EXAM TICKET No 27

in the discipline "Faculty Therapy, Occupational Diseases"

1. Atrial flutter. Definition. Aetiology. Pathogenesis. Classification. Clinical and ECG

data. Treatment (principles, methods, medicines – write prescriptions). Course and
outcomes. Prophylaxis.

Atrial flutter is a tachyarrhythmia with a regular frequent (up to 200-400 in 1 minute) atrial
rhythm. Atrial flutter is manifested by paroxysms of heartbeat lasting from several seconds to
several days, arterial hypotension, dizziness, loss of consciousness.
Reasons:
rheumatic heart defects, coronary artery disease (atherosclerotic cardiosclerosis, acute
myocardial infarction), cardiomyopathies, myocardial dystrophy, myocarditis, pericarditis,
hypertension, SSS, WPW syndrome. Atrial flutter can complicate the course of the early
postoperative period after cardiac surgery for congenital heart defects, coronary artery bypass
grafting.

Atrial flutter is also found in patients with COPD, pulmonary emphysema, pulmonary embolism.
In cor pulmonale, atrial flutter is sometimes accompanied by end-stage heart failure. Risk factors
for atrial flutter not related to heart pathology can be diabetes mellitus, thyrotoxicosis, sleep
apnea syndrome, alcohol, drug and other intoxications, hypokalemia.
Pathogenesis
The basis of the pathogenesis of atrial flutter is the mechanism of macro-re-entry – multiple re-
excitation of the myocardium. A typical paroxysm of atrial flutter is due to the circulation of the
great right atrial circle re-entry, which is bounded anteriorly by the tricuspid valve ring, and
posteriorly by the Eustachian crest and vena cava extrasystoles. At the same time, there is a high
frequency of atrial depolarization (about 300 beats per minute).
Since the AV node is not able to transmit impulses of this frequency, only half of the atrial
impulses are usually transmitted to the ventricle (2:1 block), so the ventricles contract at a rate of
about 150 beats per minute. Much less often, blocks occur in a ratio of 3:1, 4:1 or 5:1. If the
conduction coefficient changes, the ventricular rhythm becomes irregular, which is accompanied
by a spasmodic increase or decrease in heart rate. An extremely dangerous ratio of
atrioventricular conduction is the ratio of 1:1, which is manifested by a sharp increase in heart
rate to 250-300 beats per minute, a decrease in cardiac output and loss of consciousness.
Classification
Typical flutter (Type I). It is observed in 90% of patients. It is characterized by the propagation
of the macro re-entry wave counterclockwise (most often) or clockwise (much less frequently)
around the tricuspid valve. A characteristic feature of this type of TP is the obligatory repeated
passage of the excitation wave along the so-called kavotricuspid isthmus (isthmus).

Atypical flutter (Type II). Atypical TP includes all other types of atrial macro re-entry that do not
include the area of the cavotricuspid isthmus in the excitation re-entry chain.
Clinic:
The clinical presentation of newly developed or paroxysmal atrial flutter is characterized by
sudden palpitations, which are accompanied by general weakness, decreased physical endurance,
discomfort and pressure in the chest, angina pectoris, shortness of breath, arterial hypotension,
dizziness. The frequency of atrial flutter paroxysms varies from one per year to several per day.
Attacks can occur under the influence of physical exertion, hot weather, emotional stress, heavy
drinking, alcohol consumption and intestinal upset. With a high pulse rate, presyncopal or
syncopal states often occur.
For TP, the characteristic ECG criteria are:
Regular atrial rhythm (F-waves with a cycle of less than 240 ms) at a frequency of 250-350 per
minute at the same or varying RR intervals. In some cases, the frequency of ventricular rhythm
can vary significantly (usually there is a multiple conduction from the atria to the ventricles in a
ratio of 4:1 to 2:1, rarely 1:1).
The presence of F waves, which have the form of a "sawtooth" curve in a typical TP, are
especially clearly visible in the lower leads (II, III, aVF).
AF screening is recommended for patients over 65 years of age using short-term ECG recording
or palpation of the pulse or auscultation of the heart [26].
Treatment:
Therapeutic measures for atrial flutter are aimed at stopping paroxysms, restoring normal sinus
rhythm, and preventing future episodes of the disorder. For drug therapy of atrial flutter, beta-
blockers (for example, metoprolol, etc.), calcium channel blockers (verapamil, diltiazem),
potassium preparations, cardiac glycosides, antiarrhythmic drugs (amiodarone, ibutilide, sotalol
hydrochloride) are used. To reduce the thromboembolic risk, anticoagulant therapy (intravenous,
subcutaneous, warfarin) is indicated.

For the relief of typical paroxysms of atrial flutter, the method of choice is transesophageal
electrical pacing. In acute vascular collapse, angina pectoris, cerebral ischemia, and increasing
heart failure, electrical cardioversion with low-power discharges (from 20-25 J) is indicated. The
effectiveness of electropulse therapy increases against the background of drug antiarrhythmic
therapy.

Recurrent and permanent forms of atrial flutter are indications for radiofrequency ablation or
cryoablation of the macro-re-entry focus. The effectiveness of catheter ablation for atrial flutter
exceeds 95%, the risk of complications is less than 1.5%. Patients with SSSU and paroxysms of
atrial flutter are indicated for RFA of the AV node and ECS implantation.
Outcomes and prevention.
A long course of atrial flutter predisposes to the development of thromboembolic complications
and heart failure.

Patients with atrial flutter need to be monitored by a cardiologist-arrhythmologist, consult a

cardiac surgeon to decide on the advisability of surgical destruction of the arrhythmogenic focus.
Prevention of atrial flutter requires the treatment of primary diseases, reducing stress and
anxiety, stopping the use of caffeine, nicotine, alcohol, and some medications.

2. Osteoarthritis. Definition. Aetiology. Pathogenesis. Classification. Clinical options.

Diagnosis, treatment (principles, methods, medicines - write prescriptions). Course
and outcomes. Prophylaxis.
Osteoarthritis (OA) is a type of degenerative joint disease that results from the destruction of
the articular cartilage and underlying bone. The most common symptoms are joint pain and
stiffness
Reason:
Osteoarthritis is a consequence of cartilage damage. It can occur as a result of injury or
metabolic disorders in cartilage tissue. Endocrine, neurological or other pathology can also cause
osteoarthritis. All this leads to changes in the cartilage tissues up to its destruction. Since it is the
articular cartilage that ensures the normal mobility of the joint, osteoarthritis causes pain and
reduces the range of motion.
Pathogenesis:
Classification:

There are two main forms of osteoarthritis: primary (idiopathic) and

secondary, which occurs against the background of various diseases.

Localized (lesions of less than 3 joints)- Joints of the hands- Joints of the feet-
Primary
Knee joints- Hip joints - Spine- Other jointsGeneralized (lesions of 3 groups of
(idiopathic)
joints or more)- Erosive
- Post-traumatic - Congenital, acquired, endemic diseases (Perthes disease,
hypermobility syndrome, etc.) - Metabolic diseases (ochronosis,
hemochromatosis, Wilson-Konovalov disease, Gaucher disease)-
Secondary Endocrinopathies (acromegaly, hyperparathyroidism, diabetes mellitus,
hypothyroidism)- Calcium deposition disease (calcium pyrophosphate,
hydroxyapatite)- Neuropathies (Charcot's disease)- Other diseases
(osteonecrosis, rheumatoid arthritis, Paget's disease, etc.)

Clinical Options :
Single and double acute osteoarthritis.
In the "classic" form of OA, pain and dysfunction occur in one or two major cases. Background
pathological changes may be noticeable in these joints: multiple epiphysular dysplasia,
acetabular dysplasia, Perthes disease and epiphysiolysis, inflammatory joint diseases,
osteonecrosis, injuries or injuries to ligaments or menisci. In most cases, however, the
impairment is minor and can only be detected with the use of special imaging techniques
Polyarthritis
At the moment, it is the most common form of OA, although most patients never see a podiatrist.
As a rule, this is a middle-aged woman who has pain, swelling and limitation of finger
movements. The first metacarpal joint, the first metatarsophalangeal joint, the knee joint, and the
lumbar condom can be affected more or less simultaneously. These changes are especially
noticeable in the hands. The interphalangeal joints are swollen and soft, and they often look
inflamed in the early stages. Within a year, osteophytes occur, edema leads to a characteristic
nodular deformity of the distal interphalangeal joints (Heber Dehn's nodules) and, less
commonly, proximal interphalangeal joints (Bouchard's nodules); Later, the pain may disappear,
but stiffness and deformity persist. Some patients complain of pain in the knees or back and only
casually pay attention to knotted fingers. In addition, there is a close relationship between carpal
tunnel syndrome and isolated tenosynovitis. Usually, X-ray imaging reveals changes
characteristic of OA, most pronounced in the distal interphalangeal joints of the fingers
Osteoarthritis of atypical localization
Osteoarthritis is rare in the shoulder, elbow, wrist and ankle joints. If these joints are affected,
preceding pathological changes, congenital or traumatic, or some systemic disease should be
suspected.
Rapid Progression of Steoarthrosis
Very often, in patients with OA, bone destruction occurs and progresses rapidly. At one time, it
was believed that this was due to the prescription of powerful anti-inflammatory drugs,
highlighting a conditional type of "analgesic arthropathy". It has now been shown to occur
mainly in older women, and is associated with the deposition of calcium pyrophosphate
dihydrate crystals, but whether this is a cause or effect has not yet been clarified.
Diagnosis and treatment.
The diagnosis of OA is established on the basis of the patient's complaints and anamnestic data,
clinical and instrumental examination and exclusion of other diseases. An important diagnostic
factor is a thorough collection of anamnesis, which makes it possible to identify certain causes
(risk factors) for the development of OA.
X-ray examination is the most reliable method for diagnosing OA, which reveals narrowing of
the articular space, marginal osteophytes and sharpening of the tibial condyles, and subchondral
sclerosis.

If OA of the knee joints is suspected, an X-ray is taken in the anterior-posterior and lateral
projections in a standing position, for the examination of the patellofemoral joint - an image in
the lateral projection during flexion (B).

If hip OA is suspected, an X-ray examination of the pelvic bones should be performed with the
grip of both hip joints (level C).
Treatment:
Treatment of OA should be comprehensive and include non-pharmacological, pharmacological,
and surgical methods.
1. Non-pharmacological methods: patient education, weight loss, therapeutic exercises,
orthopedic devices, physiotherapeutic therapy.
2. Drug treatment.
Symptomatic treatment, fast-acting drugs.

Nalgetics Paracetamol is indicated for mild to For mild to moderate joint

moderate pain in OA without signs of pain, paracetamol is used in the
inflammation. At a dose of 3.0 g/day. the minimum effective dose, but
safety of using paracetamol in OA for 2 not higher than 3.0 g/day. (the
years has been proven. High doses are maximum single dose should
accompanied by the development of not exceed 350 mg) (A).
complications from the gastrointestinal Paracetamol can be used for a
tract, kidneys and cause an increase in long time (A).
blood pressure in men and women. The
 drug should not be prescribed to patients
with liver damage and chronic alcoholism.
It is used only during the period of
increased pain, the minimum effective
doses are prescribed for pain relief and, if
possible, not for a long time. Patients
should be informed in detail about the
advantages and disadvantages of NSAIDs,
including over-the-counter drugs.All
NSAIDs in equivalent doses have similar
efficacy, the choice of NSAIDs is
determined primarily by their safety in
specific clinical conditions.Gastrointestinal
complications are one of the most serious
NSAIDs are used in case of
side effects of NSAIDs. The relative risk of
paracetamol ineffectiveness, as
their occurrence varies for different
well as in the presence of signs
NSAIDs and dose-dependents.Selective
Nonsteroidal of inflammation (A). In case of
COX2 inhibitors have the lowest risk of
anti- severe joint pain, treatment
developing gastrointestinal bleeding. They
inflammatory should be started immediately
should be prescribed in the presence of the
drugs with NSAIDs (A). NSAIDs are
following risk factors for the development
used in the minimum effective
of adverse events: age over 65 years,
dose, prescribed for the
history of peptic ulcer disease or
shortest possible time (A).
gastrointestinal bleeding, concomitant use
of corticosteroids or anticoagulants, the
presence of severe concomitant diseases. In
patients with OA with risk factors for
gastrointestinal bleeding at the same time as
NSAIDs, it is necessary to recommend
taking a proton pump inhibitor in the full
daily dose. It is necessary to control blood
pressure and the course of chronic heart
failure while taking NSAIDs. When
prescribing NSAIDs, the possibility of drug
interactions should be taken into account
To reduce pain in OA of the
Local NSAIDs have a sufficient analgesic knees and hand joints, which is
effect in OA of the knee and hand joints, not relieved by taking
Transdermal
are well tolerated, but should be used for 2 paracetamol, or if the patient
(local) forms of
weeks with a subsequent break, since the does not want to take NSAIDs
NSAIDs
effectiveness decreases with longer orally, transdermal (local)
administration. forms of NSAIDs (A) are
recommended.
An opioid analgesic is used for a short It is used for a short period of
period (50 mg/day in the first days with a time to relieve severe pain in
gradual increase in the dose to 200-300 case of ineffectiveness of
Tramadol mg/day) to relieve severe pain if paracetamol or NSAIDs, as
paracetamol or NSAIDs are ineffective, as well as the impossibility of
well as it is impossible to prescribe optimal prescribing optimal doses of
doses of these drugs. these drugs
 In OA, corticosteroids are injected into the
knee joints to reduce pain and symptoms of Intra-articular injection of
inflammation, the duration of the effect is glucocorticoids (GLA) is
from 1 week to 1 month. It is recommended indicated for OA of the knee
Intra-articular
to use single injections of joints with symptoms of
glucocorticoids
methylprednisolone (40 mg) or inflammation (A).
triamcinolone (20 mg or 40 mg). It is not
recommended to perform more than 2-3
injections per year into the same joint.

Symptomatic slow-acting medicines

Research results Recommendations

Preparations containing chondroitin sulfate
and glucosamine have a moderate analgesic Preparations containing
effect and high safety. Data have been chondroitin sulfate and
obtained on their possible structural- glucosamine sulfate are
modifying effect (slowing down the recommended for OA to reduce
Chondroitin
narrowing of the articular space) in OA of pain, improve joint function; the
sulfate and
the knee joints (chondroitin sulfate, effect persists for several months
glucosamine
glucosamine sulfate) and small joints of the after their withdrawal, well
hands (chondroitin sulfate). Glucosamine tolerated by patients (A).
sulfate is prescribed at 1500 mg/day for 4-
12 weeks, courses are repeated 2-3 times a
year.
The experiment showed that the mechanism
of action is to inhibit IL-1β. Reduces pain, The interleukin 1 inhibitor
the effect lasts for several months after the diacerein is used to reduce pain,
Diacerein completion of treatment for OA of the knee improve joint function, and
and hip joints. Diacerein is used 50 mg 1 possibly slow the progression of
time a day, then 50 mg 2 times a day for a OA(A).
long time.
Numerous in vitro and in vivo studies have
shown that NSAS increase the level of
stimulants of tissue production and have a
Avocado and soy non-
chondroprotective effect in induced OA.
saponification compounds
NSAS reduces pain, reduces the need for
(NSAS) – piascledine is used to
Piascledine NSAIDs, and has an aftereffect for several
reduce pain, improve joint
months after the completion of treatment.
function and, possibly, slow the
The structural-modifying effect of NSAS
progression of OA (A).
has been demonstrated in 2 studies in hip
OA. Piascledine is used 300 mg 1 time a
day, for a long time.
Hyaluronic Hyaluronic acid preparations reduce pain, Hyaluronate derivatives are used
acid improve joint function, but there is greater for intra-articular administration
preparations heterogeneity in the assessment of the in OA to reduce pain (A).
outcomes of the analyzed studies. At
 present, low-molecular (molecular weight
500-730 kilodalton) and high-molecular
(molecular weight 12000 kilodalton)
hyaluronate preparations are used. Low-
molecular and high-molecular drugs show
the same results, the effect lasts from 60
days to 12 months. The treatment is well
tolerated, very rarely when injected, pain in
the joint can increase like a pseudogouty
attack.
It has a symptomatic effect (reduces pain
and improves joint function at a dose of 2.0 It is used to reduce pain and slow
Strontium
per day) and a structural-modifying effect at the progression of OA of large
ranelate
doses of 1.0 and 2.0 per day in OA of the joints (A)
knee and hip joints, used for 3 years

Surgical treatment

Research results Recommendations

Reduces pain, improves motor function,
and improves quality of life in hip OA.
It is indicated in OA with severe pain
The duration of the effect is about 10
syndrome that does not respond to
years, the frequency of infectious
conservative treatment, in the
complications and reoperations is 0.2–
presence of serious impairment of
Joint 2.0% annually. The best results of
joint functions (before the
replacement endoprosthetics were noted in patients
development of significant
surgery aged 45–75 years, with a body weight of
deformities, joint instability,
<70 kg, with a high social standard of
contractures and muscle atrophy) (A).
living.

Knee replacement surgery reduces pain

and improves motor function.

Prevention of osteoarthritis is specific. Doctors recommend wearing exceptionally comfortable

shoes and warm clothes in winter. It is important to be able to distribute the load when doing
sports and keep your weight under control. It is also advisable to eat right and lead a healthy
lifestyle.
Prognosis for osteoarthritis. If the problem is treated in time and comprehensively, then you can
significantly reduce the painful manifestations of the disease and stop the progression of the
disease.

3. Manganese intoxication: pathogenesis, clinical manifestations of acute and chronic

intoxication, treatment, prevention, examination of working capacity.
Pathogenesis:
The pathogenesis of acute processes is based on damage to the mucous and submucosal layers of
the gastrointestinal tract. Coagulation necrosis, edema and ulceration of tissues, occult bleeding
are formed. Perforation of the esophagus or stomach with the development of peritonitis is
possible. When a toxicant enters the respiratory tract, similar processes occur in the tissues of the
oropharynx, trachea, bronchi. This leads to mechanical asphyxia, death of the patient from acute
respiratory failure. An additional pathogenetic factor is a shock state.
Systemic phenomena are caused by the accumulation of manganese and potassium in the body.
At the same time, Mn is deposited inside the kidneys, lungs, heart and central nervous system,
disrupting their work. Its increased concentration in plasma is noted within an hour after
absorption from the mucous membrane of the small intestine. Further, the amount of the trace
element in liquid media is normalized. The content of K+ in the blood increases significantly,
which has an additional negative impact on the cardiovascular system.
Clinical manifestations:
Light. Symptoms are moderately expressed, mainly the upper parts of the digestive apparatus
and the oropharynx are affected. Inflammation is catarrhal-fibrinous, the pain syndrome is
insignificant, does not require the use of narcotic analgesics. There is no threat to the life of the
victim.
Moderate severity. The mouth, stomach, esophagus are damaged. Exotoxic shock phenomena
may occur. The inflammatory process acquires a catarrhal-serous character. Symptoms of
moderate damage to the urinary and hepatobiliary systems are determined. If the xenobiotic gets
inside the windpipe, swelling with breathing difficulties is noted. Consciousness is usually
preserved.
Heavy. There is a burn of the esophagus, stomach, oral cavity, small intestine. Perforation of the
gastrointestinal tract may occur. Severe exotoxic shock, impaired consciousness up to coma are
detected. Inflammation of the ulcerative-necrotic type, damage to the kidneys and liver before
the onset of multiple organ failure is revealed.
Treatment.
. Conservative therapy
At the pre-hospital stage or immediately after delivery to the hospital, lavage through a
nasogastric tube is performed. To do this, use a solution made by mixing 100 ml of 3% hydrogen
peroxide, 250 ml of 3% acetic acid and 2 liters of cool water. The procedure is continued until
the rinsing composition is clean. Visible mucous membranes are treated with ascorbic acid.
Under the influence of these drugs, the toxicant is converted to harmless compounds. After the
procedure, activated charcoal is injected at a dose of 1 g / 10 kg of weight.
Systemic treatment consists of the administration of complexing antidotes (tetacin-calcium,
unitiol). A solution of ascorbic acid 5% in the amount of 50-100 ml/day is prescribed through the
mouth. Analgesics, sometimes narcotics, are used for the purpose of anesthesia. To reduce the
swelling of the mucous membranes, the victim is inhaled sodium bicarbonate with the addition
of local anesthetics actions.
Resuscitation
In the development of shock, cardiovascular, respiratory and multiple organ failure, the patient is
indicated to be transferred to the intensive care unit, where methods of active detoxification can
be used: replacement blood transfusion, hemodialysis, forced diuresis. In case of shock, the
patient is transferred to mechanical ventilation, cardiotonics, glucocorticosteroid hormones, and
adrenaline are connected. Hypoxia caused by airway occlusion requires a tracheostomy.

Bleeding arising from ulcers of the esophagus and stomach is stopped with the use of hemostatic
drugs. In the absence of an effect from conservative therapy, hemostasis is carried out
endoscopically. The damaged area is pricked with an adrenaline solution or cauterized with
colloidal silver. Convulsions are an indication for the infusion of barbiturates, benzodiazepines
and anxiolytics. Round-the-clock monitoring of the patient's condition using an anesthetic
monitor is necessary.

Surgical treatment
It is required for uncontrolled bleeding, perforation of the gastrointestinal tract, volumetric
necrosis of the intestine, as well as in the late stages of healing with formed strictures. In the first
case, the indication for intervention is profuse or prolonged capillary hemorrhages occurring
over a large area of the esophagus. Through holes in the wall of the digestive system are an
indication for emergency surgery, since they are usually accompanied by the development of
peritonitis, which poses an immediate threat to life. Without help, the mortality rate is 100%.

In case of tissue death, the need for surgical treatment is due to the functional failure of the
digestive system and endotoxicosis, which occurs when the decay products of the intestinal wall
are released into the blood. Strictures that interfere with the passage of food are eliminated in
cases where the narrowing reaches 40-50%. Lower degrees of stenosis make it possible to
abandon surgical correction if the patient observes some food restrictions.
Prevention of potassium permanganate poisoning consists in keeping the chemical out of the
reach of children, the elderly and patients with a psychiatric diagnosis. It is strictly forbidden to
keep the solution in food containers. For bathing children, a minimum concentration of the agent
is used. The water should be pale pink, not purple or black. When working with the drug at work
or at home, it is recommended to use closed clothing and personal organ protection breathing
(mask, respirator, gas mask).