2nd Semster Q finals

Question 1

31. Syndrome of lung consolidation.

Answer 1

—DF : Significant reduction or complete disappearance of
airiness of lung tissue in a more or less common area
(segment, lobe, several lobes).
—Possible reasons :
there is 2 types:
1-Inflammatory infiltration:
1.1-Pneumonia
1.2-Infiltrative tuberculous
2-Noninflammatory etiology:
2.1-Pulmonary infarction with pulmonary embolism, thrombosis
2.2-Lung tumor
2.3-Obstructive atelectasis
—Location :
* The tops of the lungs
* The lower parts of the lungs
* Middle lobe
* Subpleural location
—Complaints :
* Cough
* Dyspnea
* Increase tº (fever)
* Pain in the side
—-Inspection :
1-Hyperemia of face (cheeks)
2-The lag part of the chest during respiration
—Palpation :
1-Pain in the intercostal space
2-Increase of vocal (tactile) fremitus
—Percussion : Dull or flat percussion note
—auscultation :
-Breath:
1-Weakened vesicular breathing
2-Bronchial breathing
-Additional respiratory sounds
* Fine cracles
* cracles (small, medium-bubbles)
* Pleural friction
-Bronchofoniya - increase
—-Laboratory diagnostics :
–Blood test:
- Leukocytosis, left shift
- ESR acceleration
–Sputum
- “Rusty”
- mucous
- purulent

Question 2

32. Lung cavity syndrome

Answer 2

—Etiology :
1-Abscessed pneumonia
2-Tuberculous cavity
3-Abscessed pulmonary infarction
4-Wegener’s granuloma
5-Gangrene
—Symptomatology :
1-Cavity size
2-Depth of its location
3-Cavity contents: air only (empty cavity), air with some amount of fluid (e.g. air and exudates).
4-Cavity communication with respiratory tract (via drainage bronchus) or isolated cavity
—Stages :
1-inflammatory infltraion of lung tissue
2-formation of pus in lung cavity
3-occures of obulitration ofthe cavity with formation of penumoscolorosis
—Clinical signs : there is 2
1- first Stage - before communication with the bronchus (isolated cavity):
1.1-Hectic fever
1.2-Cough - dry or with a small amount of sputum
1.3-General weakness
1.4-Decrease of vocal (tactile)fremitus
1.5-Dullness of percussion sound
1.6-Weakened vesicular breathing
2- second Stage - after communication with the bronchus:
2.1-Reducing signs of intoxication
2.2-Productive cough with a big amount of purulent sputum
2.3-Increased vocal fremitus
2.4-Tympanic sound
—Instrumental diagnostics:
1- Xray
2-CT
—Laboratory diagnostics:
1-Blood:
1.1-Leukocytosis
1.2-Shift left of leykoformula
1.3-ESR acceleration
1.4-Toxic granularity of neutrophils
2-Sputum:
2.1-Pus mixed with blood

Question 3

33. Syndrome pulmonary hyperinflation (emphysema)

Answer 3

—-DF : is characterized by a pathological expansion of air spaces
located distal to the terminal bronchi, and is caused by
a decrease in the elastic properties of the alveolar septa.
—-Etiology:
1-Obstructive bronchitis (CORD)
2-Bronchial asthma
3-Emphysema
—Forms of emphysema:
1. Interstitial
2. Alveolar:
2.1 nonobstructive
2.3 focal
2.4 diffuse
3-.Primary emphysema is a genetically determined deficiency of 1-antitrypsin.
4-Secondary emphysema develops against the background of chronic lung diseases.
—- Causes:
1-frequent cough (chronic bronchitis);
2-chronic obstructive pulmonary disease (COPD);
3-genetically determined deficiency of 1-antitrypsin;
4-mechanical stretching of the alveoli during forced expiration (for glass blowers, singers), musicians playing wind instruments)
—Complaints:
-Dyspnea, shortness of breath, which is expiratory in
nature and can manifest itself first with physical
exertion, and then at rest, characterizing a varyin degree of respiratory failure.
—Inspection:
1-Barrel chest
2-Diffuse cyanosis
—Palpation:
1-Rigid chest
2-Vocal fremitus weakened:
right side = lift side
—Percussion:
1-Hyperresonant percussion note
2-The lower boundary of the lung omitted
3-Tops expanded
—Auscultation:
1-Symmetrical weakened vesicular breathing
2-Common wheezing
3-Single crackles
—inestrumnetal dignostic:
1-X-ray
2-Spirography

Question 4

34. Pleural effusion syndrome.

Answer 4

—DF : this is a symptom complex due to the presence of fluid
between the layers of the pleura, due to damage to the
pleura or in connection with general disorders of water and
electrolyte metabolism in the body
–Types:
1-hydrothorax : accumulation in the pleural cavity of transudate - noninflammatory fluid;
2-exudative pleurisy : an inflammatory process of the pleura, accompanied by the accumulation of exudate in the pleural cavity - an inflammatory fluid;
3-empyema of the pleura (pyothorax): a purulent inflammatory process of the
pleura, accompanied by accumulation of pus in the pleural cavity;
4-hemothorax: accumulation of blood in the pleural cavity; most often occurs with chest injuries
5-hylothorax - accumulation of lymph in the pleural cavity,
—classificaion of Eitology :
1-infectious : most often caused by bacteria: Streptococcus pneumoniae
2-non-infectious or aseptic : accumulation of fluid in the pleural cavity due to other (noninfectious) mechanisms such as malignant tumors
—-The main pathogenetic mechanisms of the occurrence of pleural effusion:
* 1. increased permeability of pleural sheets;
* 2. increased pressure in the pulmonary capillaries;
* 3. reduction of negative intrapleural pressure
–pleural effusions are classically divided into transudates and exudates:
1-Transudative (edematous) pleural effusions develop under the influence of
extrapleural factors on the filtration of the pleural fluid. Ex > heart failure,
,cirrhosis of the liver,hypoalbuminemia
2-Exudative pleural effusions are observed in cases where pathological changes in the pleura itself develop Ex> malignant diseases,parapneumonic effusion,bacterial pleurisy, tuberculosis
—Complains:
1. Shortness of breath appears when more than 1 liter of fluid accumulates in
the pleural cavity due to a decrease in lung capacity
2. Pain in the chest occurs when the affected visceral and parietal layers of the pleura come into contact.
3. Dry cough.
—palpation : - Increased resistance chest, Vocal fremitus weakened or not determined,
—percussion:a dull sound is dull; on auscultation,
sharply weakened vesicular breathing or its absence; ↓ bronchophony
—Laboratory and instrumental diagnostic :
1-X-ray
2-Ultrasound of the pleural cavities
3-thoracoscopy

Question 5

35. Syndrome of air accumulation in the pleural cavity.

Answer 5

–DF : Pneumothorax is an accumulation of air in the pleural cavity. The air
penetrating into the pleural cavity due to ↑ intrapleural pressure
-mechansim :is based on two groups of causes:
1. Mechanical damage to the chest or lungs
2. Diseases of the lungs and chest organs
—Three types of pneumathorax:
1-closed pneumothorax, the pleural cavity is not communicated with the
environment and the volume of air entering the pleural cavity does not increase. A small amount of air can be absorbed on its own.
2-Open pneumothorax is characterized by the presence of a defect in the chest
wall, through which there is a free communication of the pleural cavity with the external environment. The pressure in the pleural cavity becomes equal to atmospheric pressure, which leads to the collapse of the lung and turning it off from breathing
3-Valvular (tense) pneumothorax,: due to damage to the lung tissue, a kind
of valve arises that allows air to pass into the pleural cavity at the moment of inhalation and blocks its exit at the moment of exhalation
—Spontaneous pneumothorax : they are two types
1-Primary : occurs in people who do not suffer from lung disease, usually in tall, thin old and men aged 20–30 years. Caused by spontaneous destruction of the subpleural apical vesicles or bullae through smoking or heredity.
* Usually pneumothorax develops at rest, in some cases - during physical work
2-Secondary : occurs in patients with existing progressive pulmonary pathology:
* Respiratory diseases – COPD, asthma, cystic fibrosis
—Complaints:
1. strong sudden stabbing pains in the chest on the side of the lesion
2. acute shortness of breath
3. dry cough,
—Palpation :
– ↑ resistance of the chest on the side of the lesion
– ↓ or even absence of vocal fremitus on the affected side
—Percussion : - tympanic sound on the side of the lesion
—Auscultation :
– ↓ or absence of vesicular breathing on the side of the lesion;
- Negative bronchophony on the side of the lesion
—main method for diagnosing pneumothorax : Chest X-ray

Question 6

36. Syndrome of bronchial obstruction (asthma).

Answer 6

–DF : a clinical symptom complex that occurs as a result of airflow limitation in the bronchial tree, mainly on exhalation,
–Diseases accompanied by bronchial obstruction :
1-Mandatory obstruction : COPD , Bronchial asthma.
2-Facultative obstruction : Acute bronchitis , pneumonia , Pulmonary tuberculosis
—Main mechanisms of bronchial obstruction :
1-Functional (reversible) : Mucosal edema
2-Organic (irreversible) : Peribronchial fibrosis
—Complaints :
1-asthma attacks of expiratory type
2-cough (initially dry, )
3-widespread dry wheezing, mainly on exhalation
—palpation : resistance of the chest and symmetrical ↓ vocal fremitus are noted.
—percussion :
1-comparative percussion: there is a box lung (hyperresonant)
2-topographic percussion - an increase in the upper and lower boundaries of the lungs, limited mobility of the lower lung edge
— auscultation : weakened vesicular breathing with prolonged exhalation
—Laboratory and instrumental diagnostics :
1-General blood analysis :
- polycythemia
- increase hemoglobin
- The decrease in ESR
2-Sputum
- Bright, viscous, scanty, vitreous
—-Instrumental methods of investigation :
1-Fibrobronchoscopy

Question 7

37. Syndrome of respiratory deficiency.

Answer 7

—DF : is the inability of the respiratory system to supply the oxygen needed tosaturate hemoglobin and remove carbon dioxide.
—types:
1-obstractive
2-restractive
3-diffusion
4-mixed
—signs :
* dyspnea
* central (diffuse) cyanosis
* enhanced work of respiratory muscles
—Pulmonary heart disease :
* is the enlargement and failure of the right ventricle of
the heart as a response to increased vascular resistance or high blood pressure in the lungs.—DF : is the inability of the respiratory system to supply the oxygen needed tosaturate hemoglobin and remove carbon dioxide.
—types:
1-obstractive
2-restractive
3-diffusion
4-mixed
—signs :
* dyspnea
* central (diffuse) cyanosis
* enhanced work of respiratory muscles
—Pulmonary heart disease :
* is the enlargement and failure of the right ventricle of
the heart as a response to increased vascular resistance or high blood pressure in the lungs.

Question 8

38. Syndrome of mitral stenosis

Answer 8

—hemodynamics abnormalities :
1-Compensation stage: the area of mitral ostium is significantly less than normal (4-6 cm to 2cm ) leads to left atrium repletion with blood. This blood had not time to move to the left ventricle, and there is also blood, arrived from pulmonary veins. It results in left atrium hypertrophy
2-Decompensation stage : left atrium contractility is decreased pressure within it increases, that leads to the pressure rise within the pulmonary veins and pulmonary capillaries. The pressure rise within the pulmonary veins ostii causes the narrowing of the pulmonary arterioles- and when pressure rising within the pulmonary artery and further overload and hypertrophy of the right ventricle
—-complaints :
1-Breathlessness, cough
2-Chest pain
3-Haemoptysis
—Physical examination :
1-Mitral facies
2-Jugular vein distension
3-Diastolic thrill at the apex
–Percussion : Increase in absolute dullness of the heart (dilatation of the right ventricle)
—Auscultatory signs :
* Accentuated S1 at the apex
* Accentuated pulmonary S2
* The diastolic murmur of mitral stenosis is of low pitch
—Blood pressure and pulse :
1-* In significant left atrium hypertrophy the left clavicular artery is compressed and pulse filling on the left arm is decreased – pulsus differens.
2-* In decreased filling of left ventricle and diminished cardiac stroke volume – pulsus parvus
3-* Mitral stenosis is frequently complicated by atrial fibrillation – pulsus irregular.
4-* Blood pressure is usually normal, sometimes the systolic pressure is slightly decreased and diastolic – increased.
—Complications :
1-Thromboembolic complications
2-Chronic heart failure

Question 9

39. Syndrome of mitral incompetence.

Answer 9

— Causes : we have 2 types :
1-* Absolute (destruction of valvular leaflets):
-Rheumatic heart disease
-Mitral valve prolapse
-Infective endocarditis
2-* Relative (dilation of left ventricle):
-Cardiomyopathy
—hemodynamics abnormalities:
-left atrium increases, dilates and hypertrophies
-overfilling and dilatation of the left ventricle
-congestion in the pulmonary circulation
-right ventricle hypertrophy
—Physical examination:
1-On precordium palpation apical impulse displacement to the left and sometimes downward is disclosed
2-Pulse and blood pressure in compensated mitral incompetence don’t change
—Percussion:
* mitral configuration with smoothed cardiac waist
* right ventricle hypertrophy cardiac dullness also shifts to the right.
—Auscultation:
Systolic murmur: a high pitched pansystolic murmur at the apex is transmitted to the left axilla.
—Complications :
* Thromboembolic complications
* Episodes of acute pulmonary edema (acute heart failure)
* Chronic heart failure

Question 10

40. Syndrome of aortic stenosis.

Answer 10

—DF : A narrowing of the outflow tract of the left ventricle in the aortic valve area with impaired blood flow from the left
ventricle to the aorta in systole
—Causes :
1- Atherosclerotic
2-Rheumatic heart disease
—hemodynamics abnormalities:
1-Decompensation stage: decrease of left ventricular
contractile capacity,
2-The left ventricular dilatation occurs, then hypertrophy and dilatation of the left atrium, followed by hypertrophy and dilation of the right heart.
—Clinical manifestations:
* anginal pains
* dizziness and syncope due to small cardiac output
* arrhythmias
— Percussion :
* displacement of relative dullness borders to
the left and aortic heart configuration
—Heart auscultation:
* diminished S1 at the apex, connected with left ventricle
overfilling and lengthening of its systole
* diminished S2 at the aorta
* rough systolic murmur,
—Blood pressure :
* pulse becomes small, slow and rare (pulsus parvus,
tardus et rarus)
* pulse pressure becomes decreased.
—Complications :
* Heart failure
* signs of decompensation stage (dyspnea, edema, swelling neck veins, liver enlargemen)

Question 11

41. Syndrome of aortic incompetence

Answer 11

—DF : a non-closure of the aortic valve leaflets resulting in
regurgitation of blood from the aorta to the left
ventricle during diastole.
—Causes:
* infectious endocarditis
* atherosclerotic lesion
* rheumatic fever
* syphilis
—Clinical manifestations :
* anginal pains
* dizziness and syncope
—General examination :
* skin pallor
* peripheral arteries pulsation: carotids
(”carotid’s dance’’- Corrigan pulse)
—Percussion data :
* displacement of relative dullness borders to the left and aortic heart configuration
—auscultation:
* diminished S1 at the apex,
diminished S2 at the aorta
* diastolic murmur
—-Blood pressure and pulse :
* pulse fast, high, big (pulsus celer, altus, magnus)
* pulse pressure is high
—Complications :
- left ventricular heart failure
- cardiac asthma attack
- coronary insufficiency with development angina syndrome;
- rhythm disturbance;

Question 12

42. Syndrome of tricuspid incompetence (organic and functional)

Answer 12

—Causes: we have 2 types
1-* Organic (rarely): endocarditis, frequently
rheumatic
2-* Relative (more frequently)- right ventricular
dilatation and right atrioventricular orifice distension
—hemodynamics abnormalities :
-During right ventricular systole because of incomplete closure of valve leaflets part of blood regurgitates back to the right atrium, in which usual volume of blood from venas cava simultaneously passes right atrium dilatation and hypertrophy
— Clinical manifestations:
1-Significant venous congestion in systemic
circulation in tricuspid incompetence:
edema, ascites
2-Skin acquires cyanotic colouring
—Physical examination :
* Neck veins swelling and pulsation,
* Positive vein pulse,
* Liver pulsation,
—Percussion :
* On percussion significant displacement of cardiac dullness borders to the right owing to right atrium and right ventricular hypertrophy is detected.
—Auscultation :
1-Diminished S1 at the xyphoid process base is found;
2-Diminished S2 at the pulmonary artery
—-Complications:
1-severe circulatory insufficiency
2-cardiac cirrhosis.

Question 13

43. Heart failure (acute and chronic)

Answer 13

–DF : it is a syndrome or a pathological condition in which the heart is unable to deliver to the organs and tissues the amount of
oxygen and nutrients necessary for normal functioning,
–Causes :
1- Impaired systolic function :
1-1. Damage to the heart muscle
* primary (myocarditis, myocardial infarction, chronic ischemic heart disease,
cardiosclerosis)
* secondary (hypo- or hyperthyroidism, anemia, obesity)
1-2. Hemodynamic myocardial overload
* pressure (hypertension of a large or small circle of blood circulation, stenotic defects)
* volume (valvular heart failure, intracardiac shunts)
* combined (combined heart defects, concomitant heart disease)
2-Disturbance of diastolic filling of ventricles :
* myocardial hypertrophy
* cardiosclerosis,
* adhesive pericarditis,
3-Heart rhythm disorders:
* atrial fibrillation, tachycardia/bradycardia.
-Types :
1-By heart dysfunction :
-systolic
-diastolic
2-By the rate of development of symptoms :
-Acute
-Chronic
3-Depending on the primary lesion of the left, right or both ventricles :
1-left ventricular (stagnation in the pulmonary circulation)
2-right ventricular (stagnation in the systemic circulation) total

Question 14

44. Hypertension syndrome - essential hypertension and secondary (symptomatic).

Answer 14

–DF : Arterial hypertension is a persistent increase in blood pressure - systolic over 140, diastolic over 90 mm Hg.
–Types:
1. Primary:, essential arterial hypertension (AH) - 90– 95%: is established in the absence of a secondary cause of increased blood pressure.

2. Secondary:, symptomatic hypertension (5-10%)
   –Casues :
3. Renal
4. Endocrine :
   – pheochromocytoma
5. Hypertension caused by damage to
   large arterial vessels (hemodynamic),
   atherosclerosis.
   —Features of Arterial Hypertension for symptomatic (secondary) types :
   * 1) relatively young age of patients with
   hypertension (up to 30 years);
   * 2) acute onset of the disease with rapid stabilization of blood pressure at high levels.
   —Grades :
   - Norm : S less then 140 / D less then 90
   -stage 1 : S 140-160 / D 90-100
   -Stage 2 : S 160-180 / D 100-110
   -stage 3 : S more then 180 /
   D more then 110
   -Hypertension in DM,RF :
   its should be mess then 130/80
   –Target Organs :
   1-Brain : Cerebrovascular disease: ischemic or hemorrhagic stroke, transient ischemic attack; chronic circulatory encephalopathy;
   2-Heart:LVH, angina pectoris, MI,
   acute and chronic heart
   failure, arrhythmias;
   3-kidneys : Microalbuminuria, ↓GFR,
   nephrosclerosis, acute and chronic
   renal failure;
   4-Vessels : dissecting aneurysm,
   damage to peripheral
   arteries;
   —Complaints :
   1-due to myocardial damage :
   * Cardialgia * Palpitation, arrhythmia
   2-due to brain damage :
   * Headaches in the occipital and temporal regions
   * dizziness, visual disturbances
   3-due to excessive activation of the RAAS :
   * Edema
   * nocturia
   –General examination :
   * Overweight or obesity
   * Signs of lipid metabolism disorders
   * swelling of the face, limbs
   * Corneal arch
   –Physical data:
   * Apical beat – is displaced to the left
   * S1 tone at the apex - weakened.
   * S2 tone on the aorta - enhanced
   * With severe LVH and its dilatation - systolic murmur of mitral regurgitation.
   * Pulse - hard, tense, large.
   –Stages :
   Stage I - mild or moderate arterial
   hypertension without target organ
   damag
   Stage II - moderate or significant
   arterial hypertension with target
   organ damage
   Stage III - moderate or significant
   arterial hypertension in the
   presence of complications or
   associated clinical conditions

Question 15

45. Coronary insufficiency syndrome.

Question 16

46. Hypersecretory syndrome of the stomach.

Answer 16

-DF : This syndrome is caused by an increase in the
production of hydrochloric acid and pepsin
activity,
-Provking factors :
* Disturbance of diet (dry eating, very hot, spicy
* food, etc.)
* Irregular nutrition
* Alcohol abuse, smoking
* Helicobacter pylori
-Causes :
1. Chronic gastritis with increased secretory activity of the stomach
* 2. Peptic ulcer with localization in the duodenum and antrum (pyloric) stomach
* 3. Duodenitis
-Complaints :
* heartburn after eating,
* sour belching;
* vomiting acidic masses, facilitating the patient’s condition;
* increased appetite;
-Mechansim of pain :
* Spastic:
* definite localization - in the epigastric region to the right of the midline and in the right hypochondrium
* irradiation in the back
* paroxysmal
-Dudenal Vs gastric :
1- Dudenal :
Pain is relave by meal ,occures 2-3h after meal
,Dark stool (malena )
2-Gastric :
Pain increasced by meal , occuers after 30 min of meal , vomating occures
- Inspection and Palpation :
* Forced position of the body (pose of the “embryo”)
* soreness in the epigastric region
-Sgins : Fibrogastroduodenoscopy
* Signs of hypersecretion (erosion, ulcers, fibrin, pinpoint hemorrhages)

Question 17

47. Hyposecretory syndrome of the stomach.

Answer 17

-DF : This syndrome is caused by a decrease in gastric secretion and is combined with a decrease in the motor activity of the stomach
-Causes :
* 1. Atrophic gastritis
* 2. Gastric ulcer
* 3. Cancer of the stomach
-Complains :
* decreased appetite;
* belching after meals
* intolerance to fatty and coarse foods, milk and dairy products;
* nausea;
* diarrhea
-mechnasim of pain :
* associated with distended stomach.
* occur after eating, sometimes immediately, often after 30-40 minutes (early pain)
* low-intensity, dull, aching pains or only a feeling of heaviness in the epigastric region, sometimes to the left of the midline, without clear localization and without irradiation. The pain disappears usually after 2-3 hours.
- Inspection and palpation :
* Weight loss
* Signs of anemia due to malabsorption of iron, vitamin deficiency
* Diffuse tenderness in epigastrium
-Sings :Fibrogastroduodenoscopy
* Hypo- / atrophy of the gastric mucosa

Question 18

48. Abdominal pain syndrome

Answer 18

1-Spastic pain :
-DF : due to spasm of the smooth muscles of the gastrointestinal tract
-Charectarstic : sharp, paroxysmal with a clear localization
-Causes : gastric colic (hypersecretion), intestinal colic, biliary colic
————————-
2-Distension pain :
-DF: associated with hypomotor dyskinesia of smooth muscles and hollow organ distension
-Charectarstic : dull pains, non-intense, without clear localization
-Causes : flatulence, hyposecretory syndrome
—————————-
3-Vascular pain
-DF : associated with a violation of the blood supply
to the abdominal cavity, as a result of this,
ischemia and necrosis develop sudden onset,
very intense, progressive,
-Casuses :mesenteric thrombosis, embolism, ischemic disease of the digestive system
————————–
4-Peritoneal pain :
-DF :based on tension of the capsule or visceral sheet of the peritoneum
-Charetrstic :peritoneal pain occurs gradually or suddenly (with perforation), increases, intense, accompanied by tension of the abdominal wall,
-Causes :peritonitis due to inflammation of the organs
(appendicitis, acute cholecystitis, acute pancreatitis) and perforation of the stomach and intestines
——————————–
5-Acute Abdomen Syndrome :
* Acute surgical pathology:
* Perforated ulcer of the stomach and duodenum
* Acute appendicitis
* Acute cholecystitis
* Acute pancreatitis
* Bowel obstruction

Question 19

49. Gastrointestinal bleeding Syndrome.

Answer 19

DF :can originate anywhere from the mouth to the anus and can be overt or occult.
-Casuses :
1-Upper tract :
* Duodenal ulcer (20–30%)
* Gastric or duodenal erosions (20–30%)
* Varices (15–20%)
* Gastric ulcer (10–20%)
2-Lower GI tract:
* Anal fissures
* Angiodysplasia (vascular ectasia)
* Colitis: Radiation, ischemic, infectious
* Colonic carcinoma
* Colonic polyps
-sings :Red flags! Several findings suggest hypovolemia or
hemorrhagic shock:
* Syncope
* Hypotension
* Pallor
* Sweating
* Tachycardia
-Types :
1.Hematemesis
2.Hematochezia
3.Melena
-Physical examination :
* indicators of shock or hypovolemia: tachycardia,
* tachypnea, * pallor, * diaphoresis, * oliguria,
-Testing :
* Complete blood count (CBC), coagulation profile,
* Upper endoscopy for suspected upper GI bleeding
* Colonoscopy for lower GI bleeding
* Flexible sigmoidoscopy and anoscopy
* Digital rectal examination
——————————————————
1-Hematemesis :
-DF :is vomiting of red blood and indicates upper GI bleeding, usually from a peptic ulcer, vascular lesion, or varix
-Charectarstic : Coffee-ground emesis is vomiting of
dark brown, granular material that
resembles coffee grounds
-Pathoginsis :It results from upper GI bleeding that has slowed or stopped, with conversion of red hemoglobin to brown hematin by gastric acid.
————————————
2-Melena :
-DF : is black, tarry stool and typically indicates upper GI
bleeding, but bleeding from a source in the small bowel
-Location : ileocecal valve
-NB! : Black stool that does not contain occult blood may result
from ingestion of iron, bismuth, or various foods and
should not be mistaken for melena
——————————————
3-Hematochezia :
-DF : is the passage of gross blood ( braight or dark red ) from the rectum and usually indicates lower GI bleeding but may result from vigorous upper GI bleeding with rapid transit of blood through the intestines.

Question 20

50. Disturbance of the evacuation of the stomach syndrome.

Answer 20

-DF : Acquired pyloric stenosis is a narrowing of the
pyloric (output) section of the stomach, which
is a consequence of stomach diseases in
adults
-Casues : peptic ulcer or tumer in the ploric orfecis
-Pathoginisis :
1-Initial stage- the muscles of the stomach are still able to overcome the obstacle that arises, and the food lingers in the stomach for a short time.
2-Progressive stage - food lingers for a longer time, the stomach grows in size, and atony of its muscles develops. As a result, food ceases to pass into the duodenum almost completely.
-Complains:
1.a feeling of fullness in the upper abdomen after eating, periodically occurring vomiting,
2.In advanced cases, the patient’s condition becomes severe, vomiting may be absent, as a result of a large loss of fluid, convulsions develop.
-Objactive data :
1.enlarged contours of the stomach in the upper abdomen
2.↓ body weight up to cachexia
3.convulsions
-Diagnosis ;
1.X-ray
* Gastroptosis
* Stomach is enlarged, stretched, hypotonic,
* Evacuation is dramatically slowed down
* On an empty stomach contains a lot of liquid and food masses
2.Fibrogastroduodenoscopy : * Pylorosthenosis

Question 21

51. Malabsorption syndrome and digestion

Answer 21

-DF :refers to a number of disorders in which
nutrients from food are not absorbed properly
in the small intestine.
-Causes ;
* Gastrectomy, Intestinal resection
* Biliary obstruction and cholestasis
* Cirrhosis
* Chronic pancreatitis, Pancreatic cancer, Pancreatic resection
* Cystic fibrosis
-Symptoms and sings :
* Chronic diarrhea
* Steatorrhea—fatty stool, the hall mark of malabsorption—occurs when > 7 g/day of fat are excreted.
* Steatorrhea causes foul-smelling, pale, bulky, and greasy stools.
* Abdominal pain, distention
* Increased flatulence
* Lose weight
* Other symptoms result from nutritional deficiencies.
* Anemia
* Amenorrhea
-Diagnosis :
1. Blood tests (complete blood count, ferritin, vitamin B12, folate, calcium, albumin, cholesterol, prothrombin time)
2. Stool fat testing to confirm malabsorption
3.Contrast x-rays

Question 22

52. Syndrome of exocrine pancreatic insufficiency.

Answer 22

-DF : is a condition characterized by deficiency of the exocrine pancreatic enzymes, resulting in the inability to digest food properly, or maldigestion. Pancreatic insufficiency causes malabsorption if > 90% of function is lost
-Causes :
* Chronic pancreatitis (the most common cause of EPI)
* Acute pancreatitis
* Cystic fibrosis
* Obstructions of the pancreatic duct (eg, from pancreatic cancer)
-Clinical picture :
* The exocrine pancreas produces three main types of enzymes: amylase, protease, and lipase.
* When lipase and protease secretions are reduced to < 10% of normal, the patient develops malabsorption characterized by steatorrhea, the passing of greasy stools. In severe cases, undernutrition, weight loss, and malabsorption of fat-soluble vitamins (A, D, E, and K) may also occur.
-Dyspeptic syndrome : * increased salivation, * air or eaten food
eructation, * nausea, vomiting, * loss of appetite, * fatty food intolerance, flatulence * weight loss
-Pancreatic diarrheas and malabsorption and maldigestion syndromes :
* are characteristic of severe pancreatic exocrine insufficiency,
* diarrhea are caused by alterations of pancreatic enzymes release and intestinal digestion,
* excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine.
-Diagnosis :
1.X Ray
2. Ultra sound

Question 23

53. Syndrome of jaundice.

Answer 23

-there is 3 types :
1-hemolytic
-Df : Hemolytic (suprahepatic or prehepatic) - high blood levels of unconjugated (indirect) bilirubin
-mechansim :Increased formation of unconjugated (indirect) bilirubin from the RBC
-Causes :
1.sickle anemia
2.Malaria
3.thalssmia
-clincial picture :
* Skin color - lemon yellow.
* The color of the urine is not changed or darker than usual.
* Stool color normal or dark
* Hepatomegaly
* Splenomegaly
-Laboratory changes:
* ↑ indirect bilirubin in the blood,
* ↑ urobilin in the urine,
* ↑ Increased stercobilin in feces
* Bilirubin is absent in the urine
————————————-
2-hepatic
-DF : Hepatic cell (parenchymal) - increased blood levels of both indirect and direct bilirubin.
-Mechansim : Hepatocyte damage
-Causes :
-hepatitis,
-cirhosis,
-liver cancer
-alcohol;
- viruses;
- medicines;
-Clincial picture :
* Skin color - yellow
* Urine is darker than usual
* The stool color is not changed or discolored.
* Hepatomegaly
* Splenomegaly
-Laboratory changes:
* ↑ direct (to a greater extent) and indirect bilirubin in the blood,
* ↑ urobilin in the urine
* urine bilirubin is determined
* stercobilin in feces is normal or ↓(reduced)
——————————————
3-mechanical
-DF :Mechanical (subhepatic or post-hepatic, obstructive) - high blood levels of conjugated (direct) bilirubin
-Mechansim ;Biliary obstruction
-Causes :
-Cholelithiasis
-Pancreatic head tumor
-Bile duct cancer
-Clinical picture :
* Skin Color: Dark Yellow
* Itchy skin
* The color of urine is very dark (like beer)
* Feces - discolored
-Laboratory changes :
* ↑ Direct bilirubin in the blood,
* ↑ bilirubin in urine
* Urobilin is absent in urine
* Stercobilin in feces is absen

Question 24

54. Syndrome of portal hypertension.

Answer 24

-DF : this is an increase in pressure in the portal vein system caused by a disturbance of blood flow in the portal vessels, hepatic veins, and the inferior vena cava
-Types :
1.Posthepatic form of Portal Hypertension : caused by difficulty in the outflow of blood from the hepatic veins. It is manifested by the development of:
-ascites,
-pain in the liver,
-significant hepatomegaly with a relatively small increase in the spleen.
2.intahepatic : the most common cause of portal hypertension
(80% of all cases). Obstruction of blood flow is in the liver itself.
* Persistent dyspeptic syndrome,
* flatulence, * diarrhea, * weight loss.
* In the later stages - splenomegaly with hypersplenism,
* varicose veins with possible bleeding * ascites.
3.Prehepatic form of Portal Hypertension : occurs with occlusion of the portal or splenic veins.
* liver is usually not enlarged
* splenomegaly with hypersplenism without bleeding and ascites,
* less frequent repeated bleeding from the veins of the esophagus, followed by ascites
-Mixed form of portal hypertension syndrome :is associated with the
development of portal vein thrombosis in patients with cirrhosis
-Manifestations:
1. Ascites
2. Signs of collateral circulation: - varicose veins of the esophagus;;
- “medusa head”;
3. Splenomegaly, hypersplenism
4.Bleeding from varicose veins
-General examination :
1.Drum sticks
2.Ascitits
3.Medusa viens
-Diagnostics:
* Ultrasound examination of the liver
* Esophagogastroduodenoscopy

Question 25

55. Hepato-lienal syndrome

Answer 25

-DF ;combined lesion of the liver and spleen, due to their close connection
with the portal vein system, the generality of innervation, and the
pathways of lymphatic drainage.
-Causes :diffuse liver damage,circulatory disorders in the portal vein system, accumulation diseases (amyloidosis), systemic blood diseases, sepsis, heart failure
-Clinical picture:
1 - with portal hypertension - a large spleen (there may be more liver), hypersplenism;
2- with congestive heart failure - spleen is slightly increased, hypersplenism is absent;
3 - infiltrative lesions can be equally expressed in both organs (with sepsis), mainly in the spleen (with hemoblastosis),
—Hypersplenism :
-DF :accompanies a significant increase in the spleen and is manifested by an increase in its normal function to remove destroyed blood cells.
-Causes :all forms of portal hypertension, granulomatosis with enlarged spleen
-Clinical picture :
*can be asymptomatic,
* sometimes manifested by a feeling of heaviness in the left hypochondrium;
* palpation - pain and enlargement of the spleen,
* hemorrhagic syndrome.
-Laboratory changes:
* anemia,
* leukopenia,
* thrombocytopenia.

Question 26

56. Syndrome of hepatic failure

Answer 26

-DF ;impaired liver function due to acute or chronic damage to hepatocytes
-Types :
1.Chronic :* hepatitis, * cirrhosis, * tumors, * heart failure;
2.Acute: * drug damage, * poisons, * sepsis, * shock,
–Main indicators of hepatic cell failure: :
* 1. Disturbance of the protein-synthetic function of the liver
* 2. Disturbance of the carbohydrate function of the liver
* 3. Disturbance of lipid function of the liver
* 4. Disturbance liver pigment function
* 5. Disturbance of the neutralizing function of the liver
–hepatic coma :
-DF ;If the underlying cause of liver disease isn’t treated, liver function deteriorates, and toxins continue to build. Some people with advanced hepatic encephalopathy lose consciousness and go into a hepatic coma
-Clincial sings :
1. Developing coma: drowsiness, marked disorientation in space, clapping tremor of the fingers, eyelids, ataxia, dysarthria, reflexes are increased, handwriting disorder, fever,
* 2. Sopor, pronounced disorientation in space.
* 3. Hepatic coma (deep coma):
* hepatic odor from the mouth,
* jaundice
–hepatic encephalopathy
-DF ;is defined as a brain dysfunction caused by liver insufficiency and/or portal-systemic blood shunting
-Clinical sings :
* 1. Mental disturbance: sleep disturbance in the form of inversion, the appearance of nightmare dreams, memory, intelligence are gradually
reduced, dementia develops.
* 2. Movement disorders: small tremor of the fingers resembles “flapping the wings of a bird”, bradykinesia, increased tendon reflexes, impaired
coordination.
* 3. Change of the encephalogram (EEG): inconstant and weakly expressed.

Question 27

57. Nephritic syndrome

Answer 27

–DF :
* this symptom complex is characterized by inflammation of the glomerular apparatus of the kidneys.
* The occurrence of acute nephritic syndrome is most
characteristic of acute post-streptococcal nephritis (especially
in children and young men), 2-3 weeks after the infection
–Causes:
* 1. Infections
* 1.1. Acute post-streptococcal glomerulonephritis
* 1.2. Other glomerulonephritis associated with
* infection: - bacterial: infectious endocarditis, sepsis; -viral: hepatitis B and C, - parasitic: malaria,btoxoplasmosis
* 2. Primary chronic glomerulonephritis
* 3. Systemic diseases:
* - systemic lupus erythematosus;
* - systemic vasculitis;
—Manifestations:
* 1. Edema (periorbital puffiness, ankle edema from latent edema to anasarca)
* 2. Urinary syndrome (brown or cola-coloured urine, proteinuria <3.5 g / day).
* 3. Arterial hypertension
* 4. Oliguria
–Complications:
1. Renal eclampsia:
* - a significant increase in blood pressure;
* - cramps;
* - visual impairment;
* - coma
2. Acute left ventricular failure:
* cardiac asthma, pulmonary edema
3. Acute renal failure

Question 28

58. Syndrome of renal hypertension

Answer 28

–DF : Hypertensive syndrome is a pathological condition,
which is based on an increase in blood pressure due
to pathology of the kidneys or renal vessels
–Hypertensive syndrome may be detected in:
* 1) parenchymal (acute and chronic glomerulonephritis
chronic pyelonephritis, diabetic nephropathy, nephrocarcinoma, polycystic kidney disease;
* 2) Vasorenal hypertension renal artery stenosis
atherosclerosis of the vessels of the kidneys, aortoarteritis
–Patogenesis:
* vasorenal or renoparenchymal genesis of hypertension
- retention of Na and water due to activation of reninangiotensin-aldosteron system (RAAS) and depression
of prostaglandin-callecrein system function
–Manifestations :
* depends on degree of BP elevation and damage of cardiovascular system. Changes in urine appears before increase of BP.
* headache, blurred vision, pain in the heart, shortness of breath
* ↑BP (especially high and persistent diastolic pressure),
* left ventricular hypertrophy
* pronounced retinopathy
* systolic murmur during auscultation of the abdomen at the site of projection of the renal arteries,
* signs of narrowing of the renal vessel during aortography
–Complications of malignant arterial hypertension:
* loss of vision (blindness),
* hypertensive encephalopathy,
* heart failure

Question 29

59. Syndrome of renal failure, uremic coma

Answer 29

–df :The clinical condition resulting from chronic
derangement and insufficiency of renal excretory and
regulatory function (uremia)
–Eitology :
* glomerulonephritis - 57.4%;
* pyelonephritis - 13.9%;
* polycystic kidney disease - 11.1%;
* diabetic nephrosclerosis - 5.1%;
* congenital and hereditary lesions of the kidneys - 3.8%;
* systemic diseases –2.2%;
* arterial hypertension - 2.0%;
* amyloidosis - 0.9%
–clinincal manfsitation :
1-Cardiovascular: High blood pressure, increased heart rate
2-Immune: Increased risk of infection
3-Musculoskeletal :Renal osteodystrophy, decreased calcium, vitamin D impairment, hyperparathyroidism, pathological fractures
4-Neurological: Peripheral neuropathy, restless legs, change in level of consciousness,
5-Gastrointestinal: Anorexia, nausea, vomiting, halitosis, metallic taste in mouth, bleeding in gastrointestinal tract
Renal: Decreased urine output, azotemia, proteinuria, hernaturia, hyperuricemia
6-Respiratory : Increased respiratory rate, Kussmaul respirations, crackles, decreased Po2
–Diagnosis :
* - a decrease in glomerular filtration rate, an increase
in the concentration of creatinine, urea, potassium,
uric acid;
* - a decrease in the specific gravity of urine (isostenuria, hypostenuria);
* - reduction in hemoglobin, erythropoietin
production;
* - metabolic acidosis;
* - violation of phosphorus-calcium metabolism;
* - reduction in the size of the kidneys and parenchyma
–Classification of chronic renal failure:
is based on the grade of severity and characteristic clinical
manifestations.
* Mild: GFR is 30—50 ml/min.
* Moderate: GFR is 10—30 ml/min.
— anemia;
— hypertension;
— osteodystrophy.
* Grave: GFR is 5—10 ml/min.
— nausea;
— anorexia;
— pruritus.
* Terminal (end-stage): GFR is < 5 ml/min.
— pericarditis; — pulmonary edema; — coma.

Question 30

60. Nephrotic syndrome

Answer 30

–DF : is a complex of symptoms, including:
* Massive proteinuria (>3.5 g/24 h)
* Hypoalbuminemia (< 35 g/l)
* Disproteinemia (hyper-α2- globulinemia)
* Dislipidemia (cholesterol increase)
* Edema (due to ↓of serum oncotic pressure and retention of Na )
-NB! : Arterial hypertension and hematuria are
not characteristic signs of nephrotic
syndrome!
–Etiology :
1. Primary glomerulonephritis (acute and chronic)
2. Kidney damage in the following conditions:
* a) infectious and parasitic diseases - chronic viral hepatitis; malaria, schistosomiasis; infectious endocarditis;
* b) systemic diseases - systemic lupus erythematosus, hemorrhagic vasculitis; rheumatoid arthritis;
* c) amyloidosis;
* d) diabetes mellitus;
* e) tumors - paraneoplastic nephrotic syndrome with
bronchogenic cancer, cancer of the parenchyma of the kidney,
stomach, colon, malignant lymphoma;
3. Drug damage to the kidneys: antiepileptic drugs, gold
preparations, mercury, D-penicillamine, antibiotics).
–Clinical manifestations
* The leading clinical sign of nephrotic syndrome is edema,
from moderate to degree anasarca with dropsy cavities
(ascites, hydrothorax, hydropericardium).
* skin - pale, dry, atrophic.
–Complications of nephrotic syndrome:
* 1. infectious (bacterial, viral, fungal), due to the low
content of immunoglobulins lost with urine proteins.
frequent pneumonia, pleurisy.
* 2. vascular - peripheral phlebo- and
arteriothromboses (pulmonary embolism, thrombosis
of the arteries of the kidney with the development of
necrosis of its parenchyma, strokes, myocardial
infarction), in connection with severe
hypercoagulation.
* In patients with NS due to severe dyslipidemia, the
development of atherosclerosis occurs earlier.
Hyperlipidemia is a factor in the progression of
glomerular damage and leads to glomerulosclerosis
–Diagnosis :
* 1. Urinalysis - high relative density (may
* reach 1,030-1,050), contains hyaline, granular,
* epithelial and waxy cylinders, white blood cells.
* 2. Immunological studies
* 3. Kidney biopsy
* 4. Blood test – hyperfibrinogenemia.