndromedar anyktaldy, Omyrtkanyn - moiyn,

keude, bel aimatarynyn kozgalysynyn shektelui, omyrtkalyk bel lordosis tegistelgen.
Thomayer, Otto, Schober's son Malara they are not less than Corsetti.
Bolzham diagnosis:Ankylosis spondylitis, satysy cache, FC-3, uveitis.

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Diagnostic criteria:
1984 boyinsha:
Құsurulardyң өte kөp zhalғasuy, 3 aidan artyқ (25zhyl)
Omyrtkanyn kozgalystarynyn shektelui
2009 boyinsha:
40
25
Physikalyk kozgalys zhattygu kezderde aurudyn basyluy
NSAIDs on nәtizhe korsetuі
4. Kutіletіn өzgerіsterdі kөrsetіp, zertteu zhosparyn құru

ZHA: ETG zhogarylauy, leukocytosis anyktaluy (keide anemia, bolus thrombocytosis)
Biochemical analysis: CRP protein zhogarylauy
Kanda IgA deңgeyinіn zhogarylauy
rf factor ballmowy
HLA-27 analyzes they still take
Synovialdy suyyktyk құramyn zertteu
Aspaptyk zertteulerde:
Radiography Zhurgizu
Zhambas bөlіginіn suyekterі men buyndar 2
Sacroiliitis anқtaluy
Keude kuys aғzalarynyn 2 Zhakty projection and radiography:

Keude kuysyndagy aғzalardy tekseru ushіn
Baska projectionlardan korinetin: zhіnіshke zhane symmetrically syndesmofitter,

omyrtkalardyn osteopeniasy
Wasps zertteuler boyinsha, naқty the diagnosis is koyuғa zhane kai kezende zhurip
zhatқanyna kosymsha malimetter beredi.
5. Emdeu zhosparyn kuru

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- emes medications
Temekiden, alkagolden bastartu
Stresstik zhagdaulardy boldyrmau
Balance diet
exercise therapy
- medications
Steroids emes kabynuga karsy preparattar:
Diclofenac
Peripheral arthritter kezinde -Sulfasalazine kabyldau 500-2000mg 2-3ret kunine
GCS therapy:
Betamethasone, buyn ishilik, 2-5mg
Gendik - engineer preparation:

Infliximab 3-5 mg/kg IV 0.2.6 aptasynda odan keyin ar 6 aptad nemese
Golimumab 50mg ai saiyn
Kosymsha: opioids analgesic, muscle relaxant zhane vitaminander tagaiyndauga bolady.

Sonday-ak, ophthalmologist consultation son tagayyndaimyz.
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
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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:
Tapsyrma:
Buyndyk syndrome, terilik syndrome, alopecia, auyk kuysynyn katty tagdayynda oyylu
zharalar, Kyzba, dene salmagynyn tusui
Anamnesis:
Ystyk kölde demalyp kelgesin, sodan keyin börtpeler payda boldy + kyzba. Өz Erkimen
Emelgen Paracetamol, Zhergiliktan Advantan (ramynda methylprednizolnolo Bar) Mayyn
Koldankan, shamaly effect Bolgan, әrey қrai әe ilya bumandarynda aura Sizimi,
auykyynynya қaty tagdayyynda tuyla tapei. Astheno-vegetative syndrome (Alsizdik,
Sharshagyshtyk)
WHA: leukocyte-3.0 x 109/l, platelet-170 x10 9/l, erythrol -3.1 x10 12/l, Hb-98 g/l, ETJ 30
mm/sag.
Leukopenia, Erythrocytopenia, anemia, ETG burn

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Terilik Syndrome -Betіnde - "kobelek" tаrіzdі erythema. Auyz kuysynyn shyryshty kabatynda - oyyk zharalar
Buyndyk syndrome -Tize, ayak bassy zhane shyntak buyndarynda auyrsynular men isingen. Buyndarynda
kozgalys auyrsyngan
Tynys alu zhүyesі boyinsha kalypty
Zhurek kantamyr zhүyesі boyinsha -Zhurek tondary tuyyktalga, rhythm dұrys, pulse 84 ret min. АҚҚ
110/70mm.s.b.b. kalypty

Zhүyeli қyzyl zhegі, zhedel damu barysy, Terіlіk (Betіnde - "kobelek" tаrіzdі erythema) Buyndyқ
(polyarthritter), oyyk zhalalar, hematologylyқ (leukopenia, hemolyzdіk anemia),
Diagnostic criteria:
kyzba
terinіn: "kobelek" belgіsi, erythema
Shyryshty kabyk oyyn zhalalary
Buyndardyk syndromed, polyarthritter
Kan ozgeristeri
Kosymsha:
Serozdyk kabyktardyn: pleurisy
Zhүrektin - myocarditis, endocarditis, mitraldi қakpaқtyn zhetіspeushіlіgі
Buyrektin: non-septic syndrome, nephritis;
Nerve zhuyesinin: meningoencephalopyradiculoneuritis, polyneuritis.

Biochemical analysis: Dyslipedemia, hypercholesterolemia, hyperenzymemia,
hyperglycemia
Immunology analysis: ANA - ZhKZh-nіn diagnostics үshin manyzdy screening test for
most tabylady. Ony 2 zhol arkyly anyktauga bolady: standard "boyinsha HEp-2 substrate
retinde paidalanyp, Tura emes immunofluorescence reaction ANA tirti men tipin anyktau
Anti-dsDNA-anyktau
Complement Zhyesinin C3, C4 component of anyktau
Ribonucleoproteinterge karsy antidene, sonymen katar: anti-snRNP, anti-Ro/SS-A, anti-
La/SS-B anyktau diagnosis koyuga arnalgan markerler bollyp tabylady.
Aspaptik zertteler:
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Keude kusynyn roentgenography

ECG, echocardiography
FGDS
Buyrek UDZ Zhane biopsyasy
Densitometry
- emes medications
Diet table number 15
Mode 2
Kunge az shygu, zhabyk kiinu
Temeki shegu totatu, exercise therapy
Vitamins D buy tagamdar tutynu
- medications
Basists Therapy:
Methotrexate 2.5mg 3-4ret aptasyna
GCS therapy:
Prednisolone 5-60mg 3-4 ret kunine nemese
Methylprednisolone 4mg 3-4 ret kunine
Steroids emes kabynuga karsy preparattar:

Diclofenac 75-200mg 1-3 to
Gendik engineerlik preparation:

Belimumab IV 10mg/kg 1rem 0.14.28 kunderi
Immuglobulinder
Clinical zhagday №10

scleroderma
Woman 40 years old

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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:
Tapsyrma:
Terilik syndrome, Raynaud's syndromes, alopecia,
buyndyқsyndrome - қoldyn ұsақ buyndarynyn auyrsynuyna zhane іsіnuіne,
Astevegatative syndrome
Anamnesis:
10zhyl auyrady, ETZh SRB zhog, kabynudy korsetedi,
ұzaқ uaқyttan take (shamamen 10 zhyldan take) kol basynyn tonuy, ұyuy, kolyn suyқ suyқ
suғa zhuganda nemese kuyzelisten keyіn kol sausaktarynyn aғaruyn bayқaғan.
Songy 1.5-2 zhylda betіnde, arkasynda kolmen baskanda іzі kalmaytyn keneigen tamyrly
örnekterdin payda bolganyn bayқағan, kol sausaktarynyn auyrsynuy, shashtyңbayty үsіsіzd,
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Emkhanasyndagy therapist darіgerine karalady, texer barysynda Etzh 30 mm/sag, SRP

zhogarylauy anyқtaldy. Scientific rheumatologist darіgerіninің kenesіne zhіberіldі.

Eky kolyndada Raynaud syndromes korinedі, kol ushtary agargan,

Diagnosis: Zhүyeli scleroderma, sozylmaly. 2kezen zhayylmaly, polysyndrome
process
Diagnosis criterion
Ulken criteria.
Scleroderma proximaldes: alakan-sausak, bashpay-sausak buyndarynan proximalds
ornalaskan sausaq zhane bashpay terisininin symmetrically kalyndauy, tygyzdaluy zhane
induratsiyasy. Ozgerister bette, moiynda, dene tulғasynyn (keude tori men құrsak) ustinde de
bolady.
Other criteria.
1. Sclerodactyly
2. Sausaktar ұshynda tyrtyқtar zhane sausaktar tompagynyn zhoyyluy.
3. Ekі zhakty basalds okpe fibrosis: okpenі roentgenologylyk standardty texergende okpede
bolatyn ekі zhakty torly nemesse syzykty – moduldі özgerister; "Uyaly okpe" tipti ozgerister
boluy mүmkin. Bul өzgerister okpenің birіnshі rettі zaқymdanuymen bailanysty bolmaulary
kerek.
Diagnosis

JKA: ETZH zhogarylauy 20mm/Sag
ҚBA: zhogarylauy fibrionogen, seromucoid, zhogarylauy CRP.
Immune surfactant: Antinuclear factor, DNA-ga AD+, AD
Topoisomerase1+
X-ray: alakan-osteolysis, teri osteocalcinosis, periarticularly
osteoparosis koremiz.
Raynaud sindo-capillaryoscopy
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6.
ZhSD-da koldanylatyn dariler:
1. Antifibrozdy kasieti bar dariler (D-penicillamine, medecasol, unithiol, diucifon,
colchicine, fermenter - lidase t.b.)
2. Tamyrga aser etetin dariler: vasodilatorlar, disaggreganttar, angioprotectorlar,
hypotensive dariler.
3. Kabynuga karsy zhane immunosuppressive dariler (corticosteroidtar, cytostaticter),
aminoquinoline preparations, antacid.
Calcium antoganisteri - Nifidipine, Amlodiping
A, B, E vitamins
Heparin zhagym mayy, dimexide
Raynaud's syndrome - Prozazin, chimes aspirin
Kabynuga karsy zhane immundyk suppresivtі aserlerge
Indomethacin, Aminoquinoline catry, Salicylattar

Internal Medicine 1 Step 2 (All Subjects)

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Internal Medicine 1 Step 2 (All Subjects)

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“S.Zh. ASFENDIYAROV ATYNDAGY KAZAKH ULTTYK MEDICINE UNIVERSITY» KEAK

Give answers to the following questions:

1. Determine the degree of hypertension, risk factors.

2. Interpret laboratory data.

3. Interpret the ECG

4. Formulate a clinical diagnosis

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

5. Provide first aid and further tactics

Angiotensin II receptor antagonists: losartan (25-100), eprosartan (600)

1) Formulate a diagnosis and justify

2) Interpret the ECG

HR: 60/R-Rx T(25mm=0.04s, 50mm=0.02s)=Heart rate 92 beats per minute.

3) Provide emergency care to the patient

twenty.Determined further treatment tactics:

4) Determine the tactics of conducting

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

Wave flicker frequency 450-600 min.

From the history of life:

2) Formulate and justify the diagnosis

segmented neutrophils - 56% - normal

2) Formulate the main and concomitant diagnoses

-Non-drug treatment. (For everyone)

Optimization of the regime of the day and loads.

pH - 6.0 normal (5-7) slightly acidic

PCR result - research

Elastometry of the liver

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

3) Formulate the main and concomitant diagnoses

4)What additional studies should be prescribed to the patient

Non-drug treatment of CP includes:

Enzyme replacement therapy for CP

Therapy of pain syndrome CP.

1) Make a preliminary diagnosis, justify it

- General anemic syndrome:weakness, fatigue, dizziness, headaches, palpitations,

2) Interpret laboratory tests

3) Make a clinical diagnosis, justify it

Microcytic hyporegenerative, hypochromicIron deficiency anemia, severe(hemoglobin-49g / l), due to

1) Preliminary diagnosis:Hyperchromic anemia of the 2nd degree of severity. B12 deficiency

2) Interpretation of laboratory and instrumental data

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

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

1) Interpret the data of complaints and anamnesis

2) Conduct an examination of the joints

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

-Examination of synovial fluid (detection of sodium monourates)

5) Make a treatment plan

Identification and correction of the treatment of concomitant diseases.

List of essential medicines:

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

Glucocorticosteroid therapy: Methylprednisolone; Methylprednisolone acetate; Methylprednisolone sodium

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

− Other types of treatment:

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

Male, 18 years old, student

1) Interpretation of complaints and anamnesis

2) Interpretation of objective examination

skin syndrome -erythema ring rash

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