Internal Diseases 6th year

Theoretical questions for the exam

Diseases of the cardiovascular system

1. Non-coronary myocardial diseases: cardiomyopathies. Classification. Main syndromes. Diagnostic criteria.

Differential diagnosis. Treatment.

Non-coronary myocardial diseases: cardiomyopathies. Classification. Clinical presentation. Diagnostic criteria. Differential diagnosis and treatment.
the main types of cardiomyopathies are: Dilated cardiomyopathy (DCM); Hypertrophic cardiomyopathy (HCM); Restrictive cardiomyopathy (RCM)
cardiomyopathy is asymptomatic in the early stages, symptoms are the same as those characteristically seen in any type of heart failure and
may include shortness of breath, fatigue, cough, orthopnea, paroxysmal nocturnal dyspnea, and edema.
The cardiomyopathy is considered dilated if the following criteria can be observed 1) left ventricular end-diastolic diameter (LVEDd) > 117% of
the age and body surface 2) left ventricular systolic dysfunction (LVSD) defined by left ventricular ejection fraction (LVEF) < 45% and/or 3)
fractional shortening (FS) < 25%.
Differential diagnosis:
Dilated cardiomyopathy should be differentiated from other causes of cardiac dysfunction, in particular acute coronary syndrome, other
cardiomyopathies (hypertrophic, restrictive, and
ARVC/D), myocarditis, pericarditis, and cardiac toxicities. Toxins.
Treatment
Alcohol septal ablation (nonsurgical procedure) – In this procedure, ethanol (a type of alcohol) is injected through a tube into the small artery
that supplies blood to the area of heart muscle thickened by HCM. The alcohol causes these cells to die. The thickened tissue shrinks to a more
normal size.
Coronary artery bypass surgery and Heart transplant
2. Non-coronary myocardial diseases: myocarditis. Classification. Main
syndromes. Diagnostic criteria Differential diagnosis. Treatment.
Myocarditis-Myocarditis is an inflammation of the heart muscle (myocardium). The
inflammation can reduce the heart's ability to pump and cause rapid or irregular
heart rhythms (arrhythmias). Infection with a virus usually causes myocarditis
Classification
3. Infective endocarditis. Classification. Main syndromes. Differential
diagnosis. Treatment. Indications for surgical treatment.
Infective Endocarditis: a microbial infection of the endocardial surface of the heart. Common site. heart valve, but may occur at septal defect, on chordae tendinae or in the mural endocardium
❖ Classification:
o acute or subacute-chronic on temporal basis, o severity of presentation and progression
o By organism
o Nativevalveorprostheticvalve
❖ Pathology
o Altered valve surface
o Platelet and fibrin deposition and platelet diseases o Bactermia
o Hemodynamic
❖ Clinical Manifestation
o Fever, most common symptom, sign (but may be absent)
o Anorexia, weight-loss, malaise, night sweats
o Heartmurmur
o Petechiae on the skin, conjunctivae, oral mucosa
o Splenomegaly
o Right-sided endocarditis is not associated with peripheral emboli/phenomena but pulmonary
findings predominate
❖ Osler’s nodes – Tender subcutaneous nodules on finger and toe tips
❖ Janeway lesion – Non tender erythematous pustules
❖ Dukes criteria is used for making diagnosis.

❖ Treatment – Antibiotics targeting specific culture positive organism ❖ Cardio stable drugs
❖ Surgery and valve replacement
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4. Risk factors for the development of ischemic heart disease. Stable
coronary artery disease, diagnostic criteria. Classification. Main syndromes.
Differential diagnosis. Treatment. Indications for coronary stenting, bypass
grafting.
5. Acute coronary syndrome. Criteria for diagnosis of ACS with
ST segment elevation. Main syndromes. Algorithm for
managing a patient with ACS with ST segment elevation.
6.
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 8.. Hypertension. Mechanisms of development. Diagnosis of primary arterial
hypertension. Classification. Main syndromes. Cardiovascular risk
stratification and prevention of cardiovascular mortality.
❖ Hypertension is the pressure of circulating systemic blood which is higher then the normal range required for optimal tissue perfusion and
organ perfusion. Modern understating can be easily explained by the fact that in systemic circulation not only blood flow is enough but a
sufficient pressure is also required which exerts pressure and leads to organ and tissue perfusion. Low blood pressure and even high blood
pressure may lead to defective perfusion, under perfusion and even target end organ damage.
❖ Etiology
o Primary Hypertension or essential
o SecondaryHypertension–Renalcauseorothers
▪ CKD, Obstructive uropathy, Atherosclerosis, Diabetes, Cushing’s, Hyperlipidaemia, Obesity etc.
▪ Endocrinology – Hypothyroidism, Thyrotoxicosis and Conn syndrome
❖ HTN classification :
Elevated : 120−139 mmHg Stage 1 : 140−159 mmHg Stage 2 : > 160 mmHg 80−89 90−99 100
❖ Follow up risk and stratification
Hypertension is the most dangerous and most underestimated slow and progressive death causing disease in the world.
HTN lead to Blood vessel wall damage and plays an important role in plaque formation and coronary disease.
▪ Heart is first organ to be affected with left ventricular hypertrophy ▪ Eyes – retinal damage, retina detachment
▪ Brain – IC haemorrhage
▪ Kidney – CKD and GFR fall
▪ Aorta – Dissection
❖ D/D includes other causes and Cardiomyopathies, Vessel deformities, Pheochormocytoma and other less
but HTN cause causes.
❖ Primary treatment is Lifestyle and Dietary changes to counter HTN (Na+ low and K+ High)
❖ Drug therapy
o Diuretic, Thiazides
o ACE–Inhibitors–(Captopril)
o Calcium channel blockers (Amlodipine) o beta blockers (Carvidolol)
o AldosteroneAntagonist
9.Diagnosis, differential diagnosis and treatment of
primary arterial hypertension.
10. Symptomatic hypertension. Classification. Main
syndromes. Diagnosis criteria, differential diagnosis. The
principles of therapy.
11. Heart rhythm disturbances. Main syndromes. Premature beats. Atrial fibrillation,
atrial flutter. Classification. Main syndromes. Diagnosis. Treatment11. Heart rhythm
disturbances. Main syndromes. Premature beats. Atrial fibrillation, atrial flutter.
Classification. Main syndromes. Diagnosis. Treatment
Cardiac arrhythmias:-A heart arrhythmia (uh-RITH-me-uh) is an irregular heartbeat. Heart rhythm problems (heart arrhythmias) occur when the electrical signals that coordinate the
heart's beats don't work properly. The faulty signaling causes the heart to beat too fast (tachycardia), too slow (bradycardia) or irregularly.
Types:-
In general, heart arrhythmias are grouped by the speed of the heart rate. For example:
a)Tachycardia (tak-ih-KAHR-dee-uh) is a fast heart. The resting heart rate is greater than 100 beats a minute. b) Bradycardia (brad-e-KAHR-dee-uh) is a slow heartbeat. The resting
heart rate is less than 60 beats a minute. Fast heartbeat (tachycardia)
Types of tachycardias include:
Atrial fibrillation (A-fib). Chaotic heart signaling causes a rapid, uncoordinated heart rate. The condition may be temporary, but some A-fib episodes may not stop unless treated. A-fib is
associated with serious complications such as stroke.
Atrial flutter. Atrial flutter is similar to A-fib, but heartbeats are more organized. Atrial flutter is also linked to stroke. Supraventricular tachycardia. Supraventricular tachycardia is a
broad term that includes arrhythmias that start above the lower heart chambers (ventricles). Supraventricular tachycardia causes episodes of a pounding heartbeat (palpitations) that
begin and end abruptly.
Ventricular fibrillation. This type of arrhythmia occurs when rapid, chaotic electrical signals cause the lower heart chambers (ventricles) to quiver instead of contacting in a coordinated
way that pumps blood to the rest of the body. This serious problem can lead to death if a normal heart rhythm isn't restored within minutes. Most people who have ventricular
fibrillation have an underlying heart disease or have experienced serious trauma.
Ventricular tachycardia. This rapid, regular heart rate starts with faulty electrical signals in the lower heart chambers (ventricles). The rapid heart rate doesn't allow the ventricles to
properly fill with blood. As a result, the heart can't pump enough blood to the body. Ventricular tachycardia may not cause serious problems in people with an otherwise healthy heart. In
those with heart disease, ventricular tachycardia can be a medical emergency that requires immediate medical treatment.
Diagnosis:-
1) Electrocardiogram (ECG or EKG)
2) Holter monitor
3) Echocardiogram
4) Stress Test
5) Electrophysiological testing and mapping
Medications:-
Antiarrhythmic drugs are medications used to convert the arrhythmia to a normal sinus rhythm or to prevent an arrhythmia. Other medications may include heart rate-control drugs and
anticoagulant or antiplatelet drugs such as

warfarin (a “blood thinner”) or aspirin, which reduce your risk of stroke or developing blood clots.It is important that you know the names of your medications, why they are prescribed,
how often and at what times to take them, what side effects may occur, and what medications you have previously taken for your arrhythmia.
Surgical Treatment:-
Arrhythmia surgery may also be recommended if you need surgery, such as valve surgery or bypass surgery, to correct other forms of heart disease. The Maze and modified Maze
procedures are two surgeries used to correct atrial fibrillation.
 12. Cardiac arrhythmias: AVRT, VT, VF. Classification.
Main syndromes. The principles of diagnosis and
treatment. Indications for surgical treatment.

Cardiac arrhythmias:-A heart arrhythmia (uh-RITH-me-uh) is an irregular heartbeat. Heart rhythm problems (heart arrhythmias) occur when the electrical signals that coordinate the
heart's beats don't work properly. The faulty signaling causes the heart to beat too fast (tachycardia), too slow (bradycardia) or irregularly.
Types:-
In general, heart arrhythmias are grouped by the speed of the heart rate. For example:
a)Tachycardia (tak-ih-KAHR-dee-uh) is a fast heart. The resting heart rate is greater than 100 beats a minute. b) Bradycardia (brad-e-KAHR-dee-uh) is a slow heartbeat. The resting
heart rate is less than 60 beats a minute. Fast heartbeat (tachycardia)
Types of tachycardias include:
Atrial fibrillation (A-fib). Chaotic heart signaling causes a rapid, uncoordinated heart rate. The condition may be temporary, but some A-fib episodes may not stop unless treated. A-fib is
associated with serious complications such as stroke.
Atrial flutter. Atrial flutter is similar to A-fib, but heartbeats are more organized. Atrial flutter is also linked to stroke. Supraventricular tachycardia. Supraventricular tachycardia is a
broad term that includes arrhythmias that start above the lower heart chambers (ventricles). Supraventricular tachycardia causes episodes of a pounding heartbeat (palpitations) that
begin and end abruptly.
Ventricular fibrillation. This type of arrhythmia occurs when rapid, chaotic electrical signals cause the lower heart chambers (ventricles) to quiver instead of contacting in a coordinated
way that pumps blood to the rest of the body. This serious problem can lead to death if a normal heart rhythm isn't restored within minutes. Most people who have ventricular
fibrillation have an underlying heart disease or have experienced serious trauma.
Ventricular tachycardia. This rapid, regular heart rate starts with faulty electrical signals in the lower heart chambers (ventricles). The rapid heart rate doesn't allow the ventricles to
properly fill with blood. As a result, the heart can't pump enough blood to the body. Ventricular tachycardia may not cause serious problems in people with an otherwise healthy heart.
In those with heart disease, ventricular tachycardia can be a medical emergency that requires immediate medical treatment.
Diagnosis:-
1) Electrocardiogram (ECG or EKG)
2) Holter monitor
3) Echocardiogram
4) Stress Test
5) Electrophysiological testing and mapping
Medications:-
Antiarrhythmic drugs are medications used to convert the arrhythmia to a normal sinus rhythm or to prevent an arrhythmia. Other medications may include heart rate-control drugs
and anticoagulant or antiplatelet drugs such as

warfarin (a “blood thinner”) or aspirin, which reduce your risk of stroke or developing blood clots.It is important that you know the names of your medications, why they are
prescribed, how often and at what times to take them, what side effects may occur, and what medications you have previously taken for your arrhythmia.
Surgical Treatment:-
Arrhythmia surgery may also be recommended if you need surgery, such as valve surgery or bypass surgery, to correct other forms of heart disease. The Maze and modified Maze
procedures are two surgeries used to correct atrial fibrillation.
12. Chronic acalculo
13. Bradycardias. Classification. Main syndromes. The principles
of diagnosis and treatment. Indications for pacemaker
implantation.
14. Chronic heart failure. Classification. Main syndromes.
Treatment.
Definition
A condition in which the heart has trouble pumping blood through the body. It may develop over a long period of time. Symptoms include
shortness of breath, problems exercising, fatigue, and swelling of the feet, ankles, and abdomen.
Etiology
-high blood pressure,
-valve disease,
-thyroid disease,
- kidney disease,
-diabetes, or heart defects present at birth can all cause heart failure
Pathogenesis :
*reduced cardiac output (CO) and increased venous pressure, associated with underlying molecular changes and subsequent damage to and
death of cardiac muscle cells.
*This is composed of three basic elements:
(1) a hemodynamic defense reaction which maintains perfusion pressure in the major organs by increasing circulating

blood volume, inducing vasoconstriction and stimulating the heart;

(2) an inflammatory response (in which the body organs act as if they were facing an exogenous agent), in which inflammatory cytokines and
reactive oxygen species play an important role;
(3) a hypertrophic response and ventricular remodeling, with structural changes in cardiac muscle cells and in the shape of the ventricular
chamber.
Classification of chronic heart failure:
Class I and II are typically considered mild heart failure, while class III and IV are considered more severe or advanced heart failure.
Stage I: High risk of heart failure but no structural heart disease or symptoms of heart failure (pre-heart failure) Stage II: Structural heart
disease but no symptoms of heart failure (pre-heart failure)
Stage III: Structural heart disease and symptoms of heart failure
Stage IV: Refractory heart failure requiring specialized interventions
Sign and symptoms
Chest pain. Fainting or severe weakness. Rapid or irregular heartbeat associated with shortness of breath, chest pain
or fainting. Sudden, severe shortness of breath and coughing up white or pink, foamy mucus.
Diagnosis
*Diagnostic tests for congestive heart failure may include:
*Resting or exercise electrocardiogram (also known as EKG, ECG, or stress test) *Echocardiogram.
*Computed tomography (CT) scan.
*Magnetic resonance imaging (MRI) scan.
*Positron Emission Tomography (PET) scan.
*Biopsy or catheterization of the heart and arteries.
Treatment
Depending on your symptoms, you might take one or more medications, including: Angiotensin-converting enzyme (ACE) inhibitors.
15. The differential diagnosis of heart murmurs. Acquired
valve disease. Main syndromes. Diagnosis. Differential
diagnosis. Treatment. Indications for surgical treatment.
treatment.

Rheumatology

1. Rheumatoid arthritis. Classification. Main syndromes. Diagnosis criteria.

Differential diagnosis of inflammatory joint lesions. Treatment.
 2. Seronegative spondyloarthropathies. Classification. Main
syndromes. Diagnosis, differential diagnosis, treatment.
Ans Seronegative rheumatoid arthritis is a type of rheumatoid arthritis in which certain antibodies are not present
in the blood (most cases of RA are seropositive -- when antibodies are present in the blood).
seronegative test for rheumatoid arthritis means that a person tests negative for rheumatoid factor (RF) and
cyclic citrullinated peptides (CCP).
Clinical presentation -Tenderness, swelling, and redness in the joints.
Pain and stiffness in the palm of the hands, knees, elbows, hips, feet, and ankles.
Inflammation.
Fatigue.
Eye redness.
Diagnosis - seronegative rheumatoid arthritis, a rheumatoid factor (RF) test and an anti-cyclic citrullinated
peptides (anti-CCP) test are performed on the blood. If these tests show positive results, X-rays and physical
examinations are also completed to accurately diagnose RA.
Treatment -Medications, including non-steroidal anti-inflammatories (NSAIDs), disease-modifying anti-rheumatic
drugs (DMARDs), and steroid shots
Physical therapy
3. Osteoarthritis. Classification. Main syndromes. Differential
diagnosis of degenerative joint diseases. Treatment. Possibilities of
surgical treatment.
Definition
Osteoarthritis (OA) is the most common type of joint disease, that can be thought of as a degenerative disorder arising from the
biochemical breakdown of articular (hyaline) cartilage in
The synovial joints, however, it involves not only the articular cartilage but the entire joint organ, including the subchondral bone and
synovium
Classification
(International Classification of Diseases (ICD))
Diseases of the musculoskeletal system and connective tissue (M00-M99)
M00-M25 Arthropathies
M15-M19 Osteoarthritis

M19.01 Primary osteoarthritis, shoulder

M19.02 Primary osteoarthritis, elbow
M19.03 Primary osteoarthritis, wrist
M19.04 Primary osteoarthritis, hand
M19.07 Primary osteoarthritis ankle and foot M19.1 Posttraumatic osteoarthritis of other joints M19.2 Secondary osteoarthritis of other
joints M19.9 Osteoarthritis, unspecified site
Differential diagnosis
1. Periarticular structure derrangement: Periarticular pain that is not reproduced by passive motion or palpation
Of the joint should suggest an alternate etiology such as bursitis, tendonitis or periostitis.
2. Inflammatory arthritis: If the distribution of painful joints includes MCP, wrist, elbow, ankle or shoulder, OA is unlikely, unless there are
specific risk factors (such as occupational, sports-related, history of injury). Prolonged stiffness (greater than one hour) should raise
suspicion for an inflammatory arthritis such as rheumatoid arthritis. Marked warmth and erythema in a joint suggests a crystalline etiology.
Arthrocentesis (aspiration of the joint) can help aid in distinuishing between these types of arthritis if the diagnosis is not clear by history,
physical exam, and radiographs. If there is any suggestion of an infected joint, it should be
Aspirated and the fluid sent for culture as well.
3. Other inflammatory / systemic condition: Weight loss, fatigue, fever and loss of appetite suggest a systemic
Illness such as polymyalgia rheumatica, rheumatoid arthritis, lupus or sepsis or malignancy. Clinical Investigation
(Signs and Symptoms: Hand)
Pain on range of motion.
Hypertrophic changes at diistal and proximal interphalangeal joints (Heberden nodes and bouchard nodes).
Tenderness over carpometacarpal joint of thumb
Clinical Investigation

(Signs and Symptoms: Shoulder)

Pain on range of motion.limiitation of range of motion, especially external rotation. Crepitus on range of motion
Clinical investigation( knee)
Pain on range of motion.
Joint effusion crepitus on range of motion
Presence of popliteal cyst (Baker cyst) lateral instability vallgus or varus deformity Clinical Investigation
(Signs and Symptoms: Hip)
Pain on range of motion.
Pain in buttock
Limitation of range of motion,
Especially internal rotation
Clinical Investigation
(Signs and Symptoms: Foot)
Pain on ambulation, especially at first metatarsophalangeal joint. Limited range of motion of first
Metatarsophalangeal joint,hallux rigidus.
Hallux valgus deformity
Clinical investigation( Spine)
Pain on range of motion.
Limitation of range of motion.
Lower extremity sensory loss, reflex loss, motor weakness
Caused by nerve root impingement. Pseudoclaudication caused by spinal stenosis

Treatment
Long-term Management
Managing symptoms, such as pain, stiffness and swelling. Improving joint mobility and flexibility.
Maintaining a healthy weight.
Getting enough of exercise
(Pain and Anti-inflammatory Medications)
Analgesics: acetaminophen, opioids (narcotics) and an atypical opioid called tramadol.
Nonsteroidal anti-inflammatory drugs (NSAIDs): aspirin, ibuprofen, naproxen, and celecoxib. corticosteroids.
Hyaluronic acid: hyaluronic acid occurs naturally in joint fluid, acting as a shock absorber and lubricant, the injections are done in a doctor’s
office.
Opioids: may ease pain if paracetamol or NSAIDs do not work, but can also cause side effects such as drowsiness, nausea and constipation.
Capsaicin cream: blocking the nerves that send pain messages in the treated area.
(Surgery)
Arthroscopy.
Osteotomy.
Arthroplasty (particularly with knee or hip osteoarthritis) Fusion
7.Systemic vasculitis. Classification. Main syndromes. Diagnostic criteria. Trea
Etiology
Osteoarthritis (OA) has a considerable hereditary component and is considered to be a polygenic disease.
Primary osteoarthritis is caused by the breakdown of cartilage, a rubbery material that eases the friction in
your joints. It can happen in any joint but usually affects your fingers, thumbs, spine, hips, knees, or big toes.
Osteoarthritis is more common in older people

Pathogenesis
4. Systemic lupus erythematosus. Classification. Main
syndromes. Diagnostic criteria. Treatment.
5. Systemic scleroderma. Classification. Main
syndromes. Diagnostic work-up. Treatment.
 6. Polymyositis. Classification. Main syndromes. Diagnostic
criteria. Treatment.
Polymyositis:-A chronic autoimmune systemic disease with a predominant lesion of the striated muscles and no skin unlike Dermatomyositis with skin lesions.
Bohan and Peter classified the idiopathic inflammatory myopathies as follows :
I - Primary idiopathic polymyositis
II - Primary idiopathic dermatomyositis
III - Polymyositis or dermatomyositis associated with malignancy
IV - Childhood polymyositis or dermatomyositis
V - Polymyositis or dermatomyositis associated with another connective-tissue disease
VI - Inclusion body myositis
VII - Miscellaneous (eg, eosinophilic myositis, myositis ossificans, focal myositis, giant cell myositis) Etiopathogenesis of these diseases is not fully understood. An
autoimmune etiology of the Idiopathic inflammatory myopathies is supported by the presence of serum autoantibodies,complement deposition in muscle tissue (in DM
patients), lymphocyte mediated cytotoxicity(CD8 T cell in Polymyositis), and general clinical improvement in response to immunosuppression.
Histopathology
In PM inflammatory infiltrates, composed of invading CD8+ T cells, also known as "killer T cells" typically involve the fascicles. Moreover, perifasicular atrophy is a
characteristic of DM only.
Muscle damage
▪ Muscle weakness of the shoulder, pelvic
girdle (proximal muscles) (95%)
climbing stairs
combing hair
toilet bowl symptom
▪ Back muscles of the neck (80%)
▪ Eye muscles (paraorbital edema) (40%)
▪ Lifting the upper eyelid (ptosis) (30%)
▪ Dysphagia, dysphonia, dysarthria (30%)
▪ Diaphragm, respiratory muscles (30%)
▪ Heart damage (25%)
Diagnostic criteria
1. Proximal muscle weakness
-symmetrical proximal muscle weakness of the shoulder and pelvic girdle
- rapid onset of weakness (from several weeks to several months)
-dysphagia or damage to the respiratory muscles
2.Needle EMG
3.Biopsy
4.Increase in the level of CPK, myoglobin, aldolase,LDH, AST, ALT
Autoantibodies
◼ The myositis-specific autoantibodies (MSAs) against ribonucleoproteins, RNA synthetases of the protein synthesis pathways are present in 20–30% of Idiopathic
inflammatory myopathy patients

◼ The MSAs might best be divided into three broad groups that include (1) anti-tRNA synthetases, (2) antisignal recognition particle (anti-SRP), and (3) others that
includes anti-Mi-2 directed against a component of the nucleosome remodeling deacetylase, antipolymyositis-scleroderma (anti-PM-Scl) directed against peptides of a
nucleolar RNA processing complex, and anti-CADM-140 directed against an important receptor involved in innate immunity
Polymyositis treatment
◼ Prednisolone 1 mg / kg / day improvement (1 week - 3 months) decrease when remission is achieved slowly! (3- 6 months) steroid myopathy (25%!?)
◼ Cytostatics:
◼ Methotrexate (15-25 mg / week)
◼ Azathioprine 100-200 mg / day
◼ CF 400-1000 mg / month
◼ MMF 1-2 g / day
◼ DMARD (rituximab)
7. Systemic vasculitis. Classification. Main syndromes.
Diagnostic criteria. Treatment
Nephrology

1. UTI. Classification. Main syndromes. Diagnostic work-

up. Differential diagnosis. Treatment.
2. UTI in pregnant women and the elderly. Main syndromes.
Differential diagnosis. Diagnostic work-up. Treatment.
3. Interstitial nephritis. Classification. Main syndromes. Diagnostic
work-up. Differential diagnosis. Treatment.
4. Glomerulonephritis. Clinical, morphological classification. The
major glomerular syndromes. Diagnostic work-up. Principles of
differentiated treatment.
5. Diagnostic work-up in nephrotic syndrome.
Amyloidosis. Diabetic nephropathy. Main
syndromes. Classification. Diagnostic work-up.
6. Chronic kidney disease. Classification. Main syndromes.
Principles of treatment in a pre-dialysis period. Indications for
hemodialysis (renal replacement therapy).
Respiratory system diseases

1. Chronic obstructive pulmonary disease. Classification. Main

syndromes. Diagnosis. Differential diagnosis. Treatment.

COPD is characterized by long-term respiratory symptoms and airflow limitation. The main
symptoms include shortness of breath and a cough, which may or may not produce mucus.
Etiology-: • Smoking
• Occupational exposure to dusts and chemicals. • Exposure to fumes from burning fuel.
• Genetics.
Pathogenesis
The molecular pathogenesis of COPD is characterized by airway inflammation; however, evidence
on the relationship between airway inflammation and epithelial apoptosis is lacking. For decades,
necrosis was considered as an accidental form of cell death that did not require any specific
molecular signaling pathways. Classification-:
A (low risk, less symptoms),
B (low risk, more symptoms),
C (high risk, less symptoms),
D (high risk, more symptoms).
clinical picture-:
Shortness of breath, especially during physical activities.
Wheezing.
Chest tightness.
A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or greenish.
Frequent respiratory infections.
Lack of energy.
Unintended weight loss
Differential diagnosis
asthma, congestive heart failure, bronchiectasis, tuberculosis
Treatment-: bronchodilator 1. Albuterol
2. Ipratropium 3. Levalbuterol
2. Bronchial asthma. Classification. Main syndromes.
Diagnosis. Differential diagnosis. Therapeutical basis.
Bronchial asthma (or asthma) is a lung disease. Your airways get narrow and swollen and are blocked
by excess mucus.
Pathogenesis- Airway inflammation is a major factor in the pathogenesis and pathophysiology of
asthma. The importance of inflammation to central features of asthma continues to expand and
underscore this characteristic as a primary target of treatment
Classification includes (1) intermittent asthma,

(2) mild persistent asthma,

(3) moderate persistent asthma,
(4) and severe persistent asthma.
Clinical presentatiomn- Shortness of breath. Chest tightness or pain. Wheezing when exhaling, which
is a common sign of asthma in children. Trouble sleeping caused by shortness of breath, coughing or
wheezing.
D/D :- COPD, cystic fibrosis, bronchitis, and aspiration syndromes can mimic the symptoms and signs
of asthma. Patients with carcinoid syndrome and sarcoidosis may have marked wheeze in the
absence of true asthma. Patients with left heart failure or pulmonary embolus may wheeze similar

During an asthma attack, also called an asthma exacerbation, the airways

become swollen and inflamed. The muscles around the airways contract and the
airways produce extra mucus, causing the breathing (bronchial) tubes to narrow.
During an attack, you may cough, wheeze and have trouble breathing
Emergency therapy would be oxygen therapy
3. Pneumonia. Main syndromes. Diagnostic work-up. Differential
diagnosis of focal infiltrative changes in the lungs. Treatment.
4. Pulmonary disseminations. Classification. Main syndromes. Differential
diagnosis of common conditions: tuberculosis, sarcoidosis, idiopathic
interstitial pneumonia, tumors. Principles of differential diagnosis.
TUBERCULOSIS
Disseminated tuberculosis is a mycobacterial infection in which mycobacteria have spread from the lungs to other parts of the body
through the blood or lymph system.
Exposure - This happens when a person has been in contact with, or exposed to, another person who has TB. The exposed person will have
a negative skin test, a normal chest X-ray, and no signs or symptoms of the disease. Latent TB infection - This happens when a person has
TB bacteria in his or her body, but does not have symptoms of the disease. The infected person's immune system walls off the TB
organisms, and the TB remains inactive throughout life in most people who are infected. This person would have a positive skin test, but a
normal chest X- ray.
TB disease - This describes the person who has signs and symptoms of an active infection. The person would have a positive skin test and
a positive chest X-ray.
ORGANS AFFECTED
Lymph node - Most common extra pulmonary organ affected ; cold abscess
Kidney - Sterile pyuria
Eyes - Phlyctenular conjunctivitis
Ears - multiple perforations in Tympanic membrane
CVS - constrictive pericarditis
Bones - Pott's spine
Adrenal - adrenal insufficiency
Liver - Simmond's Focus ( simon's focus found in Lungs )
GIT - Transverse ulcers in Ileum
Brain - RICH FOCUS
Basal Surface involved
TB meningitis - Cob web coagulum Diagnosis
1.Increase ESR
2.Increase Total leucocyte count 3.Sputum:- Early morning sample
- Petroff's method : sputum concentration method

- Staining : Zn stain - Acid fast bacilli - Culture - LJ media(slow growth)

- Bactec method(faster growth) - PCR - Nucleic acid amplification
4.Pleural Tap:- Straw coloured fluid - increase in adenosine deaminase SARCOIDOSIS
Non caseating granuloma unlike tuberculosis with caseating granuloma Organs affected
Lungs - most commonly involved organ - Interstitial fibrosis
- Unilateral pleural effusion
- Dyspnea
Lymph node - Bilateral hilar lymphadenopathy (potato nodes) Skin - Lupus pernio(violet coloured rash on nose and cheeks)
- Painful Erythema nodosumnodosum on lower limbs Eyes - Uveitis
Liver,Bone marrow,Spleen - Granulomatous lesions present Muscles - weakness
Diagnosis
1.Serum ACE increase
2.Serum calcium increase - increase in 1 alpha hydroxylase - increase in vitamin D 3.Non caseating granuloma present
Schaumann body present Asteroid body present Residual body present
4.Brocho Alveolar Lavage fluid - increase in CD4:CD8 T cells (5:1 to 15:1)
IDIOPATHIC INTERSTITIAL PNEUMONIA
Biopsy
Microscopic examination:-Cellular and fibrosing pattern(same stage lesion co exist) Bilateral reticular opacities on HRCT present.
No fibroblastic foci
TUMORS
Malignant tumors
1.Primary :- Bronchogenic carcinoma 2.Secondary :- Metastasis - Breast cancer
Biopsy:-1.Microscopic examination 2.Immunohistochemistry
- Colon cancer
- Choriocarcinoma
1.Keratin present - intercellular bridge - Pearls(Squamous cell carcinoma) p40 and p63 present.
2.Mucin and gland present(Adenocarcinoma) TTF(Thyroid transcription factor) present Nap A and ck 7 present
3.Small cells with neurosecretory granules(small cell carcinoma)

Salt and pepper chromatin present Basophilic staining(azzopardi effect) Chromogranin present
TTF present
Nap A present
Low molecular weight CK 7,8,18 present
4.Large cells - diagnosis of exclusion(Large cell carcinoma)
CD 56 present Synaptophysin present Chromogranin present.
5. Pulmonary disseminations. Classification. Main syndromes.
Approach to patient with viral pneumonia.
6. Chronic pulmonary insufficiency. Pulmonary heart. Main
syndromes. Diagnostic criteria. Treatment.
7. Acute response allergic reactions. Pathogenesis. Acute urticaria and angioedema.
Treatment principles.
The early asthmatic response After allergen exposure, inflammatory mediators, including
large quantities of histamine, are released from mast cells on the mucosal surfaces.
Histamine causes immediate bronchoconstriction and bronchospasm, resulting in
narrowing of the small airways (bronchioles).
Acute urticaria.
These are hives that last less than 6 weeks. The most common causes are foods,
medications, and infections. Insect bites and diseases may also be responsible. The most
common foods that cause hives are nuts, chocolate, fish, tomatoes, eggs, fresh berries,
and milk
Acute urticaria treatment:-non-sedating antihistamines, such as cetirizine (Zyrtec) or
fexofenadine (Allegra) short-term use of topical steroids. Antiseptic creams to prevent a
secondary infection. Soothing creams to reduce itchiness.
Angioedema is a skin reaction similar to urticaria. It is most often characterised by an
abrupt and short-lived swelling of the skin and mucous membranes. All parts of the body
may be affected but swelling most often occurs around the eyes and lips
Treatment of angioedema :-allergic and idiopathic angioedema are usually treated with
antihistamines or, occasionally, steroid medicine to reduce the swelling
Drug-induced angioedema will usually resolve if you change to a different medicine –
your doctor will advise you about this
Hereditary angioedema cannot be cured, but medicines can help prevent swelling and
quickly treat swelling when it occurs.
7. Algorithm of
Diseases of the digestive system

1. GERD. Risk factors. Clinical and endoscopic features. Diagnostic work-up.

Treatment.
2. Peptic ulcer and duodenal ulcer. Diagnostic work-up. Differential diagnosis
with symptomatic ulcers. Principles of peptic ulcer treatment. Prevention of
relapse.
 3. Chronic pancreatitis. Working classification. Clinic.
Diagnostic work-up. Treatment.
it is a benign inflammatory process and fibrosing disorder characterized by • irreversible morphologic changes, • Progressive and • permanent loss of exocrine and endocrine
function.

(TIGAR –O classification) • Toxic – Metabolic • Idiopathic • Genetic / hereditary • Autoimmune / immunologic • Recurrent acute pancreatitis • Obstructive / mechanical
Toxic / metabolic • alcohol consumption 60 – 90 % • Tobacco (changes in composition , oxidative stress) • Hypercalcemia (trypsinogen & trypsin stabilisation , calculi formation ,
direct acinar cell injury) • CRF – uremia. Idiopathic • Up to 20% of patients with CP have no known risk factors • Based on the bimodal age of onset of the clinical symptoms
– 2 distinct entities • Early onset idiopathic CP - 1. first 2 decades of life, 2. abdominal pain - predominant clinical feature, 3. pancreatic calcifications and exocrine and
endocrine pancreatic insufficiency are very rare at the time of diagnosis.
.
Genetic factors / hereditary : 1. CFTR : Cystic fibrosis is assosiated with ductal dilatation, precipitate formation, pancreatic atrophy 2. PRSS1 : chromosome 7 and regulates
trypsinogen production; mutations - intra- acinar trypsinogen activation - resistant to inactivation - activate other proenzymes - episodes of acute pancreatitis – chronic
pancreatitis
15. Genetic factors / hereditary : 3 . SPINK 1 - serine protease inhibitor Kazal type 1 • regulates the premature activation of trypsinogen • SPINK1 mutations are not enough
to trigger pancreatic inflammation. • they lower the threshold for its development and influence the severity of the disease.
Auto immune / immunological • rare but distinct form of CP characterized by specific histopathologic and immunologic features • Autoimmune diseases , viral infections
(coxsackie) • hallmarks are 1. periductal infiltration by lymphocytes and plasma cells 2. granulocytic epithelial lesions & destruction of the duct epithelium 3. venulitis
Obstructive • scars of the pancreatic duct, • tumors of the ampulla of Vater & head of the pancreas, • Trauma • Main pancreatic duct obstruction may lead to stagnation and
stone formation by pancreatic juice • Leads to recurrent pancreatitis – periductal fibrosis - chronic pancreatitis
Diagnosis • Functional tests • Imaging
Functional tests • fecal elastase 1 level is the preferred noninvasive study to diagnose pancreatic exocrine insufficiency • Normal - > 200 μg/g feces • mild to moderate 100 -
200 μg/g • severe pancreatic exocrine insufficiency< 100 μg/g • Lipase and amylase are of minimal diagnostic value
Imaging • Test of choice previously - ERCP • Test of choice now - CECT • CT has specificity of 85% to 100% for the diagnosis of chronic pancreatitis • dilated pancreatic duct
(68%), parenchymal atrophy (54%), and pancreatic calcifications (50%). • Other findings include peripancreatic fluid, focal pancreatic enlargement, biliary duct dilation, and
irregular pancreatic parenchyma contour
Treatment-Analgesics. Analgesics are pain reducers.
Enzyme Therapy.
High-protein, High-calorie Diets.
Puestow Procedure (Longitudinal Pancreaticojejunostomy)
Whipple Procedure (Pancreaticoduodenectomy)
4. Chronic hepatitis. Classification. Process activity
criteria. Basic therapy. The principles of treatment
of autoimmune hepatitis.
Definition:
Chronic hepatitis is a common reason for persistently abnormal liver function test and forms the background for
the development of much cirrhosis and hepatocellular carcinoma. It is defined as persistence of liver injury with
raised aminotransferase levels or viral markers for more than 6 months.
CLASSIFICATION:
*chronic persistent hepatitis and chronic lobular hepatitis, to the more severe form, formerly called chronic active
hepatitis.
*Common causes include hepatitis B and C viruses and certain drugs. Most people have no symptoms, but some
have vague symptoms, such as a general feeling of illness, poor appetite, and fatigue.Chronic hepatitis can
progress to cirrhosis and ultimately liver cancer and/or liver failure

PROCESS AND ACTIVITY:

Chronic HBV infection results mostly from vertical transmission from mother to neonate. HBV-infected neonates
and children typically experience an immunotolerant phase with normal alanine aminotransferase levels despite
high levels of circulating HBV DNA and HBe antigen, the secreted form of the HBV core antigen.
CRITERIA
Chronic hepatitis B: HBsAg positive for more than six months, serum HBV DNA greater than 20,000 IU per mL
(lower values of 2,000 to 20,000 IU per mL often occur with HBeAg-negative chronic hepatitis B), persistent or
intermittent elevation in alanine transaminase (ALT) or aspartate transaminase (AST) levels, and liver
BASIC THERAPY
Treatment for chronic hepatitis B may include: Antiviral medications. Several antiviral medications — including
entecavir (Baraclude), tenofovir (Viread), lamivudine (Epivir), adefovir (Hepsera) and telbivudine (Tyzeka) — can help
fight the virus and slow its ability to damage your liver.
5. Chronic hepatitis. Classification. Process activity criteria.
6. Liver cirrhosis. Classification. Diagnosis. Treatment of ascitic syndrome, portal hypertension syndrome
(conservative)
7. Liver cirrhosis. The causes and mechanisms of development of liver insufficiency. Stages. Treatment.
8. Chronic acalculous cholecystitis. Diagnostic criteria, differential
diagnosis. Principles of treatment.

Definition:
*Chronic cholecystitis is swelling and irritation of the gallbladder that continues over time.
The gallbladder is a sac located under the liver. It stores bile that is made in the liver. Bile
helps with the digestion of fats in the small intestine. Diagnosis:
Gallbladder wall thickening greater than 3 mm. Striated gallbladder (ie, gallbladder wall
edema) Ultrasonographic Murphy sign (ie, localized gallbladder tenderness)
The test of choice for chronic acalculous cholecystitis is a cholescintigraphy nuclear scan
(HIDA) with the administration of cholecystokinin (CCK). This study examines the function of
the gallbladder. After the radionuclide is administered, CCK is given to stimulate the
gallbladder to empty.
Differential diagnosis:
biliary colic, acute cholangitis, viral hepatitis, alcoholic hepatitis, acute pancreatitis, acute
appendicitis, and irritable bowel syndrome.
Treatment:
* elective laparoscopic cholecystectomy. It has a low morbidity rate and can be performed as
an outpatient surgery. * Treatment for cholecystitis usually involves a hospital stay to control
the inflammation in your gallbladder. Sometimes, surgery is needed. At the hospital, your
doctor will work to control your signs and symptom

9. Chronic inflammatory bowel disease. Ulcerative colitis.

Diagnostic work-up. Treatment. Complications. Indications
for surgery.
10. Chronic inflammatory bowel disease. Crohn's
disease. Complications. Indications for surgery.
11. Differential diagnosis of chronic diarrhea. The main pathogenic
variants. "Basic" and pathogenetic therapy.
12. Differential diagnosis of chronic constipation. Classification of
obstipation syndrome. Diagnostic algorithm. Indications and using the
laxatives.
Hematology

1. Iron deficiency anemia. Main syndromes. Diagnostic work-up. The

principles of IDA therapy.
2. Megaloblastic anemias. Main syndromes. Diagnostic work-
up. Diagnosis and differential diagnosis. Principles of therapy
for megaloblastic anemias.
3. Hemolytic anemias. Main syndromes. Diagnostic work-up.
Differential diagnosis of hemolytic anemias (hereditary,
acquired). The principles of therapy
 4. Differential diagnosis in cytopenia. Main syndromes.
Diagnostic work-up. Myelodysplastic syndromes. Aplastic
anemias. Principles of therapy for aplastic anemia.
Differential diagnosis in cytopenia involves considering conditions like myelodysplastic
syndromes (MDS) and aplastic anemias. Main syndromes associated with cytopenia include
anemia, thrombocytopenia, and neutropenia.

Diagnostic work-up for cytopenia includes a thorough medical history, complete blood count,
peripheral blood smear, bone marrow biopsy, and cytogenetic testing. Differentiating between
MDS and aplastic anemias is crucial.

Myelodysplastic syndromes involve abnormal cell development in the bone marrow, leading to
cytopenias. Aplastic anemias result from bone marrow failure, often due to immune-mediated
destruction.

Principles of therapy for aplastic anemia may include immunosuppressive therapy (such as
anti-thymocyte globulin and cyclosporine), hematopoietic stem cell transplantation in suitable
cases, and supportive care like blood transfusions and infection management.

Consultation with a hematologist is vital for accurate diagnosis and the development of an
appropriate treatment plan based on individual patient characteristics. Regular monitoring is
essential for assessing treatment response and managing potential complications.
5. Hemorrhagic conditions: coagulopathies. Classification.
Main syndromes. Principles of diagnostic work-up and
treatment.
Hemorrhagic conditions related to coagulopathies can be classified into inherited and acquired
disorders. Inherited disorders include hemophilia and von Willebrand disease, while acquired
disorders encompass conditions like liver disease and disseminated intravascular coagulation (DIC).
Main syndromes associated with coagulopathies involve prolonged bleeding, easy bruising, and in
severe cases, spontaneous bleeding.
Diagnostic work-up includes assessing bleeding time, prothrombin time (PT), activated partial
thromboplastin time (aPTT), and specific factor assays. Genetic testing may be necessary for
inherited disorders, and additional investigations like liver function tests can help identify
underlying causes.
Principles of treatment vary based on the specific coagulopathy. For hemophilia, replacement
therapy with clotting factors is essential. In von Willebrand disease, desmopressin and factor
replacement may be used. Management of underlying conditions is crucial for acquired
coagulopathies.
Consultation with a hematologist is vital for accurate diagnosis and developing a tailored treatment
plan. Regular monitoring helps assess treatment efficacy and prevent complications associated with
bleeding disorders.
 6. Hemorrhagic conditions: platelet abnormalities. Classification.
Main syndromes. Principles of diagnostic work-up and
treatment.
Platelet abnormalities leading to hemorrhagic conditions can be classified
into quantitative and qualitative disorders. Quantitative disorders involve a
decrease or increase in platelet count, while qualitative disorders relate to
abnormalities in platelet function.
Main syndromes associated with platelet abnormalities include petechiae,
easy bruising, and prolonged bleeding after minor trauma.
Diagnostic work-up includes a complete blood count (CBC) to assess platelet
count, peripheral blood smear, and specific platelet function assays. In
qualitative disorders, testing may involve platelet aggregation studies.
Identifying the underlying cause is crucial for appropriate management.
Principles of treatment depend on the specific platelet abnormality. For
quantitative disorders, such as immune thrombocytopenia, treatment may
involve medications to increase platelet production or immune-suppressants.
In qualitative disorders, antiplatelet medications might be used.
Consultation with a hematologist is essential for accurate diagnosis and the
development of a personalized treatment plan. Regular monitoring helps
assess response to treatment and manage potential complications.
7. Acute leukemia (lymphatic, myeloid). Classification. Main syndromes.
Diagnostic work-up. Diagnosis. The principles of therapy.
8. Multiple myeloma. Classification. Main syndromes. Diagnostic
work-up. The principles of diagnosis and treatment.
Multiple myeloma is a type of cancer that affects plasma cells in the bone marrow. It can be classified
into different stages based on factors like the presence of symptoms and specific laboratory values.

Main syndromes associated with multiple myeloma include bone pain, fatigue, anemia, kidney dysfunction,
and susceptibility to infections.

Diagnostic work-up involves blood and urine tests, including serum protein electrophoresis,
immunofixation, and measurement of monoclonal proteins. Imaging studies, such as X-rays or MRI, can
help assess bone involvement. Bone marrow biopsy is essential for confirming the diagnosis and
determining the extent of plasma cell infiltration.

Principles of diagnosis include the presence of clonal plasma cells in the bone marrow, along with
evidence of end-organ damage (CRAB criteria: hypercalcemia, renal insufficiency, anemia, and bone
lesions).

Treatment typically involves a combination of chemotherapy, immunomodulatory drugs, proteasome

inhibitors, and stem cell transplantation for eligible patients. Supportive care, including medications for
bone health and infection prevention, is also crucial.

Consultation with a hematologist or oncologist is essential for accurate diagnosis and the development of
a personalized treatment plan. Regular monitoring helps assess treatment response and manage
potential complications.

Myeloma is divided at the highest genetic level into two subtypes:

disease that is hyperdiploid (h-MM), and disease that is non-hyperdiploid
(nh-MM)
The diagnosis of multiple myeloma requires increased numbers of
immature, abnormal, or atypical plasma cells in the bone marrow; a
monoclonal protein in the serum or urine; or characteristic bone lesion
The type of cancer suspected Your signs and symptoms
Your age and general health
The results of earlier medical tests Treatment
Dexamethasone+ lenalidomide+ Bortezomib (protease inhibitor) - 100%
response rate
Autologous stem cells transplantation
Radiation therapy
 Chronic lymphocytic leukemia (CLL) is a type of cancer that
affects B lymphocytes. It is often classified into different
stages based on factors such as lymphocyte count,

9. Chronic Lymphatic Leukemia. Classification. Main syndromes. presence of anemia or thrombocytopenia, and the size of
lymph nodes and organs.

Diagnostic work-up. The principles of diagnosis and treatment. Main syndromes associated with CLL include fatigue,
lymphadenopathy (enlarged lymph nodes), splenomegaly
(enlarged spleen), and susceptibility to infections.
Chronic lymphocytic leukemia is monoclonal expansion of Diagnostic work-up involves a complete blood count (CBC),

mature(naïve) B cells in blood flow cytometry to analyze lymphocyte markers, and

immunoglobulin testing. Imaging studies like CT scans or

Causes – 1. deletion 13q ultrasounds may be used to assess lymph node and organ
involvement. Bone marrow biopsy is often performed to

2.Trisomy 12
confirm the diagnosis.

Principles of diagnosis include the presence of an absolute

Diagnosis- flow cytometry( will give us the CD markers of the lymphocytosis in the peripheral blood, along with
characteristic immunophenotypic findings.
cell proliferating )
Treatment decisions in CLL depend on the stage, symptoms,
CBC and specific genetic characteristics. Watchful waiting may
be appropriate for asymptomatic cases. Treatment options

Treatment- fludarabine , cyclophosphamide,rituximab or include chemotherapy, immunotherapy, and targeted agents.

Prognostic markers, such as the presence of specific

bendamustin and rituximab genetic mutations, guide treatment decisions.

Bone marrow transplant

Consultation with a hematologist or oncologist is essential
for accurate diagnosis and the development of an
individualized treatment plan. Regular monitoring helps
assess treatment response and manage potential side
effects.

Chronic Myeloid Leukemia. Classification. Main syndromes.

Diagnostic work-up. The principles of diagnosis and
treatment.
Chronic Myeloid Leukemia (CML) is a type of leukemia
characterized by the presence of an abnormal chromosome
known as the Philadelphia chromosome.

**Classification:**
CML is typically classified into three phases: chronic phase,
accelerated phase, and blast crisis. The majority of patients
are diagnosed in the chronic phase.

**Main syndromes:**
Common symptoms include fatigue, weight loss, abdominal
discomfort, and an enlarged spleen.

**Diagnostic work-up:**
Diagnostic tests include a complete blood count (CBC), bone
marrow biopsy, and cytogenetic analysis to identify the
presence of the Philadelphia chromosome or the BCR-ABL
gene fusion.

**Principles of diagnosis:**
Confirmation of CML diagnosis is based on the presence of
the Philadelphia chromosome or BCR-ABL gene fusion.

**Treatment:**
Tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib,
and dasatinib, are the mainstay of CML treatment. These
drugs target the abnormal BCR-ABL protein. Allogeneic
stem cell transplantation may be considered for certain
cases, especially in advanced stages or if TKIs are not
effective.

Regular monitoring of response to treatment, including

molecular testing for BCR-ABL transcripts, is crucial.
Consultation with a hematologist or oncologist is essential
for accurate diagnosis and the development of an
appropriate treatment plan.
10. Chronic Myeloid Leukemia. Classification. Main syndromes.
Diagnostic work-up. The principles of diagnosis and treatment.
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