PATHOLOGICAL PHYSIOLOGY

FIRST PART

1a. Disease: definition of the concept, classification of diseases, stages of disease progress,
options for the outcome (completion) of disease.

Definition: Disease is the disruption of normal functioning of the body in case of

exposure to harmful factors, resulting in decrease of its adaptive capabilities, working
activity and increases the likelihood of death.
Classification:

• Etiology: common reason of the disease. For example, there are the infectious
and uninfectious diseases. Diseases caused by an intoxication (food,
professional), genes violations and chromosomal mutations (hereditary
diseases) etc.
• Topographic-anatomical: is based on the organ principle: the cardiovasculars
diseases, diseases kidneys, diseases of nervous system etc. Classification of
the functional systems: blood system, digestive system, musculosceletal
apparatus diseases etc.
• By age and sex: they distinguish children disease, elderly and senile age
disease
• Environmental: The air temperature, atmospheric pressure, solar light, macro
and micro element in drinking water, soil and food products affect the health
status of the population of certain regions.
• For common pathogenesis: there are disease of allergy,
inflammatory,neoplastic and other origin.
• Social: they are occupational disease, disease in wartime and disease of
civilization.
• By the nature of the course: they may be acute and chronic
• Depending on methods of treatment: there are surgical and therapeutic
disease.
Stages of disease progress:

• The latent period: last from the first effect of an etiological factor on a body
to the first clinical sign of the disease.
• The prodromal period: time interval from the first sign of disease precursors
to the occurence of the developed clinical picture
• The period of expressed manifestation: characterized by complete
development of the clinical picture: convulsion in the case of insufficiency of
parathyroid gland, tripple triad (hyperglycemia, glycosuria, polyuria) in case of
diabetes mellitus
 • The disease outcome or completion.

Options for the outcome:--

They can be:--
Convalescence ( complete and incomplete), Remission, Recurrence, Complication,
Transition, the Death or terminal state.

• The convalescence: is the state when all the disease signs disappear and
organism restores its adaptation possibilities completely. When the convalescence is
incomplete the disease consequences are expressed. They remain for a long time or forever. The
convalescence is provided by the urgent (emergency) and lasting protectively-compensational reactions
of the organism.
• The remission: is the temporal state improvement of the patient, which is
displayed by the disease progressing slowing down or cessation, the partial
reverse development or the disappearance of the pathological process clinical
signs.

• The recurrence is the new disease display after its seeming or incomplete
cessation.

• The complication is secondary as for reference to the disease pathological

process.

• The transition in the chronic form signifies that disease courses slowly with
the protracted remission periods ( months and even years). So, many diseases
acquire chronic nature in old age ( chronic pneumonia, chronic colitis).

• The terminal states are the boundary ones between life and death. This is
also the dying, which include a few stages: preagony, agony, clinical death,
biological death.

Preagony is characterized by the diverse duration (during hours, days) of deep violations of the vitally
important organism functions. The dyspnea, the decreasing of the arterial pressure, the darkening down
of the consciousness, which are observed in this period. Gradually the pre-agony gets across in the
agony.

Agony is characterized by the gradual turning down of all organism functions. The agony lasts 2-4
minutes, sometimes more. The clinical death is such condition when all of the visible sparks of life have
already disappeared (the breathing and the heart work are ceased, however the metabolism still
continues). The life can be restored on this stage.
The biological death is characterized by the irreversible changes in the organism.
2a. Terminal states: preagoniy, agony, clinical death, biological death. The most important
methods of resuscitation, or revival of the body.
The preagony is characterized by the diverse duration (during hours, days)
of deep violations of the vitally important organism functions. The dyspnea,
the decreasing of the arterial pressure, the darkening down of the
consciousness, which are observed in this period. Gradually the pre-agony
gets across in the agony.
The agony is characterized by the gradual turning down of all organism
functions. The agony lasts 2-4 minutes, sometimes more.
The clinical death is such condition when all of the visible sparks of life have
already disappeared (the breathing and the heart work are ceased, however the
metabolism still continues). The life can be restored on this stage.
The biological death is characterized by the irreversible changes in the organism.

Methods of resuscitation:

The reanimation includes number of measures which are done to restore blood circulation
and breathing:
- heart massage,
- artificial lungs ventilation, heart
- The indirect heart massage is widely used for the renewal of blood circulation, it can
be used at once after the clinical death setting in any conditions and even not by
specialist.
- The artificial ventilation of the lungs also must be started as soon as possible.
- The heart fibrillation is observed in the terminal period ordinary. In such cases the
electric defibrillation is used.

All of these measures are directed to renewal of cerebral cortex function. The
respiratory centre is main parameter. It is the main pacemaker of cerebral rhythms and
the impulses, which promote the appearance of the electric cortex and the subcortical
centres activity, vasomotoral one also. The renewal of the independent breathing
promotes renewal of the blood circulation.

3a. Etiology. Classification of etiological factors, risk factors, conditions for the disease
occurrence.
Definition: The etiology is the study of disease beginning, causes and conditions. The
notions of causality and determinism are base of etiology.
Classification: There are exogenous (external) and endogenous (internal).
The exogenous factors are:

a) physical – mechanical influence, radiation, high and low temperature, electric

current, overloading, zero-gravity and others;

b) chemical – the inorganic and organic compound;

c) biological – viruses, rickettsias, bacterias, Protozoas, helmints, Arthropodes; d) psychic – a
word;
e) social – society development level, traditions and others.
The endogenous factors are: heredity, constitution, age, sex, organism reactivity.

The main condition for occurrence of the disease-:

The conditions of the disease beginning are the different factors. All the
conditions are divided into two groups, according to the disease beginning
influence.
1. The conditions which increase cause action and promote disease
development. For example, viruses are the cause of acute respiratory diseases,
and cooling, tiredness, immunodeficiency are cooperant conditions. Sometimes
these conditions can matter decisive. Without the definite conditions, in spite of
cause presence, the disease does not arise (for example, the food products
allergy).

2. The conditions which weaken the cause action and prevent the disease
development. They are the nutrition, correcting day routine organization,
physical culture, correct care of sick. Sometimes the conditions may neutralize
completely the cause action (for example, the presence of natural or acquired
immunity to the infectious diseases).
The main conditions for the occurence of the disease is the reactivity, ie the
ability of an organism to respond to the action of pathogenic factor with defined
protective reaction, most of which are imperfect and may themselves damage
organs and tissues

4a. Concept about pathogenesis, destructive and adaptive-compensatory, local and

general phenomena in pathogenesis.

The pathogenenesis is the study about the mechanisms of the development, the course and
the end of disease.
Adaptive mechanism: adaptation means the adaptation of the organisms to conditions
of existence with the help of adequate changes of function, metabolism and structure
of its organs and systems. The adaptative mechanism were created to evolve and are
aimed at maintaining homeostasis. Adaptative mechanisms are always alert and
involved in the response to a specific signal. This is their homeostatic role
Destructive mechanism: another situation occurs during illness, in this case, the influence
of pathogenic factor is so powerful that the normal adaptive mechanism fails, and
homeostasis is disrupted. The body temperature, level of glucose in blood pH is changed,
this is when the destructive process begins.
At this point into the reaction, other mechanisms join which is called compensatory.
The compensation is the state, which develops as the realization result of the
compensatory reactions and processes, directed to renewal of changed homeostasis along
with pathogenic factors influence. The compensation liquidates the damage consequences.

The local violations-- They can bring to local changes of the organism proper conditions. So,
inflammation, neoplasms, burns – are the local violations. However if their expression
arrives to definite level they can cause the development of general violations: fever,
cachexia, burn disease.
The general violations-- They can be displayed by general changes. So, in diabetes mellitus
(general disease) the local processes – furuncles, defeats of the joints, nerves, kidneys, eyes
retina develop secondary. The general changes of the lipid metabolism in the organism
conduce frequently to the development of atherosclerosis that can be displayed by such
local defeats as myocardium heart attack, strokes, the gangrene of lower extremity.

5a. Barotrauma. Pathogenic effects of high and low atmospheric pressure.

Barotrauma: is caused by the pathogenic effect of modified atmospheric atmospheric

pressure on an organism.
EFFECT OF LOW ATMOSPHERIC PRESSURE:- people feel this at height or on a
nonhermetic aircraft or mountains. pathological changes occuring in such conditions are
caused by two factors: low partial pressure of oxygen which could lead to hypoxic hypoxia
and decreased atmospheric accompanied by a complex on syndrome, the syndrome of
decompression.
The gases contained in the body cavities are expanded and the person feels the pain in the
ears and frontal sinuses, joint, abdomen(high altitude fratulence). During the rapid
lowering of the atmospheric pressure the syndrome of explosive decompression develops.
Its causes instantaneous death.
Reasons for explosive decompression can be--

• Rupture of the lungs, heart and large vessels

• Boiling of the blood and other body fluids at the body temperature
• The acute form of hypoxia
 •
EFFECT OF HIGH ATMOSPHERIC PRESSURE: people feel, when they are immersed in water
to a considerable depth during diving and caisson works. As a result, the pain occurs in the
ears because of pressure on the eardrums; with a sharp and quick dip the injury of the
pulmonary alveoli is possible.

So, In the hyperbaric condition people should breath the air or gas mixtures under high
pressure, resulting in additional quantity of gas dissolved in the blood and tissue saturation.

6a. Pathogenic effect of the thermal factor: hyperthermia and hypothermia, frostbite and
burn (combustion), colds. Use of high and low temperatures in medicine.

Pathogenesis of thermal injury is due to complex pathological disorders and compensatory

reactions, which are the strain of physical and chemical thermoregulation(heat loss and heat
production).
HYPERTHERMIA: Hyperthermia is elevated body temperature due to failed
thermoregulation that occurs when a body produces or absorbs more heat than it releases.
If the balance between heat production in the body and its return to the environment is
disturbed, hyperthermia(overheating) develops.
In the stage of compensation, the only thermo- regulatory mechanism is perspiration and
evaporation.
In the stage of decompensation, the cardiovascular system is the main. Tachycardia is the
first symptom of overheating, and then there is excitation of the CNS and then dyspnea.
Acute over heating with rapid increase in body temperature is called heat stroke(fever,
excitement, and depresion of cns).

HYPOTHERMIA:Hypothermia is defined as body core temperature below 35 degrees. It can

occur due to extreme exposure to cold, decrease heat production or increase heat loss. The
overall effect of low temperature may cause a decrease in the body temperature and
develop hypothermia.
There are two stages:

In the compensation stage the bodies temperature is at original level, what the body
does here is to limit the heat transfer by reducing sweating, thermal conductivity, and
thermal radiation.
In the decompensation stage, not only does the body temperature decrease, but also,
the intensity of metabolic processes, oxygen consumption and vital functions are
inhibited.

FROSTBITE: the local effect of low temperature causes frostbite, this frost bite is
caused by violation of local circulation due to spasm of peripheral vessels, platelet
formation and direct damaging effect of low temperature of the cytoplasm.
BURN: the local effect of high temperature leads to burn and is manifested by local
destructive and reactive changes. There are four degrees of burn:

• Skin redness(erythema)
• Acute excudative inflammation
• The partial skin necrosis and ulceration
• Deep necrosis of skin and tissues

+High temperatures can be used to sterilize medical equipments

+Low temperature can be used to store medication, preserve organs.

Classification of burns:

(1) First-degree burns ( partial-thickness burns) are characterized by hyperemia without significant epidermal
damage; they generally heal without intervention.

(2) Second-degree burns (partial-thickness burns) are characterized by blistering and destruction of the epidermis
with slight damage to the underlying dermis; healwithout intervention.

(3) Third-degree burns (full-thickness burns) are characterized by damage to the epidermis, dermis, and dermal
appendages; skin and underlying tissue are often charred and blackened;often require skin grafting.

Complications of burns (1) Inhalation of smoke or toxic fumes results in pulmonary or systemic damage. (2) Hypovolemia
results from fluid and electrolyte loss. (3) Curling ulcer (acute gastric ulcer associated with severe burns) (4) Infection -
Pseudomonas aeruginosa.

7a. Types of ionizing radiation. The primary mechanism of action of ionizing rays.
Mutagenic, carcinogenic and somatic effects of ionizing rays.
Ionizing radiation is radiation that carries enough energy to free electrons from atoms or
molecules. Medicines that are called Countermeasures could help speed up the excretion
process of this ionizing radiation if exposed

Types are:
-Alpha: they are positively charged and made up of two protons and two neutrons from the
atom’s nucleus. They have the greatest ionization. This particle lack the energy to penetrate
the outer layer of the skin, but when inside the body it can be very harmful. Stopped by sheet
of paper

-Beta: these are small fast moving particles, more penetrating than alpha pariticle, but are
less damaging to living tissue. Stopped by layer of clothing, wood, few mm of aluminium

-Gamma: these have the smallest ionization, but they have a very high penetrating power.
Gamma rays can pass completely through the human body and they can cause ionizations
that damage tissue and DNA. Stopped by several feet of concrete or few inches of lead

-X-rays: belong to electromagnetic radiations. X-rays arise of substance or the X-ray tube
anode electrons internal atoms

The mechanism of ionizing radiation -: direct and indirect ones.

Direct way is the straight ionizing radiation influence upon high molecular connections of an
organism: proteins, lipids, enzymes, nucleic acids, nucleoproteins, lipoproteins. The energy
absorbed with macromolecule, migrates in there and breaks the most labile connections.
Proteins lose their enzyme and immune properties after such irradiation. Nucleic acids and
their albuminous complexes – nucleoproteins are very sensitive to radiation.

Indirect radiation action is connected to water radiolysis. In result positively and negatively
charged ions with oxidizing and regenerative ability get produced first. They react with the
activated water molecule and in combinative way, form hydrogen peroxide H2O2,
hydroperoxyde HO2, atomic oxygen O, superoxide radical O2, etc. Water radiolysis products
are very chemically active. They reach biologically important molecules and get them
oxidized.

Mutagenic ionizing rays - directly affects DNA structure by inducing DNA breaks. All these
changes induce cell death and mitotic failure. The risk of a mutation exists for all kinds of
radiated cells is somatic and sexual, but their appearence consequences of are different.
These can lead to Genic and chromosomal aberrations, translocations, mosaicism or
aneuploidy.
Carcinogenic/ Somatic - somatic cells get divided intensively, and may cause their ability to
uncontrollable duplications. From them malignant tumours or leukosis develop

8a. Forms of acute radiation sickness. Clinical periods of the marrow form of acute
radiation sickness. Principles of radioprotection.
Acute radiation sickness: This term designates the general injury of an organism with the big
ionizing radiation doze.
Forms:

• marrow (a doze of 1-10 Gr)

• Gastrointestinal (a doze of 10-50 Gr)
• Cerebral (a doze of 50 Gr)

Marrow forms has four clinical periods:-

The initial period: last from several hours to 1-3 days, it is characterized by the reaction of
the nerve receptors and hormonal cells on the direct and mostly indirect effects of
irradiation. It is manifested by nervous excitement, headache, disorder of internal organs,
nausea, vomiting and diarrhoea. Body temperature could rise which would be as a result of
violation of thermoregulation. In severe cases, radiation shock is possible.
The latent period: lasts 1-2 weeks. Mitosis activity of bone marrow cells increases.
Leukopenia, lymphopenia, thrombocytopenia and reticulocytopenia. this is the period of
imaginary well being, when the manifestation associated with excessive excitation of the
nervous and endocrine systems, has disappeared and typical symptoms of the radiation
disease are still absent.
Period of marked manifestation: during this period, radiation lesions develop, leukemia,
thrombocytopenia are in progress, haemorrhagic, enteric, bone marrow injury syndrome
occur. In the oral cavity there is inflammation of the tongue, gums, and tonsils, food
consumption becomes difficult.
Death or recovery: maximal mortality is observed in the period of acute granulocytopenia
and thrombocytopenia. Hemorrhages and death are the main causes of death. For recovery,
the signs are improvement of health and normalization of blood cell content.
Principle of radioprotection:

• Time
• Distance
• shielding
OR (optional if the previous principle is not correct)
 • Justification: this means that new activities are permitted only when they associated
with a reasonable benefit for the individual and society
• Dose limitation: the dose should not exceed certain limit values
• Optimization: this requires that the likelyhood of exposure, number of exposed and
individual dose affecting a patient should be kept as low as possible.

9a. Pathogenic action of chemical factors. Exogenous and endogenous poisons. Addiction
to poisons: alcoholism, drug addiction, substance abuse.
Chemicals are capable of damaging cells. Most damaging chemical are carbon monoxide,
insecticides, trace metals such as lead.

Chemical agents can injure the cell membrane and other cell structures, block
enzymatic pathways, coagulate cell proteins and disrupt the osmotic ionic balance of
the cell.
-Exogenous poisons originates from outside organism and is harmful when taken by
patient (lead, food, drugs e.t.c)
-Endogenous poisons are poisoning from substances within an organism, tissue
or cell (uraemis, ammonia)

Drug addiction is a chronic, often relapsing brain disease that causes compulsive drug
seeking and use, despite harmful consequences. Addiction can be to alcohol, drugs,
substances even substances that are toxic to humans, as it can cause gene mutation
in a pregnant person and affect the child mental and physical growth, and also
various teratogenic effects.

10a. Pathogenic action of biological factors, their species. Input gates of infection, ways of
generalization of the infectious process, interaction between microorganism and
macroorganism.

Pathogenic action: The biological agents may cause a variety of health effects in
humans, such as infectious diseases, acute toxic effects, allergies and even cancer.
Biologic agents differ from other injurious agents that they are able to replicate and can
continue to produce their injurious effects.
Biological factor or agents include : Bacteria, Fungi, Virus, Bacterial endotoxins,
Mycotoxins, Peptidoglycans, β-glucans, Allergens (high molecular weight), Plant fibres etc.

Viruses enter the cell and become incorporated into its DNA synthetic machinery.
Certain bacteria elaborate exotoxins and interfere with cellular production of ATP. Other
bacteria like gram negative bacilli release endotoxins that cause cell injury and increased
capillary permeability.
Protozoas is an informal term for a group of single-celled eukaryotes , either free-living or parasitic , which feed on organic
matter such as other microorganisms or organic tissues and debris Helmints

Parasitic worms, also known as helminths, are large macroparasites ; adults can generally be seen with the naked
eye. Many are intestinal worms that are soil-transmitted and infect the gastrointestinal tract. Other parasitic worms
such as schistosomes reside in blood vessels.

Arthropodes is an invertebrate animal having an exoskeleton , a segmented body, and paired jointed appendages .
Arthropods are characterized by their jointed limbs and cuticle made of chitin , often mineralised with calcium carbonate
. The arthropod body plan consists of segments, each with a pair of appendages.

Ways of generalization of the infectious process- system and local infections

Localised infections-once an infectious process initiated, the disease may remain localized
or it may spread

Systemic infections- when the infection spreads throughout the body it is said to have
become a systemic or generalized infection example is military tuberculosis caused by
mycobacterium tuberculosis

Interaction between microorganism and macroorganism.

Positive interaction- mutualism, syntrophism, commensalism, photo cooperation Negative

interaction- predation, parasitism, competition, ammensalism.

11a. Types of mutations. The most important mutagens, mechanisms of the structure
violation of chromosomes and genes, anti-mutation mechanisms.

A mutation is a change in the amount or the structure of the DNA of an organism. This
produces a change in the genotype, which may be inherited by cells derived by mitosis or
meiosis from the mutant cell.

Mutations occurring in gamete cells are inherited, where as those occurring in somatic cells
can only be inherited by daughter cells produced by mitosis. this are known as somatic
mutations.

Influence of mutagens can lead to: somatic mutation, germ(gametic) mutations, gene
mutations, chromosomal mutations
There are 3 main types of mutations:
1. Chromosomal mutations (changes in number of chromosomes).
Eg translocation, duplication, inversion and deletion.
2. Chromosomal aberrations (changes in structure of
chromosomes).
 Trisomy 21(down syndrome ), trisomy 18(edward), trisomy 13(patau).
3. Gene (point) mutations (changes in structure of the nucleotides
of DNA). Eg silent, nonsense, missense.

The most important mutagen:

PHYSICAL MUTAGEN

the most important physical mutagen is the ionizing radiation, which damages the genetic
apparatus either directly or through the products of radiolysis. Sometimes the mutation is
caused by a very small dose of radiation, and such dose doesn't cause the radiation
disease.
CHEMICAL MUTAGEN
The most powerful chemical mutagens are the analogs of purine and pyrimidine bases
and also alkullen agents , desaminize agents (nitritic or nitrous acid), and substances that
in the process of metabolism can turn into nitrites, nitrosamines.
Among the chemicals that are constantly accumulating in the environment there are many
mutagens (agricultural:- pesticides, herbicides; production of epoxy resins, phenol,
formaldehyde, food products:- acetaldehyde, which is used in the production of
preservatives etc.). The chemical mutagens may also be medicines, especially cytostatics
(inhibitors of DNA synthesis, derivatives of folic acid, analogs of purine and pyrimidine
bases and their derivatives — bromouracil, aminopurine).

BIOLOGICAL MUTAGEN
The biological mutagens include virus of the infectious mononucleosis, chicken pox,
hepatitis, measles, rubella, and mumps. So, if pregnant women had rubella or viral hepatitis, there are
spontaneous abortions, and chromosomal aberrations are determined in the fetal cells. The children (born by these
women) are often diagnosed the chromosomal diseases. The waste products of some pathogenic fungi (aflatoxin) can
also be mutagens.

Exogenous mutagens can induce the formation of endogenous mutagens — the active
forms of oxygen, free radicals, radiotoxins, etc.

Mechanism of the structure violation of chromosomes and genes:

Antimutation Mechanisms:

In the body there are numerous mechanisms that prevent mutations, restore the
mutant gene that prevent its implementation or compensate violations caused by
it. At the molecular level the compensatory reaction means inactivation of
endogenous mutagens (e.g., reactive oxygen) with natural antioxidant systems.
The genetic apparatus is characterized by certain reliability. Not every replacement of
the nitrogenous base in the DNA molecule leads to mistake in the case of its
reduplication.

The double nature of the DNA spiral is one of factors of such reliability, as in the case of
mono- chain damage of the DNA molecule the recovery is taken place according to the
matrix of other normal chain.

In addition, in the cell there is the system of enzymes of reparation of damaged DNA; these
enzymes recognize the defect, cut this fragment with the help of endonuclease (via
restriction), split it (under the action of exonuclease), synthesize a normal fragment (by
using polymerase) and inserted it (by ligase). This protective mechanism restoresabout 95 %
of spontaneous mutations.

12a. Diagnostic methods of of hereditary diseases.

Methods of Examination: genetic, biochemical, cytological, study of sex chromatin,

genealogical, population statistical method, twin method.

✓ The genetic method helps to identify the mutation restructuring or gene

variations at the DNA level with monogenic hereditary' diseases. There are two
possibilities.
The direct DNA diagnosis is to determine gene mutations at the level of the nucleotide
sequence of the modified gene using the polymerase chain reaction (PCR), specific probes.
The indirect diagnosis- Altered DNA are called DNA markers. If the nucleotide sequence
of the modified gene is established by means of biochemical tests (presence of
biochemical products of this gene).

✓ By the biochemical method they detect the enzymopathies, which is diagnosed

by the degree of activity of the enzyme or the products of the reaction catalyzed
by this enzyme.

✓ The Cytological Method. The Study of Karyotypes. During the cell division at the
stage of prophase the chromosomes can be seen under the microscope, and in
the metaphase it’s possible to define their number and morphological features.
The karyotype can be analyzed in the bone marrow cells.
The quantitative pathological karyotype and structural changes of the genetic apparatus caused by the chromosomal
mutations that are manifested by ruptures, dicentric and ring-shaped chromosomes, their fragments, and chromosomal
associates. They arose in the studied lymphocytes already in the culture and show chromosomal instability of the
genetic apparatus of the patient.
 ✓ The Study of the Sex Chromatin. The sex chromatin is detected in the
interphase nuclei
(Barr’s bodies) and is the spiral X-chromosome in that case, when the chromosome set
has two of them and more. The normal sex chromatin can be detected only in female.
If there are several X-chromosomes in the cell, the number of sex chromatin is equal to their quantity minus
one. By the way, not every somatic cell contains the female sex chromatin.An example for using the
immunological method may be the identification of heterozygosity in the hemophilia A for detection of
antibodies to antihemophilic globulin.

✓ The population-statistical method is used to establish the genetic etiology of

the disease in a particular family. It consists in comparing the frequency of
occurrence of the disease in the family of the patient with the frequency of this
disease in the population (according to the medical statistics).

✓ The geneological method: i.e pedigree drawing allows determining the type of
inheritance and the risk of recurrence of hereditary disease in the family of the
patient.

✓ The twin method: by using the twin method it is possible to distinguish the role
of genetic factors and environmental factors. The genetical twins are genetically
identical and the difference between them is determined only by environmental
factors.
✓ Dermatogliphycal method consists of analysis of hereditary conditioned hands
skin drawings, fingers tips.

13a. Types of inheritance of diseases, examples, characteristics.

The genetic pattern of a disease may be classified as autosomal dominant; autosomal

recessive; X-linked recessive; X-linked dominant; triplet repeat mutations; genomic
imprinting; mitochondrial; or multifactorial.

Autosomal Recessive Disorders:

If the mutant gene is recessive, the disease develops only in the homozygous state of the
gene, i.e. in that case the child receives the abnormal gene from both parents (being
heterozygous carriers of the trait they remain healthy). In such way the fermentopathias are
inherited.
Example Cystic fibrosis, Phenyketonuria, Galactosemia, Homocystinuria, Lysosomal storage
disorders, Alpha 1 antitripsin deficiency

Autosomal Dominant Disorders: The mutation of dominant genes can be seen in both the
homo- and heterozygous state. Those dominant carriers of those mutant genes survive and
inherit the pathology that don’t substantially disrupt viability, don't prevent reproduction,
and therefore they are little subject to natural selection. The dominant gene mutations lead
to the well-known phenotypes.
Example Marfan Syndrome, von willbrand disease, huntington’s disease etc

X-Linked Recessive: males with a mutant recessive gene on the X chromosome have the
condition, while daughters of affected males are obligate carriers, who in many situations
are asymptomatic. Example Hemophilia A.

X-Linked Dominant: are similar to X-linked recessive, but both males and females show
disease.
Example fragile X syndrome The disease with the polygenic type of inheritance

Y-linked: Y chromosome infertility, some cases of Swyer syndrome ( A condition is

considered Y-linked if the mutated gene that causes the disorder is located on the Y
chromosome , one of the two sex chromosomes in each of a male's cells. Because only
males have a Y chromosome, in Ylinked inheritance, a mutation can only be passed from
father to son )

14a. Chromosomal diseases, causes and mechanisms of development, phenotypic

manifestations.

Chromosomal disease: this disease are caused by chromosomal mutation in the germinative
cell of one parent that manifest itself in the offspring.
Causes :

• errors during meiosis

• Errors during mitosis
• Exposure to teratogenic substances
Mechanism of developement: this occurs when there is an error in the cell division resulting
in cells with too few or too many copies of chromosome.
Examples of chromosomal disease

Down syndrome: The pathogenesis involves 1) meiotic nondisjunction (95%) the

karyotypes are 47, XX, +21; 47,XY,+21, 2) Robertsonian translocation (4%) the
karyotypes are 46,XX,t(15q21q); 46,XY,t(15q21q), or 3) mosaicism due to mitotic
nondisjunction during embryogenesis (1%) the karyotypes are 46,ХХ or XY / 47,
XX or XY, +21.

Clinical finding/phenotypic manifestation: can include intellectual disability;

mongoloid facial featuresflat face, low-bridged nose, and epicanthal folds);
Brushfield spots (speckledappearance of the iris); muscular hypotonia; broad short
neck; palmar (simian)crease; and congenital heart defects.

Patau syndrome (trisomy 13): is caused by nondisjunction. The risk increases with maternal
age.
Clinical findings/phenotypic manifestation: can include intellectual disability; cleft lip
and/or palate; cardiac defects; renal abnormalities; microcephaly; holoprosencephaly; and
polydactyly. The very poor prognosis is due to severe congenital malformations.

Klinefelter syndrome is caused by meiotic nondisjunction and is a common cause

of male hypogonadism. The most common karyotype is 47,XXY.
Clinical findings/phenotypic manifestation: include testicular atrophy, infertility due to
azoospermia, eunuchoid body habitus, high-pitched voice; female distribution of hair;
and gynecomastia.
Lab studies show elevated FSH and LH with low levels of testosterone.
Turner syndrome is a common cause of female hypogonadism. The most common
karyotype is 45,X. The second X chromosome is necessary for oogenesis and normal
development of the ovary. Clinically, patients fail to develop secondary sex
characteristics and have short stature with widely spaced nipples. Other features include
gonadal dysgenesis with atrophic streak ovaries; primary amenorrhea; and infertility.

Clinical features involving other organ systems include cystic hygroma and webbing
of the neck; hypothyroidism; congenital heart disease (preductal coarcta¬tion of
the aorta and bicuspid aortic valve); and hydrops fetalis.

Trisomy of the X chromosome: most patient are absolutely normal, women sometimes do
not have any evident clinical consequences. Some of them are normally developed have
children, but more frequently this syndrome declares itself through the hypergonadism,
decreased fertility and intelligence
Trisomy of the type XYY: Men have a very high growth: their sexual development can
be normal and even of enhanced fertility, the level of intelligence is normal or average,
there is a tendency to aggressive behaviour

15a. Principles of prevention and treatment of hereditary diseases.

The etiological prevention of genetically determined diseases means to prevent
exposure or neutralization of mutagenic agents. In prevention of the hereditary diseases,
there are some social factors (restrictions of marriages between close relatives, fight
against prejudices that lead to exclusion based on racial and religious grounds).
TREATMENT:--
The pathogenetic therapy involves correction of the gene damaged by mutation or
replacement of the defective gene with normal, that is, the genetic therapy is the targeted
manipulation of genetic material (the genetic engineering).

Any gene can be isolated from the body and cloned. A new genetic material can be taken
into the genome together with the virus particle, previously depriving it from the ability to
replication) or with the complex of liposomes. It’s possible to isolate and cultivate cells of
the patient, to introduce the extraneous genes, and repose these cells to the same patient.

The substitutive therapy means the introduction of antihemophilic globulin (factor VIII) to
the patients with the haemophilia A; it increases their lifetime, and makes it possible for
some of them to have the normal lifestyle, and even to have children. Gammaglobulin,
Hormones (insulin, thyroxine), enzymes, metabolites, etc. have the same applications. Using
the method of genetic engineering they create fanciful forms of microorganisms capable to
synthesize proteins (interferon, hormones, enzymes, etc.) useful for people

The symptomatic therapy: in the case of mental disorder in hereditary disease it is

recommended to use psychotropic medicines.so, the seadative therapy inporoves the
quality of life of patient with emotional disorders, symptoms of agitation and agression.
Administration of sex hormone for the grils with turners syndrome and boy with klinefelters
syndrome contribute to the developement of secondary sexual characteristics, the onset of
mestruation in girls and in some cases increases the potency in young men and positive
effect on the mental condition of patient.
To stimulate mechanism of own immune protection they use immuno-modulators and
antioxidants. The surgery is very effective in such maldevelopment as the cleft lip or cleft
palate. The colon with the hereditary polyposis has to be removed due to risk of malignancy.

16a. Individual reactivity, role of age, sex, heredity and environmental factors.

Individual reactivity is the ability of the individual to react by change of vital activity
to response of adequate or extreme stimuli of the environment. Individual reactivity is
aimed to preserve or restore of homeostasis and to maintain the health and save the
life of the individual.
Individual reactivity is determined by age, sex, heredity, constitution, and functional
conditions of organism’s regulatory systems, external environmental influences. Individual
reactivity could be specific, non specific, pathological and physiological.
Role of Age: some diseases arise only in infant organism (measles, roseola, small pox,
rachitis, scarlet-fever) but not in adult’s one. Children are less adapted to sharp changes of
air temperature, but infant organism is more resistant to the hypoxia (oxygen deficiency),
than adults. Resistance of the old organism to the infection reduces, but the number of
cancer-ill adults and atherosclerotic-ill increases. Old people have very slowly developing
inflammatory reaction.

Role of Sex: The dependence of the reactivity on sex can beexplained by the morphological
and physiological peculiarities of men and women. Reactivity of a female organism varies
during the menstrual cycle time, pregnancy, climax. Resistance of a women to the hypoxia,
hunger, and bleeding is better, than men’s. Women live longer, than men. But men are
physically stronger.

Role of Hereditary: Heredity - individual reactivity factor. Human genotype determines how
to respond to environmental factors - its norm of reaction.
Reaction norm - is determined by genotype range of adaptive reactions of the organism - its
adaptation in time and space.

Environmental factors: individual reactivity can be changed as a result of influence of

factors of the external environment. Some changes of an ecological situation can prevent
development of disease, and others on the contrary provoke the development of disease.

For example, small dose of an ultraviolet irridiation increases resistance of an organism to

the infectious disease, promote synthesis of vitamin D in the organism, but a large promote
the development of skin burn.

17a. The role of the constitution in human pathology, the concept of diathesis.

Constitution is a unique complex of morphological, functional, mental and biochemical

features of the organism, which determines its individual reactivity( adaptation capacity
and pathological predisposition) and is formed on the hereditary basis under the
influence of the environment.All people belong to some constitutional type.

Classification of constitutional type: morphological, biochemical, serological, temperament

and psychic(higher nervous) activities
Hyppocrate (firstly) had determined the individual peculiarities of the person determined
his reaction on the external environment and caused disease course peculiarities.
Hyppocrate had divided all people on four types:
 • choleric
• phlegmatic
• Melancholic
• Sanguinic.

Sigaud had divided all people into 4 morphological types. This classification is based on the
peculiarities of the anatomic structure of the person.Constitution types by Sigo are:

• respiratory type
• digestive type
• muscular type
• brain type

Krechmer has offered the classification, based on the functional peculiarities of an

organism.Constitution types by Krechmer are:

• asthenic
• athletic
• Digestive
Constitutional types by Chernoruzkiy. He determined due to the size of costal arcs angle of
a person.

• Asthenic (less than 90 degree)

• Normosthenic (90 degree)
• Hypersthenic (more than 90 degree)

А.А.Bogomoletz has offered the classification, which characterizes the connective tissue
peculiarities. Constitution types by Bogomoletz are:

• asthenic type,
• fibrosis type,
• pastosis type, • lipomatosis type.

William sheldon has based his classification on development of derivatives of a specific germ
layer
• Ectoderm( dolicomorphic and hypotrophic)
• Endoderm( brachymorphic and hypertropic)
• Mesoderm(normotropic)
I.P Pavlov distinguished 4 constitutional type (as the type of hippocrate)
• Choleric which he distinguished into the strong, mobile and unbalanced
 • Sanguinic : into the strong, balanced and mobile
• Phelgmatic: into the strong balanced and slow
• Melancholic: weak

Concept of diasthesis:
Diathesis is the manifestation of the abnormal constitution, which is characterised
by the abnormal reaction of an organism to the physiological and pathological
influences. Diathesis appears the most frequently during the childhood, because the
homeostatic regulation mechanisms are imperfect.
There are 4 types of the diathesis:

• exudative-cataral,
• lymphohypoplastic, • nervous-arthritic,
• asthenic.
Exudative- catarrhal: Very intensive exudative processes, allergy reactions and long
disease course, characterize the development of the inflammation in such patients,
who are suffering from the exudative-cataral diathesis. Allergic reactions are the
result of the high level of immunoglobulines in the patient’s blood, so bronchial
asthma, and anaphylactic shock саn develop very often.
Lympho-hypoplastic: The patients, who are suffering from the lymphohypoplastic
diathesis, are usually pale, theirs muscular tissue is developed deficiently, the
lymphatic nodes size is increased. The aytoallergic diseases arise in these patients
very often.
Nervous-arthritic diathesis cause the obesity intensification, nervous system irritability,
diseases of joints, skin diseases, psychological disorders in some patients.
Astenic diathesis is characterized by adynamia; lability of vascular reactions and
gastroptosis.
Diathesis is not a fatal condition of the patient. The environment can promote
or inhibit its manifestation. The causes of many forms of diathesis, probably,
are hereditary pathology of different enzymes.

18a. Aging, changes in the body, disorders of the nervous, endocrine and immune systems
during aging, progeria. Principles of geriatrie protection.

Ageing is a progressive deterioration of various functions after an organism attains

reproductive maturity
Changes in the body Changes that accompany ageing can be identified at the various levels
of biological organization of an entire organism.
Heterochroneity and heterotopicality of ageing upon reaching certain age, the capacity for
adaptation sharply decreases and the organism dies
Changes of the systems and organs

✓ In the nervous system- neural cells decreases and the number of glial cells or
elements increases in some layers of the brain cortex along with their constancy in
other brain areas. Lipofuscin is accumulated in the neuronal body. Rate of impulse
conduction also decreases, memory declines, creative activity and ability to study
decreases

✓ In the endocrine system-the function of sexual glands is weakened, significant

changes occurs in the thyroid gland, decrease insulin level in blood, weakened
activity of thyroid gland, in general decrease metabolic activity

✓ In the immune system- decrease reactivity to alien antigen, immune deficit, increase
in frequency and intensity of immune reactions against its own
antigensautoimmunity and potential inclination to the lymphoproliferative diseases
Progeria(Hutchinson-Gilford progeria syndrome) -is a specific type of genetic disorder that
causes children to age rapidly. The getic mutation occurs randomely and its non-hereditary.
Patients born with progeria live to an age of mid-teens to early 20’s. Severe cardiovascular
complications usually develop by puberty, resulting in death.
Principles of geriatrie protection-there are 3 main principles i.e

• Variability of capabilities within an aged group is more pronounced than younger.

• Hypokinetcs-describes the physiology of inactivity( immobility ) which is the losses in
functional capabilities.
• Optimal health- is the state of complete physical, mental and social well being. There
are some cumulutive effects ie biological, physiological, anatomical. Prventing
impairements and disability is a key principle in geriatric rehabilitation.

19a. The role of connective tissue in organism resistance. Violation of the structure and
function of the connective tissue.

The role of connective tissue in organism resistance

Connective tissue, which surrounds the vessels and penetrates into a tissue, executes the
Protective function too. The most powerful and complex barrier surrounds the nervous
system And organs of reproduction.
The nervous cells are the most sensitive to the internal Environment changes. The
hematoencephalic barrier permeability is various in different sites of The central nervous
system.
Other examples of resistance are hematoophtalmic (blood-eye tissue), hematolabirintic
(blood-lymph of a labyrinth), hematoovarial (blood-ovarium tissue), hematotestical (blood
testicular tissue), placenta (mother’s blood-fetus blood).
For example, hemato-encephalic barrier in the area of hypothalamus pass all substances,
Which are in the blood. The information about the chemical structure of blood is necessary
for The hypothalamus functions correction. The delay of the information can be dangerous
for life.

• Hematoencephalic barrier includes the endothelium of the brain capillaries, their

basal Membrane, the glia and the brain coats.
• Hematoencephalic barrier structure: slots between Endothelial cells of the capillaries
are absent; glial cells cover all surface of the capillary; basal Membrane is very
dense.
• The peculiarity of the hematoencephalic barrier structure promotes protection of
the brain Against the influence of toxic substances. But in some cases this property
complicates the Treatment of some diseases of the nervous system.

Violation of structure and function of connective tissue -:

• The permeability of barrier amplifies when The temperature of body increases.

• The protective function of barriers is dependence on nervous and humoral
influences, on a state Of the external and internal environment.
• The alcohol has specific influence up Hematoencephalic barrier.
• The permeability of this barrier increases during initial stage of alcoholism, so
various toxic Substances influence up the brain. Then permeability of the barrier
decreases, that provokes Violation of nutrition of the brain.
• Alcoholic psychoses, degradation of the person, premature Aging develop in such
patients. The alcohol easily damages reproductive system, poisons a Foetus.

20a. Protective mechanisms of reactivity, types of resistance, violation of phagocytosis

and complement system.
Protective mechanism is regulated by three physiological levels: nervous system,
endocrine system, and local, tissue-specific mechanism. The systems determining reactivity
are nervous system, endocrine system, immune system, monocyte- macrophages system.

Types of resistance: active and passive resistance, primary and secondary resistance,
specific and nonspecific resistance.

✓ Active resistance is a result of the organism adaptation to the long-time pathological

factor influences.
 ✓ Passive resistance is a result of anatomical and physiological peculiarities of each
organism.

✓ Primary (congenital) resistance is a result of the inherited peculiarities of an

organism and it manifest itself after birth of the person.

✓ Secondary (acquired) resistance is a result of organism functional reactions changes,

which occur during the whole life.

✓ Unspecific resistance is the opposition to the influence of many pathological agents.

✓ Specific resistance is the opposition to the defined agent influence, for example,
microorganisms; its result is activation of the immune system.

Violation of phagocytosis and complement system:

Lysosomal storge diseases-tay-sachs disease, GM2 gangliosidosis deficiency, niemann pick

dieases types A and B, gaucher disease, mucopolysaccharidoses
Chediak higashi syndrome, chronic granulomatous diseases is an inherited defect in
phagocytic cells so that they are unable to produce superoxide and related toxic
metabolites.
Disorders of the complement system- there ae hereditary and acquired changes of the
complement system.
C1 deficiency blood system loses its bactericidity,
C2 deficiency causes decrese of bactericidal acitivity of the blood serum,
C3 deficiency causes high mortality,
C5 deficiency determines the development of severe intestinal infections caused by gram
negative bacyteria
C7 deficiencies leads to the development of the diffuse connective tissue diseases
Decrease acitivity of phagocytosis occurs under the influence of gluocortoocoids, mediator
of the nervous systems acytecholine with a deficiency of certain hormones, vitamins and
water electrolye imbalance.

21a. System of mononuclear phagocytes, its role in the development of pathology,

methods of their study.
System of mononuclear phagocytes (SMP) is represented by a group of cells which has a
phagocytic function, its degree of activity depends on the degree of protection of the
organism and the emergence of allergic and immune deficiency diseases. SMP has three
main features—

• mutual function (all these cells are capable to phagocytes);

• mutual derivation (all these cells derive from the stem cell of red bone marrow);
• mutual structure (all these cells have one nucleus).
The mononuclear phagocyte system includes:- Monocytes ,Macrophages/histiocytes, and
dendritic cells. Macrophages/histiocytes are tissue based cells that have an important
phagocytic function and produce a variety of Bioactive substances that play roles in
inflammation and fibrosis.
ROLE IN PATHOLOGY
The mononuclear phagocyte system has two specific functions-

- phagocytosis of Foreign material

- processing and presentation of antigens to T cells by antigen presenting cells.
The pathology of SМP cells can be hereditary and can occur during life. The hereditary
defects of the enzymes myeloperoxidase, glucose-6 phosphate dehydrogenase, enzymes of
glutation system, lysosomal hydrolases provoke the violation of macrophages protective
functions.
Primary metabolism violations of an organism (diabetes mellitus, obesity, atherosclerosis,
uremia), malignant tumors, intoxication can cause the defects of macrophages too.
The inflammatory response (inflammation) occurs when tissues are injured by Bacteria,
trauma, toxins, heat, or any other cause. ... This helps isolate the foreign Substance from
further contact with body tissues. The chemicals also attract white Blood cells called
phagocytes that “eat” germs and dead or damaged cells.
METHODS OF STUDY

 Obtaining and Culturing Mononuclear Phagocytes

 The Culture of Mononuclear Phagocytes
 Murine Mononuclear Phagocytes from Bone Marrow
 Culture of Human Monocytes in Microplates and Enzymatic Assays for
Following Their Maturation
 Obtaining Adherent Cells from Spleen, Kupffer Cells, Mononuclear Phagocytes
from Disaggregated Neoplasms and Granulomas
 Fc and C3 Receptors
 Identification of Mononuclear Phagocytes by Ingestion of Particulate
Materials, such as Erythrocytes, Carbon, Zymosan, or Latex
 Quantitation of Number of Mononuclear Phagocytes, Adherent
 Mononuclear Phagocytes by Inverted Phase Microscopy, DNA in
Mononuclear Phagocytes
 Chemotaxis of Human and Murine Mononuclear Phagocytes
 Growth of Macrophage on Collagen, Elastin, and Glycoprotein-Coated Plates
as a Tool for Investigating Macrophage Proteinases
 Destruction of Listeria monocytogenes in Vitro, Candida albicans,
Toxoplasma, Rickettsiae, Leishmania, Viruses
 Extraction, Identification, and Quantitation of
Lipids Synthesis, Cellular Turnover, and Mass
of Cholesterol
22a. Immunodeficiency diseases: definition of the concept, classification, examples,
characteristics.
Immunodeficiency, also known as immunocompromising, is a state in Which the immune
system’s ability to fight infectious diseases and cancer is Compromised or entirely absent.
Most cases are acquired (“secondary”) due to Extrinsic factors that affect the patient’s
immune system.
Classification
Immune deficiency diseases may be classified as primary or secondary.
Primary immune deficiencies result from genetic or development abnormalities in the
acquisition of immune maturity.
Secondary deficiencies result from diseases or drugs that interfere with the expression of a
mature immune system.
EXAMPLES
• Ataxia-telangiectasia.
• Bruton’s X-linked agammaglobulinemia.
• Complement deficiencies.
• DiGeorge syndrome. • Hypogammaglobinaemia.
• Job syndrome. • Leukocyte adhesion defects.
• Agammaglobulinemic. • Wiskott-Aldrich syndrome.

Examples of secondary immunodeficiency diseases:-

• AIDS
• Cancer of immune system like leukaemia
• Immune complex disease (viral hepatitis)
• Multiple myeloma (cancer of plasma cells)
Symptom (Characteristics)
• Frequent and recurrent pneumonia, bronchitis, sinus infections, ear infections,
Meningitis or skin infections.
• Inflammation and infection of internal organs.
• Blood disorders, such as low platelet counts or anemia. Digestive problems, such as
cramping, loss of appetite, nausea and diarrhea.
• Delayed growth and development.

23a. Immunosuppressive conditions. AIDS. Principles of immune correction.

Immunosuppression means that the immune system does not function properly. This can
be caused by disease or induced by medications such as chemotherapy and
immunosuppressants.
Immunosuppression arises in cases like—

• Protein loss (blood loss, kidney and liver insufficiency)

• Tumors of lymphoreticular system
• Corticosteroids, ionizing radiations • Bacterial, viral or fungal infections.
AIDS stands for acquired immune deficiency syndrome. It's also called advanced HIV
infection or late-stage HIV. AIDS is a set of symptoms and illnesses that develop when an
advanced HIV infection has destroyed the immune system
Stages of Infection HIV–
• Stage 1: Infection.
• Stage 2: Asymptomatic.
• Stage 3: Symptomatic.
• Stage 4: AIDS/Progression of HIV to AIDS.
HIV attacks a specific type of immune system cell in the body. It’s known as the CD4 helper
cell or T cell. When HIV destroys this cell, it becomes harder for the Body to fight off other
infections. When HIV is left untreated, even a minor Infection such as a cold can be much
more severe.

Principles of immune correction.

(1) ability to detect and fight off infection;
(2) ability to recognize a host’s own cells as “self,” thereby protecting them from attack;
(3) a memory from previous foreign infections; and
(4) ability to limit the response after the pathogen has been removed.

24a. Allergy: definition of the concept, causes, characteristics of allergic reactions by

Coombs’ and Gell’s.

Allergy is a immune response which is followed by damage of own tissues. It is often

caused by allergens.
CAUSES:
-Exogenous allergen: Dust, medicine pollen, food, industrial allergen
-Endogenous allergen: Autoallergen

Classification of allergic reactions by coombs

1. Type 1 hypersensitivity or Anaphylactic: atopic bronchial asthma, pollinosis,
atopic dermatitis. This occurs under the influence of mediators , the permeability of
vessel and chemotaxis of neutrophils and eosinophils increase which lead to
inflammatory reactions can cause bronchospasm, spams of GIT muscles, spasm of
uterus in women, decrease arterial pressure and heart insufficiency.
2. Type 2 hypersensitivity or Cytotoxic: blood transfusion, rhesus incompatability
of mother and fetus. Occurs due to antibodies that developed to antigen of the cell
binds to cells and cause their damage or even lysis (cytolitic action). Damage of cells
with the antigen properties may be caused by activation of complement components of
which damage cell membrane, activation of phagocytosis of cells covered with
antibodies due to activation of T lymphocytes, natural killers and K lymphocytes.
3. Type 3 hypersensitivity or Immune complex: food allergy, auto allergic diseases,
rheumatoid arthritis, systemic lupus erythematous. If immune complexes (mediators
C3a, C5a, C4a), lysosomal enzymes are placed on canalicular apparatus of kidney
inflammation with alteration, exudation and proliferation (glomerulonephritis) occurs. If
on lungs alveolitis occurs. If on skin dermatitis occurs. Inflammation may lead to
formation of ulcers, hemorrhages and thrombosis in vessels.
4. Type 4 hypersensitivity or Delayed type: Transplant rejection. Lymphotoxin
interferon shows a cytotoxic action and decreases activity of cell. Allergic reaction of
delayed type may develop due to -Direct cytotoxic action of sensitized T lymphocytes on
target cells, which acquired auto-allergen properties
25a. Stages of allergic reactions.

Allergy occurs when a person reacts to substances in the environment that are harmless to
most people. These substances are known as allergens and are found in dust mites, pets,
pollen, insects, ticks, moulds, foods and some medications.
In the development of allergic reaction there are three stages:
• Immunological stage. It covers all the changes in immune system during the
penetration Of an allergen into the organism, formation of antibodies or sensitized
lymphocytes and Their binding with the repeatedly entering allergen.
• Pathochemical stage. Its sense is in formation of biological active substances. The
Stimulus to their formation is the binding of allergen to antibodies or sensitized
lymphocytes At the end of immunological stage.
• Pathophysiological stage. It is described by pathogenic action of formed mediators
onto
Cells, organs and tissues of the organism with a clinical display

Types of allergies: • Type I or anaphylactic reactions • type II or cytotoxic reactions • type III or
immunocomplex reactions and • type IV or cell-mediated reactions.

26a. Autoallergy, mechanisms of autoantigen formation.

Autoallergic or autoimmune diseases develop as a result of the antibody or T-killer cells

capable to react with antigens of its own body.
Auto allergens may cross link effector cell bound IgE autoantibodies and by release of
inflammatory mediators, lead to immediate type symptoms or IgE mediated presentation of
autoallergens may activate autoreactive T cells to release proinflammatory cytokines,
contributing to the magnitude of the allergic tissue reaction.
Autoallergic diseases are diseases such as rheumatoid arthritis and systemic lupus
erythematosus.
Autoantigen is a normal or complex of proteins and sometimes DNA/RNA that is recognized
by the immune system of patients suffering from specific autoimmune disease Autoantigens
are the result of mutation, neoantigen formation or exposure of previously hidden
selfantigens. Viral infections and drugs can create neoantigens that stimulate an immune
response

27a. Basic principles of prevention and treatment of allergic reactions in practice.

Prophylaxis of an allergic disease depends on its character and group of the allergens.
It consists of measures of preventing of penetration of given allergen into the organism and
preventing of the influence of different irritating factors on the organism. If sensitization has
already occurred and allergic diseases has already started, the following measures are
appropriate.
1. Suppression of antibodies and sensitized lymphocytes production with the helpof
immune depressants, ionizing radiation, cytostatics, specific lymphocyte vaccines and
monoclonal antibodies.
2. Specific desensitization by Bezredka. Desensitization is provided by little doses of
the antigen, which do not cause severe reactions. The doses are introduced repeatedly after
certain intervals of time, during which produced mediators get inactivated in the organism.
The main dose of the antigen is introduced after antibodies binding. This method is effective
in introduction of foreign medical vaccines.
3. Inactivation of biological active substances. For this purpose antihistamine
preparations, inhibitors of proteolytic enzymes etc. are introduced.
4. Protection of the cells from the influence of biological active substance and also
normalizing of functional disorders in organs and systems (narcotic, spasmolytic substances,
receptor blockers etc.).

28a. Arterial and venous hyperemia, causes of occurrence, characteristics, consequences.

ARTERIAL HYPEREMIA

Arterial hyperemia is the enhanced blood filling of an organ because of the reinforced Blood
inflowing through arterial vessels.
CAUSES OF OCCURRENCE -: Pathological arterial hyperemia is observed when the part of
body or all organism exposes to the influence of unusual factors of external or internal
environment – microbe toxins, chemical substances, biologically active substances etc.
Arterial hyperemia characterizes such signs as:--

• redness, dilatation of small arteries, Capillaries and veins, arteries

• pulsation, the increasing of the volume of hyperemic site, rising Of turgor, the
increasing of the pressure in the vessels, local temperature rising.

CONSEQUENCES -: Under the microscope the increasing of blood flowing and of amount of
functioning Capillaries is visible. In hyperemic organ the metabolism is enlarged. In the
patients with Atherosclerosis the arterial hyperemia can result in the negative superventions
( the vessel Rupture and haemorrhage).
VENOUS HYPEREMIA

Venous hyperemia is the increasing of blood supply of and organ or tissue because of the
Difficulties of blood outflow through the veins.
Causes of occurrence -: Venous congestion is caused by such causes, as thrombosis,
embolism, pressing of veins by tumor or enhanced neighboring organ. The outflow of blood
from veins of greater circle slows in insufficiency of right heart and decreasing of attracting
force of thorax (exudative pleurisy, hemo- and pneumothorax).
Venous hyperemia characterize the signs:

• redness with the cyanotic hue; cyanosis is explained by the piling up of restored
Haemoglobin over 30 % from general amouamoun
• local decreasing of the temperature as a result Of the limited inflow of arterial blood
and surplus heat emission)
• slowing-down of blood Stream;
• rise of blood pressure in veins distal from the impediment
• the increasing of the volume of the hyperemic tissue (edema) because of the
transsudation of liquid from vessels.
CONSEQUENCES -:
 dystrophic changes, atrophy, excessive growth of CT, cirrhosis, phelobosclerosis
 Further follows a sclerosis and Consolidation (induration ) of organs. These
phenomena are known under the names of liver Cirrhosis, cyanotic induration of the
spleen and kidneys.

29a. Ischemia, stasis: types, causes, characteristics, role in pathology.

The ischemia (local anemia) is called the diminished organ or tissue blood supply because of
the insufficient inflow of arterial blood.
There are three types of ischemia by the mechanism of their beginning
-Compressive ischemia: Squeezing of artery by tumor, scar, ligature, bandage
-Obturational ischemia: partial or fully closing of lumen of artery by thrombus, embole or
sclerotic plague.
-Angiospastic ischemia: various chemical and biological irritants which narrow the vessels
(trauma, cold, ergotoxine)

A/C to the place of ischemia is occurrence:- Brain ischemia- stroke, Limb ischemia, Bowel
ischemia, Cardiac ischemia/Coronary ischemia.
Cause: Ischemia is caused by a decrease in blood supply to a tissue or organ. Blood flow can be
blocked by a clot, an embolus, or constriction of an artery. It can occur due to gradual thickening of
the artery wall and narrowing of the artery, as in atherosclerosis. Trauma can also disrupt blood
flow.
Signs of ischemia: pallor of the ischemizated site, the decreasing of its volume, local
decreasing of the temperature, pain, the appearance of the paresthesias.
A speed of blood flowing in the arterial vessels beneath the impediment is slowed, the
blood pressure is low, amount of functioning capillaries is diminished.
The consequences of ischemia depend on the depth of anoxaemia. It can get through
without trace or complete by the necrosis of the ischemisated site – the infarction,
gangrene.

STASIS – this is a blood motion stop in the vessels of microcirculative stream, chiefly in the
capillaries.
There are three varieties of a stasis

• True (capillary) stasis: caused by cold and heat, acid concentrated salt solution.
Infectious toxic stasis in extremities of patients with louse borne typhys. Caused by
sladge phenomenon (intracapillary erythrocytes aggregation)

• Ischemic and Venous

Occurs when blood Is reduced ( e.g heart failure or shock when veins are dilated as some
medication therapies .)
When skeletal muscle contraction is reduced ( e.g immobility , paralysis of extremities
anaesthesia)
Bed rest reduce the blood flow of legs by the 50%

30a. Thrombosis, embolism: causes, characteristics, role in pathology.

Thrombosis-coagulation of blood in lumen of blood vessels or heart cavities with formation
of a thrombus. A clot of blood (lymph), that formed, is called thrombus.
CAUSES: Three primary factors (Virchow triad ) influences predispose to thrombus
formation –
Two local causes-- (1. endothelial abnormality or 2. blood flow abnormality)
One general cause --(3. hyper- coagulation or change in blood composition)
Thrombosis characteristics: in the area affected will be swollen, redness or Discoloured skin,
tenderness or pain in the area, feeling of warmth in the Affect area.
Thrombosis role in pathology is the formation of a blood clot, known as Thrombus, within a
blood vessel. It prevents blood from flowing normally Through the circulatory system.

The embolism is obstructing up of lymphatic or blood vessels by the particles (еmbols),

which in norm in blood and lymph do not meet.
Embolism is subdivided on exogenous and endogenous.
The exogenous embolism may be: air, gaseous, bacterial, parasite, made by foreign bodies.
Endogenous embolism subdivides on: thrombembolism, fatty, tissue, embolism by amniotic
fluid.
Embolism characteristics: • pain, swelling and tenderness in the area • heavy ache in the
Affected area • warm skin in the area of the clot • • red skin, depending on the embolism , •
Will appear shortness of breath • drooping of the face • weakness or numbness • slurred
Speech, • stabbing pain in chest • dizziness.
Role in pathology: usually occurs as consequence of a thrombosis, Accompanying illness or
injury. Sometime is created for a therapeutic reason, to stop Bleeding or to kill a cancerous
tumour by stopping the blood supply, this therapy is called Embolization.
Complication is the embolism of pulmonary artery. It arises in the patients with thrombosis
of lower extremities and the cavity of right heart. Embolism of greater circulation
reverberates on the structure and function of the organs, into which the embols are
brought.

31a. Cell damage: characteristic, necrosis, apoptosis, autophagy.

Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due
to external as well as internal environmental changes. Cell damage can occur in many ways
such as injury from physical agents, radiation injury, chemical injury, injury from biologic
agents and injury from nutritional imbalances
Necrosis refers to cell death in an organ or tissue that is still part of a living person.
• With prolonged necrosis, most organelles are disrupted and there occurs karyolysis,
karyorrhexis and pyknosis.
• It is characterized by cell swelling, rupture of the cell membrane, and inflammation.
• The cell can undergo liquefaction (i.e., liquefaction necrosis); it can be transformed
to a gray, firm mass (i.e. coagulation necrosis); or it can be converted to a cheesy
material by infiltration of fatlike substances (i.e.caseous necrosis).

Apoptotic cell death involves controlled cell destruction and is involved in normal cell deletion
and renewal. For example, blood cells that undergo constant renewal from progenitor cells in
the bone marrow are removed by apoptotic cell death. Its activation is observed after ionizing
radiation, hypoxia, under effects of microbes’ waste products.

Autophagy - a type of a cell death that occurs in the absence of chromatin condensation but
accompanied by massive autophagic vacuolization of the cytoplasm. Massive vacuolization of
the cytoplasm, engulfing of intracellular organelles and cytoplasmic materials.
Accumulation of double membrane autophagic vacuoles, little or no uptake by phagocytic
cells in vivo.
Cellular stresses, such as nutrient deprivation, activate autophagy genes that create vacuoles
in which cellular organelles are sequestered and then degraded following fusion of the
vesicles with lysosomes. The digested materials are recycled to provide nutrients for the cell.

32a. Inflammation: definition of the concept, the main components of the inflammatory
reaction, local features.

It is a typical pathological process, which arises after damage of tissue and consists of three
main vessel-tissue components -alteration; -violation of microcirculation, exudation and
migration of leucocytes; -proliferation.
Main components of inflammatory reaction :

✓ Alteration: Damage of the tissue and formation of the biological active substances
are the main effects of the alteration. Primary alteration is the result of pathological
agent influence on a tissue.
Secondary alteration is the consequence of the primary alteration and that arises even
at the absence of the damaging agent. Metabolism disorder (local acidosis, hyperosmia,
hyperoncia), violation of microcirculation, free radicals formation, biological active
substances action, lysosomal enzymes (damaged cells origin) conduce its development.

✓ Exudation: Violation of microcirculation and emigration of leucocytes in the center

of an inflammation. The first stage of microcirculation violation is the short-term
spasm of vessels (arterioles), the second is the arterial hyperemia, the third stage is
the venous hyperemia, the fourth stage is the prestasis, and the stasis is the fifth
stage.
The stages of leukocytes emigration are

• edge standing
• penetration through the vessels wall
• move in area of inflammation.

Types of exudates are: serous; fibrinous; purulent; rotten; hemorrhagic.

✓ Proliferation: Tissue regeneration. It depends on

1.Interaction of the connective tissue cells between each other
(endotheliocytes, fibroblasts, macrophages, lymphocytes);
2.Interaction of the connective tissue cells and fibrous element (collagen,
proteoglicans, fibronectine);
 3. Interaction of the connective tissue cells, blood cells and parenchymal
cells.

Local features :
SWELLING (lat. - tumor) - is the result of exudation
REDNESS (lat. - rubor) - is the result of arterial hyperemia
HEAT (lat. - calor) - is the result of arterial hyperemia and impermanent intensification of
metabolism in the focus of inflammation.
PAIN (lat. - dolor) - pain is the result of the painful receptors irritation by biological active
substances, metabolites, and pressing of painful receptors by exudate
LOSS of a FUNCTION (lat. - functio laesa) is the result of the functional active tissue injury.

33a. Mediators of inflammation: classification, biological effects.

Mediators of an inflammation, as the signal's system, provide the exchange of the information
between the cells, which cooperate and destroy the pathological agent. The system of
mediators not only provokes various responses of tissues, but also is responsible for their
interrelation. Therefore inflammation has stereotyped components, such as alteration,
vascular response, exudation, phagocytosis, and proliferation.
Classification:
1) HUMORAL : Humoral mediators are characterized by the widespread effects;
spectrum of their influence is very wide.
-complement system proteins
-bradykinin
-kallidin
-Coagulative proteins

2) CELLULAR : The effects of cellular mediators are local.

-histamine
-serotonin
-lymphokines (IL-1, IL-6 et all.)
-monokines
-prostaglandines
-leucotriens
-lysosomal enzymes

Biological effects:
1) Histamine : vasodilation; increases permeability of the capillaries; activation of
leucocytes emigration; Stimulation of phagocytosis; increases adhesive property of the
vessels endothelium; pain.
 2)lnterleukin-1 : Muscles --> pain; joints --> pain; CNS --> somnolence; Liver --> Protein
synthesis activation; Thermoregulative center --> fever.

34a. Alteration in inflammation. Physicochemical changes in the center of inflammation.

The first stage is alteration, with which all forms of an inflammation begin. This stage is
characterized by the violation of cells structure and function, of fibrous structures, of the
microcirculatory system, nervous derivations.

The damages of tissues are characterized by the disorder of proteins, fats, and carbohydrates
metabolism, physical-chemical and morphological changes of tissues. The more complicated
protein fibrous derivations (collagen, elastin) can also be destroyed.
Necrobiosis and necrosis can take place in tissues. It is the reversible (sublethal) damage of
cells, if they can adapt and restore their structure and function, and the irreversible (lethal)
damage of cells, which is characterized by irrevocable change of cells structure.

There are two type of the alteration: primary and secondary.

The primary alteration is the result of the influence of the pathological (flogogenic) agent on
a tissue. Metabolic and structural changes arise therefore. Various cells react differently:
some cells perish, others - remain alive, and others become activated. The activated cells are
responsible for the creation of following stages of an inflammation.

The secondary alteration is the consequence of the primary alteration and it arises even at
the absence of the damaging agent.
The signs of cells damage are the follows: the lessening pO2; limitation or termination of 02
consumption by cells; the decrease of ATP and ADP and the increase of the inorganic
phosphorus concentration; the intensification of glycolysis, which cause the accumulation of
lactic acid and piruvate acid; the decrease of cells pH.

The decrease of ATP concentration reduces the activity of ionic pumps of cells membranes,
the parity of Na, K, Ca and Mg in cytoplasm is violated, and the activity of biochemical systems
of cells is violated too. Then content of water in cells changes, the synthesis of protein
decreases, the density of cytoplasm raises, the amount of H+ increases, the outlines of the
cell change. These changes are reversible.

The constant deficiency of energy provokes the rise of permeability of organelles membranes
and swelling of the cell takes place. These changes are the result of the significant damage of
cells membrane structures.

Free radicals and peroxides play the significant role in this process. They are the result of
hypoxia of the damaged tissues and the violation of biochemical processes in cells. The
accumulation of free radical substances exceeds the possibility of the cell to neutralize them.
Therefore these substances damage membrane structures of the cell.
35a. Violation of local blood circulation in area inflammation, stages, pathogenesis.
Disturbance of the microcirculation in the inflammation area.
stages of disturbance of the microcirculation in the inflammation area.
-1 stage: short time spasm of vessels (arterioles, 10-20 seconds till several minutes)
-2 stage: Arterial hyperemia (20-30 minutes, less than an hour
-3 stage: Venous hyperemia
-4 stage: Prestasis
-5 stage: Stasis
Spasm (constriction) of arterioles is a result of vasoconstrictive adrenergic nerves
stimulation by the catecholamines. Catecholamines stimulate -adrenoreceptors and
promote the contraction of smooth muscles of vascular wall.
The duration of first stage is short, because the depot of catecholamines in the nervous
endings is exhausted very fast and monoamineoxydase destrois the released mediators.
The activation of cholinergic nerves and the excretion of acetylcholine promote the
development of the second stage of microcirculation violation – the arterial hyperemia.
This mechanism is short- term, because acetylcholinesterase destrois acetylcholine.
The significant duration of this stage is stipulated by the excretion of vasoactive mediators
of the inflammation, which influences on the walls of arterioles and precapillaries
(histamine, serotonine, bradykinine, kallidine, prostaglandines).

36a. Exudation in inflammation. Mechanisms of its development. Types of exudates.

Exudation is the release of fluid and dissolved blood plasma components from blood vessels
into the tissue. In a broad sense, this concept includes the emigration of leukocytes.
The exudation is based on the following mechanisms: 1)

increasing the permeability of the vascular wall involving;

a. Activation of microvesicular transport through endothelial cells.
b. Formation of end-to-end transcellular channels in endotheliocytes
c. Increase in a gleam of intendothelial cracks (occurs as a result of reduction and
rounding of endotheliocytes).
d. Desquamation (exfoliation) of the endothelium. Is a manifestation of primary and
secondary Alteration.
e. Depolymerization of substances that connect endothelial cells and are components
of the basement membrane of the vascular wall
2) increase in hydrostatic pressure in vessels;
3) increase in osmotic and oncotic pressure in the tissue.
The increase of vascular wall permeability provokes exudation, emigration of leucocytes.
The permeability of microvessels increases first of all (especially of venules). The
amplification of exudation provokes: of reologic properties blood change and micro
perfusionas the result of blood condensation; of laminar blood stream violation; of plasma
structure change after the output into the tissue proteins; of microvessels compression by
the edematic liquid.
Types of exudates
-Serous: promotes washing off of microorganisms and their toxins from the damaged
surfaces. But the serous exudate in brain coats can squeeze the brain and violate its
function. The serous inflammation of lungs alveolar septs can cause the development of
acute respiratory insuffiency syndrome.
-Fibrinous: contain plenty fibrinogen which forms clots of fibrin in tissues. E.g corynebacteria
diphtheria, pneumococcus
-Purulent: smell bad, consist of many viable leukocytes and purulent bodies (perishing
leukocytes), cells detritus , microorganisms, proteins (especially globulins). Seen in
staphylococcus, gonococcus, meningococcus
-Rotten: invasion of rotten microorganism in purulent inflammation
-Hemorrhagic: erythrocytes impurity to exudates. E.g Siberian ulcer, small pox, influenza
combination forms of inflammation are characterized by connection of one type of exudate
to another

37a. Emigration in inflammation. Stages of emigration. Sequence of the output of

leukocytes, their role in area inflammation.

In most cases of acute inflammation, neutrophils migrate first (process lasts about 6-24
hours). In 24-48 hours, monocytes emigrate most actively. Lymphocytes emigrate a bit later.
Lymphocytes emigrate first time during virus infection and tuberculosis and eosinophils
emigrate during allergic reactions.
Stages of migration
-Edge standing
-Penetration through vessel wall -Move
in area of inflammation.
Leukocytes regulate of the cells cooperation and delete the alien agents or the detritus of
defective tissues.
The neutrophiles (microphages) destroy pathological agents due to the following properties:
the absorption of the foreign agent (phagocytosis), the microbicydity and cytotoxicity (these
are the mechanisms of the foreign agent destroy by such biooxidants as superoxide anions,
hydroxyl- radicals, singlet oxygen, peroxide),the intra-and extracellular lysis.

38a. Mechanisms of proliferation in inflammation, the role of mitogens and keylongs.

Reparation, regeneration, mechanisms of sclerosis.
Proliferation phase is a phase of the reparatory regeneration. The restoring of the damaged
tissues structure depends on the interaction of connective tissues cells among themselves
(fibroblasts, macrophages, labrocytes, lymphocytes, endotheliocytes), on the interaction of
connective tissues cells with the intercellular matrix (collagen, proteoglicans, fibronectine),
on the interaction of connective tissue cells with blood cells and parenchymal ones.
The process of cells proliferation is regulated by substances, which can stimulate (mitogens)
or oppress (keilones) the reproduction of cells.
Mitogens stimulated cell division by increasing the amount of G1 cyclins.G1 cyclin-CDK leads
to active G1/S cyclin-CDK by increasing the transcription of G1/S cyclin and removing an
inhibitor of G1/S cyclinCDK.
Mechanisms include cross reactivity with CNS myelin antigens, triggering an already
expanded autoreactive immune repertoire or a self-limited infection of the brain that
releases myelin antigens.
The reparative stage of inflammation begins when phagocytes actively swallow the
microorganisms or the tissues detritus. At that time labrocytes activate interaction with
macrophages, fibroblasts, and intercellular matrix, clotting blood system and promote the
excretion and the synthesis of substances, which stimulate proliferative processes
Regeneration-It means the proliferation of predecessors of the destroyed parenchymal cells
mechanism of sclerosis: heterogeneous multisystem connective tissue disease with
autoimmune component of unknown origin, characterized by microvascular lesions,
inflammation, and immune system activation, leading to progressive fibrosis of conjunctive
tissues of the skin and internal organs.

39a. Fever: definition of the concept, types of fever by origin, the role of pyrogens. The
difference between fever and hyperthermia.
Fever is increase in body temperature above normal 36.5 degrees due to problems with
thermoregulation but in practice a person is usually not considered to have a significant
fever until the temperature is above (38 C).
Types of fever by origin
-Febris continua (permanent fever): 1 degree difference between morning and evening. In
croupous pneumonia, first period of abdominal typhus
-Febris remitens (indulgence fever): 1-2 degrees difference or more between morning and
evening. Viral infections, sepsis, 2nd period of abdominal typhus
-Febris intermittens (alternating fever): period of rising temperature (paroxysmus 40
degrees or higher single peak) followed by a period of normal temperature. Seen in malaria.
-Febris hectica (hectic/ exhausting fever) : 3-4 degrees increase, sometimes temperature
goes below norm. TB, malignant tumor
-Febris inverse (inverse fever): Max temperature in the morning, minimum in evening. Seen
in sepsis, TB
-Febris recurrens: Rising temperature 5-8 days, then normal (non fever period) few days.
Recurrent typhus, malaria
-Febris undulans: slow increase of body temperature then normal slowly, looks like a wave.

Pyrogen -is a substance that induces fever. Can be

-Exogenous: bacteria (lipopolysaccharides which stimulates interleukin 1 and 6)
-Endogenous: are cytokines such as interleukin 1 and 6 that are part of immune system.
They are produced and activated by immune cells and cause the increase in
thermoregulatory set point in hypothalamus
Difference between fever and hyperthermia
 Fever is the elevation of body temperature due to the resetting of the hypothalamic
set point in response to endogenous or exogenous pyrogens.
 Fever is a typical pathological process. Hypothermia is the elevation of body
temperature above the hypothalamic set point due to the failure of the body’s heat
dispersing mechanisms(thermoregulation failure).

40a. Stages of fever, mechanisms of changes in the processes of heat production and heat
loss.

Stage 1: heat production prevails over heat emission. The peripheral vessels narrows,
diminishes and influx of warm blood peripheral tissues, diminishes sweat separate and
evaporation
Stage 2: stage of high standing. In this stage heat production becomes equal as heat
emission. On temperature up degree in second stage distinguish such types of fever: -
subfebrile fever: up to 38 degrees
-Moderate fever: 38-39 degrees
-High fever: 39-41 degrees
-hyperpyretic fever: above 41 degrees
Stage 3: action of interleukin 1 on thermoreglation centre ceases. Centre of heat production
is oppressed.
Mechanism of heat production
Metabolism is the body’s main source of heat production. The sympathetic
neurotransmitters, epinephrine and norepinephrine, which are released when an increase in
body temperature is needed, act at the cellular level to shift metabolism so energy
production is reduced and heat production is increased. This may be one of the reasons
fever tends to produce feelings of weakness and fatigue.
Thyroid hormone increases cellular metabolism, but this response usually requires several
weeks to reach maximal effectiveness. Fine involuntary actions such as shivering and
chattering of the teeth can produce a threefold to fivefold increase in body temperature.
Shivering is initiated by impulses from the hypothalamus.
Mechanism of heat loss
Most of the body’s heat is produced by the deeper core tissues (i.e., muscles and viscera),
which are insulated from the environment and protected against heat loss by the
subcutaneous tissues.
Adipose tissue is a particularly good insulator, conducting heat only one third as effectively
as other tissues.
Heat is lost from the body through radiation and conduction from the skin surface; through
the evaporation of sweat and insensible perspiration; through the exhalation of air that has
been warmed and humidified; and through heat lost in urine and feces.
Normal body temperature in the area muscular axillary area 36,3-36,9 С°
Normal body temperature in the oral cavity is 36,8-37,3 С°
Normal body temperature in the rectum is 37,3-37,7 С°

41a. Changes in organs and systems in fever: pathogenesis, characteristics. The biological
significance of fever for an organism.
Changes in organs and systems in fever:
Smooth muscles in peripheral arterioles in the skin : Muscles relax causingvasodilation.
More heat is carried from the core to the surface, where it is lost by radiation. Skin turns
red.
Sweat glands : Glands secrete sweat onto surface of skin, where it evaporates. Water has a
high latent heat of evaporation, so it takes heat from the body.

Erector pili muscles in skin (attached to skin hair) : Muscles relax, lowering the skin hairs
and allowing air to circulate over the skin, encouraging convection and evaporation.

Skeletal muscles : No shivering

Adrenal and thyroid glands : Glands stop releasing adrenaline and thyroxine.

Behaviour : Stretching out, finding shade, swimming, removing clothes.

Biological significance of fever for an organism :

Fever, as regulations, renders positive influence on sick organism. It is instrumental in
convalescence. In the same time fever is followed with undesirable changes in the organism.

Fever is negatively for the growing and reproduction of some microorganisms. For example,
gonococcus and treponems perish at the temperature of 40-40,1 C

Fever creates inauspicious sphere for development of some types of the pneumococcus,
prevents to reproduction of some pathogenic viruses.

Typical example is oppression of the reproduction of poliomyelitis virus Fever decrease

resistibility of microorganisms to medical preparations, stimulates immunological answer of
the organism on encroachment of infectious agent.

The fever activates phagocytosis, antibodies synthesis rises, T-lymphocytes increase the
multiply synthesis and secretion of interferon, which makes antiviruses action. Fever is a
strong stressor.

Attached to fever rises activity of hypothalamic kernels, after takes place an activation of front
pituitary gland part and of suprarenal glands cortices. These phenomena is typical for general
adaptation syndrome.

Fever also affects the cardiovascular system by causing tachycardia; rise of the activity of
sympatical nervous system, straight hormones dominance of thyroid on heart, rises shock
heart volume. Increase in cardiac output on 25-30%

42a. Tumors: definition of concept, characteristics. Methods of experimental study of

tumors.

Tumor or neoplasm is a typical pathological process which is characterized with an

unlimited, uncontrolled, independent and endless increase in tissue growth and cellular
anaplasia
Anaplasia is a condition of cells in which they have poor cellular differentiation, losing the
morphological characteristics of mature cells and their orientation with respect to each
other and endothelial cells.
Types of anaplasia
-Morphological anaplasia: atypic cultural and tissue
-Biochemical anaplasia: tumour cells metabolism percularities
-Functional anaplasia: loss or perversion of tumour cell function
-Immunological anaplasia
Methods of simulation of tumors in the experiment:
Induction: inducing cancer cells in rats or mouse
Transplantation: moving of neoplastic cells from one organism to another (transplantation
conditions, factors that affect the growth of transplanted tumors, transplantation strains),
Explantation (explantation strains/cultivation of tumour in culture medium), the induction
of tumors (main groups of chemical carcinogens, tumor induction by physical factors, the
role of viruses in the occurrence of tumors)

43a. Carcinogens, classification, mechanisms of carcinogenesis.

Carcinogen is any substance that is directly involved in causing syndrome Classification:
1. Chemical : Includes polycyclic aromatic hydrocarbons, aromatic amines and amides,
nitrosamines and nitrosamides.
2. Physical: To physical factors belong ionizing and ultraviolet rays. The ionizing rays
cause genetical and chromosomal mutations.
3. Biological: Oncogenic viruses

Mechanism : Neoplastic growth beginning and development in multistage process. The

main three stages are: transformation, promotion, progression.

Transformation. The first stage (transformational stage) is followed with the cell oncogene
activation. The cell acquires unusual property, which is called immortalisation. This is a
potential unlimited division, immortality ability. However, the presence of active oncogene is
a readiness to division only. A cell with active oncogene can resist in latent (condition) for
years. It does not display itself with anything.

Promotion. Supplementary influences upon immortalisated cell, are necessary to exit it out
of the latent state, for giving a push to irrepressible division. These are provoking factors,
which are supplementary doses of chemical cancerogenes or xrays, retroviral superinfection.
They are named promotors.
Progression is the very last and the most protracted stage of neoplastic growth development.
The clearest determination of this notion Fulds has given: uProgression is a neoplasm
development in a way of constant, irreversible, qualitative changes of its one or a few
signs".Progression is not just quantitative tumor growth, but native change of its biological
properties. One of the major Fuld’ s principles is an independent progression of separate
neoplastic signs. Its essence is the following: each tumor sign (morphological anaplasia
degree, hormones dependence degree, invasive growth capacity, metastasing ability)
evolutionizes irrespectively to the other signs, however to the malignisation side always.
Neoplastic growth progression reflects tumor admiring to autonomy.

It holds a neoplastic cell much more further from maternal. The main progression index is
organs and tissues structure loss by the tumor with simultaneous cell differentiation
lowering.Neoplastic growth progression reflects in its clinical symptoms and therapy
possibilities.
For example, some tumors (mammal gland cancer, uterius corpus, prostata) on the definite development stages react to
hormones. In other words, these neoplasms are hormone dependent. Tumor cells lose the specific receptors and stop
reacting to the hormones influence during the progression. Neoplastic growth becomes hormone independent. It is not
sensitive to hormonal therapy.

44a. Starvation: types, stages of the complete starvation.

Starvation( fasting, deficiency or deprivation) is a condition that occurs when the body does
not receive enough nutrients or enough quantity or does not assimilate them due to a
disease.
Types for its origin starvation may be physiological or pathological pathological
1.Complete starvation-absolute deprivation without water, The person eats no food at all, it
can sometimes be with or without water (absolute starvation).
2.Incomplete starvation(quantitive malnutrition)-body receives all the nutrients but
insufficient quantity of energy value. It is also called Chronic Malnutrition- The person eats
food but the caloric energy intake is too low to maintain the organism's life.
3.Partial starvation( qualitative)-when there is insufficient intake of one or more food
components with normal energy value of food.
Stages of complete starvation

-Ist Stage – period of energy wastage; first period of complete starvation is characterized by
intensified expenditure of carbohydrates, therefore respiratory quotient is increased to 1.0.
the level of glucose in the blood is reduced lower than 3mM/L. increased protein catabolism
and activation of gluconeogenesis
-IInd Stage- adaptation period; longest period of starvation- the respiratory coefficient
decreases to 0.7, proving pereferential oxidation of fats.
-IIIrd Stage- period od tissue disintegration and disorganization of metabolism of substance;
terminal period is characterized by sharp increase of the protein breakdown of vital organs
which are used as energetic material. The respiratory rate equals 0.8
-The forth stage, changes of organs and systems- there is atrophy of tissues and
parenchymatous organs.

45a. Features of tumor tissue, types of anaplasia. Influence of a tumor on an organism,

signs of benign and malignant tumors.

Tumor (Neoplastic growth) - is the typical pathophysiological process in appearance of tissue

excrescence. It is described by potential unlimited growth, growth unregulation and atypic
cells anaplasia.

Features:

1. Tumor cells have autonomous growth. Cultural growth is controlled at two levels -
organism and tissue ones. Organism level of control is realized with aid nervous and
endocrine systems. Tissue level - with aid biologically active substances - mitogenes and
keylones. Autonomy of tumor cells develops gradually. The first tumor cell gets partially
hormonal regulated (hormone dependent tumor). Later it is perfectly irresponsible for
hormones (hormone independent tumor).

2. Anregulation of growth : Lack of reaction to effects that inhibit the growth of normal
cells. Hormonal-dependent tumor is a tumor that partially retains the ability to the
control effects of hormones. Non-hormonal tumor - a tumor that completely loses its
ability to the control effects of hormones

3. Anaplasia: Structural and biochemical organization simplification of tumor cells,

coming back to embryonic state. Neoplastic cells lose a capacity to differentiation and
can not form the specific tissue complexes.

Types of anaplasia : -morphological; -biochemical, -physical, -chemical, -functional,

immunological

Tumor influence : Hormonal disorders causing acromegaly, hyperhydration,

hyperthyroidism, ulcers, galactorrhea, virilization, bone breakdown.
Glucose consumption increase : causing hypoglycemia, acidosis, increase cardiac output.
Increase iron consumption : causing anemia
Death of tumor cells : causing hyperkalemia, hyperuricemia Also there is increase in BP,
tumor cachexia etc.
Micro > Expansile growth with well- > Vary from well to poorly
circumscribed borders (anaplastic) differentiated
> Tend to be well > Tumor cells vary in size and differentiated shape
(pleomorphism)
> Resemble the normal tissue > Increased nuclear to counterpart
from which cytoplasmic ratios
they arise > Nuclear hyperchromasia and
> Noninvasive and never prominent nucleoli metastasize > High
mitotic activity with
abnormal mitotic figures
> Invasive growth pattern
> Has potential to metastasize

46a. Starvation: types, stages of the complete starvation.

Starvation( fasting, deficiency or deprivation) is a condition that occurs when the body does
not receive enough nutrients or enough quantity or does not assimilate them due to a
disease.
Types for its origin starvation may be physiological or pathological pathological
1.Complete starvation-absolute deprivation without water, The person eats no food at all, it
can sometimes be with or without water (absolute starvation).
2.Incomplete starvation(quantitive malnutrition)-body receives all the nutrients but
insufficient quantity of energy value. It is also called Chronic Malnutrition- The person eats
food but the caloric energy intake is too low to maintain the organism's life.
3.Partial starvation( qualitative)-when there is insufficient intake of one or more food
components with normal energy value of food.
Stages of complete starvation

-Ist Stage – period of energy wastage; first period of complete starvation is characterized by
intensified expenditure of carbohydrates, therefore respiratory quotient is increased to 1.0.
the level of glucose in the blood is reduced lower than 3mM/L. increased protein catabolism
and activation of gluconeogenesis
-IInd Stage- adaptation period; longest period of starvation- the respiratory coefficient
decreases to 0.7, proving pereferential oxidation of fats.
-IIIrd Stage- period od tissue disintegration and disorganization of metabolism of substance;
terminal period is characterized by sharp increase of the protein breakdown of vital organs
which are used as energetic material. The respiratory rate equals 0.8
-The forth stage, changes of organs and systems- there is atrophy of tissues and
parenchymatous organs.
47a. Features of incomplete (quantitative) and pa tial (qualitative) starvation, deficiency
of vitamins and microelements. Protein-caloric insufficiency. Incomplete starvation
undernourishment occurs more frequently than complete. It occurs when the body doesn’t
chronically receive enough energy with food for energy use. As such starvation is prolonged.
Basic metabolic proesses decreases in adaptive mechanisms to 30-35% instead of 10-20% at
the full starvation. On 20-25% decreases the thermo production. There is often anemia. The
bradycardia and low blood pressure are observed, breathing is weakened, the sexual instinct
is also suppressed.
Partial starvation
In the carbohydrate deficiency in food the main disorders are associated with the increased
ketogenesis in the liver, where fats are transported as a result of lower glycogen levels.
Carbohydrates are synthesized as a result of glucogeogenesis Insufficient intake of fats in
the energy aspect can be corrected with the help of carbohydrates and proteins. All aldult
ought to receive daily 5g of fats.
Protein deficiency occurs when the amount of protein in diet doesn’t provide the body’s
nitrogen balance and necessary level of plastic processes. If food doesn’t have one or more
of the essential amino acids the nitrogen balance becomes negative
Vitamin deficiency is displayed by hypo and avitaminoses.
Their causes are external and internal.
The external causes are: feeding deposition, climatic conditions and labour conditions. A
need for vitamin depends on the correlation of food substances. For example, lack of Vit C
causes scurvy, nicotinic acid-pellagra, thiamine-beriberi, calciferole-rachitis.
Deficiency of vitamins
Vitamin A- Retinopathy, night blindness Vitamin B1- Beriberi
Vitamin B2- Angular cheilitis, red dry tongue, sore throat
Vitamin B3- pellagra (3d - dermatitis, diarrhea, dementia)
Vitamin B6- microcytic anemia, glossitis
Vitamin B12- Megaloblastic anemia Vitamin C- Scurvy, Gingivitis
Vitamin D- Rickets, Osetomalacia
Vitamin E- Dry Skin, neural problems
Mineral deficiency the most hard is the chloride sodium loss. Or example dysentery,
diarrhea, vomiting, vegetarians. Low potassium causes nervus muscle excitiability. Iron
deficit causes anemia, flourin deficit causes caries and iodine deficit causes endemic goiter.
Protein-caloric insufficiency The clinical and pathophysiological manifstations of protein
caloric deficiency were called alimentary dystrophia. The disease began when reducing the
energy value of food on 50%. The lack of complete protein,cold,physical and nervous strain
ar the main etiological factors of the alimentary distrophia
Deficiency of Microelements Sodium- nauseas, vomiting Muscle weakness, spasms or
cramps, seizures Potassium- heart palpitations, Fatigue, Muscle damage, weakness or
spasms, Tingling or numbness. Calcium- Muscle spasms, heart palpitations Iodine- Goitre
Protein-Caloric Insufficinecy- Kwashiokor- (Children), Marasmus

SECOND PART

1b. Violation of catabolism and anabolism of carbohydrates. The concept of

hypoglycemia and hyperglycemia.
Ans:- Disorder of catabolism of carbohydrates
As a result of insufficient absorption of carbohydrates in intestine . Splitting of
polysaccharides in the intestine occurs rarely because amylase is produced by salivary
, pancreatic and intestinal glands , the process ends with oligosaccharide of digestion
by membrane .
Disorder of anabolism of carbohydrates
is the inhibition of synthesis and deposistion of glycogen in the liver for eg. In the case
of severe damage of epithelial cells of liver ( hepatocytes ) in hepatitis , or poisoning of
carbon tetrachloride , chloroform or under conditions of hypoxia . the carbohydrate
metabolism is changed significantly in the hypovitaminosis specially of group B
because these vitamins are co – enzymes of many enzymes .
Normal glucose level 3.3-5.5 mmol/l
Hypoglycemia
-Glucose levels lower than 3.3mmol/l
- Symptoms: Confusion, delirium, tachycardia, dizziness, coma
 - causes : starvation , physical load , renal glycosuria , hyperinsulinemia ,pathology of
liver ( in ability to form glucose while fasting), glycogenoses( disorder of breakdown
or synthesis of glycogen )

Hyperglycemia

-Glucose levels higher than 5.6mmol/l

-Symptoms: Blurred Vision, fruity smelling breath, (Tachypnoe) Kussmaul’s breathing

frequent urination, coma

- causes : cushing syndrome , hyperthyroidism , acromegalia , stress, insufficiency of

insulin.

2b. Type 1 diabetes mellitus: etiology, pathogenesis.

Ans:- Diabetes mellitus, commonly known as diabetes, is a metabolic disease that causes high
blood sugar. The hormone insulin moves sugar from the blood into your cells to be stored or used
for energy. With diabetes, your body either doesn't make enough insulin or can't effectively use the
insulin it does make
Etiology - insulin-dependent diabetes mellitus is an autoimmune disease caused by
destruction of the insulin- producing cells within the pancreatic islets due to the
presence of islet cell- specific autoantibodies.

Pathogenesis - –the relationship of genetic and immune mechanism due to location of

gene in the MHC system on the chromosome 6 in the locus that controls the immune
response of the body , the presence of certain antigens is indicative for the peculiarities
of the immune status of the organism . virus and chemical diabetogenis penetrating
into the Beta cell of the islets of the langerhands may have direst toxic effects on them
or initiate immune reaction to proteins of these cells in the carries of specific antigen of
the MHC regales of initial mechanism the Distruction of Bcell causes absolute insulin
deficiency

Stages of pathogenesis -
• The stage of genetic predisposition , (several months to 10 years)
• The stage of provocative action ( 1 to 2 days)
• The stage of primary autoimmunelation of the Beta cells , ( 2 to 3 months to 3 to 4
years) the distruction of B cells occurs mainly by the mechanism of delayed type
hypersensitivity but the deficiency of insulin has not been felt at ( since more than
90% of B cells should die
• The stage of lain diabetes there are no clinical symptoms but with the glucose load
the intolerance to it is determined the duration correspond to the third stage.
• The 5th stage the stage of the over diabetes which is manifested by the clinical
picture of the diabetes , the hyperglycemia , glucosuria , polyuria ,polydipsia and
 ketonemia. This period has an acute onset . over the time there are signs of
microangiopathy

During the course of this type of diabetes mellitus, the so-called long-term
complications of diabetes invariably occur to some extent in all patients. These
complications include retinopathy, nephropathy, neuropathy, angiopathy and premature
atherosclerosis.

3b. Type 2 diabetes mellitus: etiology, pathogenesis.

Ans:- Type 2 diabetes mellitus is a type of diabetes mellitus that is caused by hyperglycemia
and hyper insulinemia. The type 2 diabetes is through insulin resistance. Also the insulin
resistance maybe primary and secondary....pre receptor, receptor and post receptor.
Etiology :- Type 2 diabetes can occur when the body becomes resistant to insulin. Cells are
not able to absorb glucose as a result of this resistance. If glucose does not get into the cells,
there will be too much glucose in the blood , There are two forms of type II diabetes: a)
obesity; b) without obesity.
The risk of developing Type 2 diabetes increases with: -

• Family history of diabetes (in particular parents or siblings with diabetes)

• Obesity ( 20% over ideal body weight or BMI > 25.0 kg/m²)
• Membership of some ethnic groups - Age > 45 years
• Previously identified impaired fasting Glucose(IFG) or impaired glucose tolerance(IGT)
• Hypertension ( 140/90 mmHg in adults)
• HDL cholesterol level <1.0 mmol/L (<0.38 g/L) and/or a triglyceride level > 2,3 mmol/L (>2,0 g/L)
• Reduced physical activity

Symptoms of DM Type 2

o Polyuria Excessive urination

o Polydipsia Excessive thirst o
Polyphagia Excessive
hunger

Pathogenesis :- 1. Genetic factors - the predisposition is not linked to the main complex of
histocompatibility, the development is due not to one but to many genes. Therefore, this
type of diabetes is a polyetiological disease.
2. Dysfunction of -cells of the pancreas - the number of -cells is reduced, their
response to glucose load is not manifested by an increase in insulin secretion. This has been
linked to amyloidosis of the islets of Langerhans.
Amylin is produced by secretory granules of cells together with insulin. It induces apoptosis -
cells. It is apoptosis caused by amyloidosis that leads to the development of insulin
dependence as CD 2t progresses. In some patients, the cause of the disease was the
synthesis of an abnormal, less active insulin molecule as a result of a mutation in the insulin
genelocated on chromosome 11.
 3. Insulin resistance - occurs on a genetic basis or as a result of external
influences. Factors that form insulin resistance are a decrease in the number of receptors
and their affinity for insulin on target cells.
Chronic resistance of receptors entails chronic hyperfunction of cells and hyperproduction
of insulin, which in turn increases the resistance of receptors. If you do not take treatment
and do not break the vicious circle, the cells may be unable to withstand long-term stress,
and diabetes will occur

Main causes of insulin- resistance and glucose- resistance:

1. The pre receptor causes are:

- pancreatic:

● the maturity onset of diabetes of the young subtype 2 is associated with the autosomal
dominant inheritance
of the defect in glucokinase in B-cells, which reduced their sensitivity to glucose.

● The decreased sensitivity of the B-cells to glucose can Leo be caused by the absence or defect
of the GLUT -2 on their membrane

● Accumulation of amylin and amyloid in the islet of langerhans decreases the sensitivity of B-
cells to the
stimulating effect of glucose. ● Lack of D-cells eliminates the inhibition of A-cells and B-cells

● The insensitivity of the A-cells to the braking effect of insulin or glucose.

● The destruction of proinsulin and / or disorder of its proteolysis with reduction of thenumber
of functional
insulin.

● The genetic anomalies of the insulin structure, which inhibit insulin binding to the receptor on
the target cells

- Extra pancreatic:

● the activation of proteases and accelerated proteolysis of insulin

● The chromium, selenium, and vanadium deficiency.the receptor

2. The receptor causes;

● the decreased number of insulin receptors

● Their decreased sensitivity to insulin •

3. The post receptor cause is the disorder of signal transmission From insulin receptor To intracellular enzyme
systems. The pathogenesis of type 2 diabetes ordinarily involves the development of insulin Resistance associated with
compensatory hyperinsulinemia, followed by progressive beta-cell impairment that results in decreasing insulin secretion
and hyperglycemia.

4b. The symptoms of diabetes mellitus, pathogenesis.

Ans:- signs and symptoms of type 1 diabetes and type 2 diabetes are:
• Increased thirst
 • Frequent urination
• Extreme hunger
• Unexplained weight loss
• Presence of ketones in the urine (ketones are a byproduct of the breakdown of
muscle and fat that happens when there's not enough available
insulin)
• Fatigue
• Irritability
• Blurred vision
• Slow-healing sores
• Frequent infections, such as gums or skin infections and vaginal infections

Pathogenesis of Type 1 Diabetes Mellitus –the relationship of genetic and immune

mechanism due to location of gene in the MHC system on the chromosome 6 in the
locus that controls the immune response of the body , the presence of certain antigens
is indicative for the peculiarities of the immune status of the organism . virus and
chemical diabetogenis penetrating into the Beta cell of the islets of the langerhands
may have direst toxic effects on them or initiate immune reaction to proteins of these
cells in the carries of specific antigen of the MHC regales of initial mechanism the
Distruction of Bcell causes absolute insulin deficiency

Stages of pathogenesis -
• The stage of genetic predisposition , (several months to 10 years)
• The stage of provocative action ( 1 to 2 days)
• The stage of primary autoimmunelation of the Beta cells , ( 2 to 3 months to 3 to
4 years) the distruction of B cells occurs mainly by the mechanism of delayed
type hypersensitivity but the deficiency of insulin has not been felt at ( since
more than 90% of B cells should die
• The stage of lain diabetes there are no clinical symptoms but with the glucose
load the intolerance to it is determined the duration correspond to the third
stage.
• The 5th stage the stage of the over diabetes which is manifested by the clinical
picture of the diabetes , the hyperglycemia , glucosuria , polyuria ,polydipsia and
ketonemia. This period has an acute onset . over the time there are signs of
microangiopathy

During the course of this type of diabetes mellitus, the so-called long-term
complications of diabetes invariably occur to some extent in all patients. These
complications include retinopathy, nephropathy, neuropathy, angiopathy and premature
atherosclerosis.

Pathogenesis of Type 2 diabetes mellitus:- 1. Genetic factors - the predisposition is not

linked to the main complex of histocompatibility, the development is due not to one but to
many genes. Therefore, this type of diabetes is a polyetiological disease.
2. Dysfunction of -cells of the pancreas - the number of -cells is reduced,
their response to glucose load is not manifested by an increase in insulin
secretion. This has been linked to amyloidosis of the islets of Langerhans.
Amylin is produced by secretory granules of cells together with insulin. It induces apoptosis -
cells. It is apoptosis caused by amyloidosis that leads to the development of insulin
dependence as CD 2t progresses. In some patients, the cause of the disease was the
synthesis of an abnormal, less active insulin molecule as a result of a mutation in the insulin
genelocated on chromosome 11.
3. Insulin resistance - occurs on a genetic basis or as a result of external
influences. Factors that form insulin resistance are a decrease in the number of
receptors and their affinity for insulin on target cells.
Chronic resistance of receptors entails chronic hyperfunction of cells and hyperproduction
of insulin, which in turn increases the resistance of receptors. If you do not take treatment
and do not break the vicious circle, the cells may be unable to withstand long-term stress,
and diabetes will occur

5b. Abnormal metabolism of lipids. Obesity: types, causes, pathogenesis.

Ans:- Abnormal metabolism of lipids :
Enhancement of lipogenesis. This mechanism is basic when obesity is due to :
(a) entry of fatty acids from chylomicrons and VLDL into fat cells (overeating, cere-bral
obesity, hyperinsulinism);
(b) increased formation of fatty acids from glucose in adipocytes (excessive
carbohydrate intake, hyperinsulinism, hyperfunction of the adrenal cortex);
(c) increased activity of lipogenesis enzymes (hyperinsulinism).
Inhibition of lipolysis. The basis of this mechanism is a decrease in the activity of
hormonesensitive lipase in adipocytes. This happens with: (a) hypodynamia; (b)
hypothyroidism; (c) disturbances of sympathetic innervation.
The impairment of fat metabolism can be due to disturbances of:
1) digestion and absorption of lipids in the small intestine;
2) lipid transport with the blood;
3) lipid deposition in adipose tissue;
4) fatty function of the liver;
5) lipid metabolism in peripheral tissues;
6) nervous and hormonal regulation of fat metabolism.

Obesity is the excessive deposition of fat in the adipose tissue that occurs with long-term
excess of energy coming and accumulation of energy substrates over their consumption.
 The common indicator of normal or abnormal accumulation of fat in the body is the body mass index (BMI), which assesses the
conformity of the mass and the surface of the human body, with the formula: BMI = weight/height in kg/m2. Under the normal deposition
of fat BMI ranges from 18.5 to 25 kg/m2. BMI greater than 30 kg/m? means development of the obesity. Classification:
Depending on the etiology there are the primary
(alimentary, constitutional, hereditary) and secondary,
or symptomatic (cerebral, endocrine) obesity.
According the pathogenetic classification of the obesity : hypertrophic and hyperplastic.
Etiology:
The internal and external factors that change human behavior regarding food cause the
obesity. The excessive eating is the main factor of the development of obesity, and its cause
the disorder of the regulation of eating behaviour (the appetite).
Pathogenesis:
Pathogenesis of the obesity is a primary or secondary disturbances of lipostatis. The obesity
affects the functioning of the organism. Fat deposition in the myocardium causes a
significant reduction in the contractile function of the heart.
The obesity is often accompanied by the atherosclerosis, increased blood pressure, blood
clotting, and thrombosis. The pulmonary ventilation is decreased, lung capacity is reduced;
there is a tendency to the hemostasis and chronic inflammation of organs of the respiratory
tract. The dyspnea occurs even with little physical load. The circulatory and respiratory
hypoxia develops. The abdominal obesity is a risk factor of diabetes mellitus of type II.

6b. Disorders of lipoprotein metabolism, the role of occurrence of

atherosclerosis.
Ans:- Disorders of lipoprotein metabolism :
1. Hyperlipoproteinemia (an increase in the content of lipoproteins in the blood
plasma).
2. Hypolipoproteinemia (a decrease in their concentration in the blood plasme
3. Dislipoproteinemia (violation of the ratio between individual clena plasma
lipoproteins, the appearance of their modified forms).
4. Hyperlipaciidemia (an increase in the content of free fatty acids in the blood).
Atherosclerosis is the deposition of lipids (fat-like substances) in the walls of vessels of medium and large size,
narrowing of blood vessels and lumen).

The role of occurrence of atherosclerosis:-

Atherogenic dyslipoproteinemia is the quantitative and qualitative changes in plasma lipoproteins that promote the
development of atherosclerosis

a) increased levels of cholesterol and triacylglycerol-rich low density (LDL) and very low
density lipoproteins (VLDL) in plasma;
 b) the appearance of abnormal lipoproteins, called 'modified', in the blood. These
include glycosylated, acetoacetylated lipoproteins; lipoproteins associated with products
of lipid peroxidation; complexes of lipoprotein-antibody, etc.

c) a decrease in plasma levels of high density lipoproteins (HDL). LDL, VLDL and
'modified';
lipoproteins have been termed atherogenic, and HDL is anti-atherogenic.

7b. Atherosclerosis: definition of the concept, stages of development and its

pathogenesis.
Ans:- Definition : Atherosclerosis is the variable combination of changes in arteries intimae,
which consists of focal accumulation of lipids, complicated carbohydrates, blood substances,
fibrous tissue and calcium, and associated with changes in media.

Stages of development:
1 stage - FOAM CELLS : Macrophages have main role: A. They have "scavenger"-
receptors so Cholesterol comes in macrophage only due to concentration gradient. B.
They can accumulate a lot of
Cholesterol inside the cell (process is controlled by HDL). C. Modified LDL stimulate
macrophages activity

2 stage - LIPID SPOTS : They are formed on different parts of arterial system (in elastic
and elastic-muscle type of vessels)

3 stage - FIBROUS PLAQUE : Vessel narrowing takes place, Stage unalterable

4 stage - COMPLICATIONS : Thrombosis, ulcerations, Calcification

Pathogenesis:
1. Increase in LDL level in blood, hypertension, hemodynamic stress, toxins in cigarette
smoke all lead to endothelium damage.
2. This leads to platelat adhesion, proliferation of myointimal cells causing collagen
synthesis.
3. Endothelium damage also causes diffusion of plasma proteins into intima, migration
of monocytes into intima, oxidation of LDL, all leading to formation of foam cells.
4. Formation of foam cells releases cytokines which again lead to proliferation of
myointima cells which ultimately causes collagen synthesis.
8b. Hereditary diseases of amino acids metabolism: phenylketonuria,
albinism, alpathonuria.
Ans:- Metabolism of amino acids depends on the activity of corresponding enzymes.
Inherited disorders of synthesis of enzymes lead to the fact that an essential amino acid
doesn't participate in metabolism, but accumulates in the biological fluids of the organism: in
the blood, urine, feces, sweat, and cerebrospinal fluid.
The clinical picture in such cases is due to:
1) The presence of a sufficiently large amount of the substance that would be
metabolized with the help of blocked enzyme;
2) Deficiency of the substance, which would be formed.

Phenylketonuria : Hereditary violation of phenylalanine metabolism is phenylketonuria, a

disease with an autosomal recessive type of inheritance. Its cause is a genetic defect of the
enzyme phenylalanine hydroxylase which normally converts phenylalanine to tyrosine. In the
absence of this enzyme, the oxidation of phenylalanine goes by the pathway for
phenylpyruvate formation. However, this path is dead-end, since phenylpyruvate cannot
undergo further transformations. Phenylalanine accumulates in the blood and tissues, and
then is excreted with the urine. Excess phenylpyruvate in the blood of newborns disrupts the
normal development of the brain and causes mental retardation, incurable dementia.

Alkaptonuria : Hereditary violation of Tyrosine

Alkaptonuria is due to insufficiency of homogentisic acid oxidase which converts this acid
into maleic acetoacetic acid. As a result, homogentisic acid appears in the blood and urine.
The latter,when standing in air, as well as adding alkali to it, becomes black which is
explained by the oxidation of homogentisic acid with air oxygen and the formation of
alkapton. Homogentisic acid passes from the blood into the tissues - cartilages, tendons,
ligaments, the inner layer of the ans rial wall. This can led to appearence of dark spots in
the ears, nose, and sclera.

Albinism : Hereditary violation of Tyrosine

Albinism is caused by a deficiency of the enzyme tyrosinase. As a result, Sometimes severe

changes in the joints develop, merit melanin is not formed in the skin and hair. The body,
devoid of pigment, becomes very sensitive to the action of ultraviolet radiation.

9b. Dehydration: types, causes and mechanisms of development.

Ans:- Dehydration is a deficit of total body water caused by exerting oneself in hot and humid
weather, sweating, vomiting, diarrhea, osmotic diuresis, excess sodium. It develops in the
cases, when the excretion of water exceeds its supply (the negative water balance).

Types of dehydration are :

 Iso-osmolar dehydration : when Na levels is normal 135-145 mmol/l. there is an equal loss
of water and electrolytes. Seen in excessive seating when there isn't enough intake of
water, repeated vomiting, diarrhea and severe bleeding.
The classic examples is : acute blood loss and significant skin burns, when the body evenly loses salts and water
accompanied by a decrease of volume of the extracellular fluid without changing the amount of water inside the cells.

Hypoosmolar dehydration : when Na levels are below 135mmol/l decrease of osmotic

pressure of extracellular fluid and is observed in case of loss of salts
- Occurs in pancreatitis, burns, addisons disease, ketonuria, cystic fribrosis, renal acidosis and diuretics abuse.
- The hypoosmolar dehydration also occurs as a result of loss of sodium in the urine due to insufficiency of the cortex
substance of the adrenals (Addison disease), in the intense use of diuretics, and at the polyuric phase of the acute renal
failure.
- Because in the case of the hypoosmolar hypohydration major fluid loss is observed in the extracellular compartment,
then signs of dehydration with reduction of CBV are quickly developed: the decreased skin turgor, dry mucous
membranes, tachycardia, orthostatic hypotension, weak pulse in the jugular veins, and oliguria.

Hyperosmolar dehydration : Na levels are above 145mmol/l develops at loss of water

therefore osmotic pressure of intracellular liquid is increased. This occurs when loss of
water exceeds loss of electrolytes.

- Occurs in diarrhea in children, diabetes mellitus and insipidus, end stage of renal failure, heat stroke.

- The hyperosmolarity (hypernatremia) is especially severe in the early childhood, lt is caused by the high level of
ansiotensin II and aldosterone in the blood, reduced glomerular filtration rate, low concentration ability of the kidneys,
relatively large surface area of the body, shortness of breath and imperfect regulatory mechanisms for the excretion of
excess sodium.

- As a result, in the children of the first years of life the hyperosmolar dehydration in the acute diseases of the digestive
tract, accompanied by vomiting and/or diarrhea, as well as in the case of excessive sweating and hyperventilation, which
occur in the fever and in hot weather, occurs more frequently than in adults, and is a severe complication that may lead
to death.

Causes:
The causes may be the limitation of water intake to the body (water starvation, disorder of
swallowing (dysphagia), esophageal atresia, and comatose state, etc.) or increased water loss
(diarrhea, vomiting, blood loss, polyuria, hyper-ventilation, sweating, loss of fluid exudate and
transudate in burn, etc.), and the combination of these disorders. mechanisms of
development :

The loss of body water without sodium causes dehydration. Water is lost from the skin,
lungs, gastrointestinal tract, and kidneys. Dehydration results when water losses from the
body exceed water replacement. It may be caused by failure to replace obligate water
losses.

10b. Edema: definition of the concept, types, pathogenesis.

Ans:- The swelling or edema occurs as a result of increased water filtration from capillaries
into the interstitial space under the influence of the increased hydrostatic pressure of the
blood at the venous termination of the capillary, or as a result of inhibition of the osmotic
 sucking of the interstitial fluid by proteins of the blood plasma in the decrease of oncotic
blood pressure or/and increase of oncotic pressure of tissues.

There are general and local edemas.

General edemas are manifestation of extracellular hyperhydration, local are

connected with the dislocation of fluid balance in the limited site of a tissue or organ.

Types of edema :

Hydrostatic edema: hypervolemic edema, congestive edema

Oncotic edema: due to proteinuria, starvation, liver cirrhosis
Membranogenic edema: Quinck;s edema
Lymphogenic edema: Violation of lymph formation and circulation

Pathogenesis:- Oedema is caused by mechanisms that interfere with normal fluid balance
of plasma, interstitial fluid and lymph flow. The mechanisms may be operating singly or in
combination to produce oedema:

1. Decreased plasma oncotic pressure :- The examples of oedema by this mechanism are seen in the following conditions:
i) Oedema of renal disease e.g. in nephrotic syndrome, acute glomerulonephritis.
ii) Ascites of liver disease e.g. in cirrhosis of the liver.
iii) Oedema due to other causes of hypoproteinaemia e.g. in protein-losing enteropathy.

2. Increased capillary hydrostatic pressure :- The examples of oedema by this mechanism are seen in the following
disorders:
i) Oedema of cardiac disease e.g. in congestive cardiac failure, constrictive pericarditis.
ii) Ascites of liver disease e.g. in cirrhosis of the liver. iii) Passive congestion e.g. in mechanical obstruction due to thrombosis of
veins of the lower legs, varicosities, pressure by pregnant uterus, tumours etc. iv) Postural oedema e.g. transient oedema of feet and ankles
due to increased venous pressure seen in individuals who remain standing erect for longtime such as traffic constables.

3. Lymphatic obstruction :- The examples of lymphoedema include the following: i) Removal of axillary lymph nodes in radical
mastectomy for carcinoma of the breast produces lymphoedema of the affected arm. ii) Pressure from outside on the main abdominal or
thoracic duct such as due to tumours, effusions in serous cavities etc may produce lymphoedema. At times, the main lymphatic channel may
rupture and discharge chyle into the pleural cavity (chylothorax) or into peritoneal cavity (chylous ascites). iii) Inflammation of the lymphatics
as seen in filariasis (infection with Wuchereria bancrofti) results in chronic lymphoedema of scrotum and legs known as elephantiasis. iv)
Occlusion of lymphatic channels by malignant cells may result in lymphoedema.
v) Milroy’s disease or hereditary lymphoedema is due to 97 abnormal development of lymphatic channels. It is seen in families and the
oedema is mainly confined to one or both the lower limbs

4. Tissue factors (increased oncotic pressure of interstitial fluid, and decreased tissue
tension)
:- These are as under:
i) Elevation of oncotic pressure of interstitial fluid as occurs due to increased vascular permeability and inadequate removal of proteins by lymphatics.
ii) Lowered tissue tension as seen in loose subcutaneous tissues of eyelids and external genitalia.

5. Increased capillary permeability :- The examples of oedema due to increased vascular permeability are seen in the
following conditions:
i) Generalised oedema occurring in systemic infections, poisonings, certain drugs and chemicals, anaphylactic reactions and anoxia.
ii) Localised oedema. A few examples are as under:
Inflammatory oedema as seen in infections, allergic reactions, insect-bite, irritant drugs and chemicals. It is generally exudate in nature.
Angioneurotic oedema is an acute attack of localised oedema occurring on the skin of face and trunk and may involve lips, larynx, pharynx
and lungs. It is possibly neurogenic or allergic in origin.

6. Sodium and water retention. :- The examples of oedema by these mechanims are as under:
i) Oedema of cardiac disease e.g. in congestive cardiac failure.
ii) Ascites of liver disease e.g. in cirrhosis of liver. iii) Oedema of renal disease e.g. in nephrotic
syndrome, acute glomerulonephritis.

Reason and mechanism classification :

Cardiac edema : It occurs mainly as a result of the venous stasis and increased venous pressure, which is accompanied by e.
creased filtration of the blood plasma in the capillaries. The developing hypoxia leads to disorder of the trophic and increasing
permeability of the vascular wall. The retention sodium and water caused by activation of RAAS is of great importance.
Renal edema : In pathogenesis of the edema in the acute renal failure primary importance is the decrease of the glomerular
filtration rate, which uses water retention in the body. Also sodium reabsorption increases in the proximal bules, likely the secondary
hyperaldosteronism plays a role, as aldosterone antagonist- spironolactone (synthetic steroid) - provides the diuretic and natriuretic
effect. In the nephrotic syndrome the main mechanism of the edema is the decrease of the oncotic pressure of the blood as a result
of the proteinuria, which leads to the hypoproteinemia.
Liver edema : Damage: In the development of the edema due to the liver damage the hypoproteinemia plays an important role,
due to impaired protein syn- hesis in the liver. A certain value is the inactivation of aldosterone disorder. In of the liver cirrhosis the
impaired blood circulation in the liver and increase of the hydrostatic blood pressure in the portal vein lead to the ascites
development.
Cachexical edema : Causes of the cachexical (of hungry) edema is the alimentary dystrophia (starvation). On the basis of its
pathogenesis there is the reduction of the oncotic blood pressure due to the hypoproteinemia, which is caused by disorders of
protein synthesis and increased permeability of the capillary walls, associated orders of the vascular trophicity. Inflammatory and
toxic edema : Can be due to bee sting, poisonous insects Allergic edema
Neurogenic edema
Myxedematous edema

11b. Disturbance of electrolyte metabolism (sodium, potassium, chlorine,

magnesium): causes, pathogenesis.

Ans:- Sodium
Pathological sodium retention- this may be due to a significant decrease of the glomerular
filtration rate or enhanced reabsorption of sodium under the influence of aldosterone and
angiotensin 2 in the secondary hyper aldosteronism, which is observed in the cases of the
heart or liver failure and nephrotic syndrome.

Primary hyperaldosteronism is caused by the formation of aldosterone producing tumor in

the cortical substance of the adrenal gland doesn’t cause a significant delay of sodium and
water.
Sodium deficiency- occurs due to disorder of its reabsorption in the kidneys with
insufficiency of the cortex substance of the adrenals and the introduction of diuretics or loss
of sodium in diarrhea or swating

Potassium

Hypokalemia may be caused by insufficient food intake of potassium; primary and

secondary aldosteroninsm; excessive secretion or administration of glucocorticoids(
cushing’s disease and syndrome), potassium loss with vomiting, diarrhea, treatment with
diuretics .
Hyperkalemia occurs in the case of kidney falure, hypoaldosteronism and hypocortiicocism,
acidosis, insulin deficiency and excessive introduction of potassium

Chlorine

Hypochloremia most often occurs in the vomiting and intense sweating. Besides, causes of
the hypochloremia may be due to the use of chlorine diuretics. The decrease of chlorine in
the blood blasma of more than 20mML causes the development of the severe alkalosis
Hyperchloremia occurs in the renal failure or with the relatively greater loss of sodium and
water than chlorine that occurs in the tubular acidosis, deficiency of mineralocorticoids and
diarrhea. The main result of the hyperchloremia is development of the acidosis

Magnesium

Hypomagnesemia occurs in reduction of its getting into the organism decreasing the
intestinal absorption and increasing excretion of urine. Main causes is alcoholism.
Hypermagnesium most often the result of hypervitaminosis of vitamin D, occurs in kidney
failure and the using preparations containg magnesium.

12b. Disoder of calcium-phosphorus metabolism: etiology, pathogenesis of

the main manifestations.
Ans:- Calcium

Hypocalcemia- common to all newborns to sudden stoppage of this macroelement from mother. It is
observed in absolute or relative deficiency of parathyroid hormone and or
active forms of vitamin D, renal and liver failure, enteritis, pancreattis,
transfusion of the citrate blood, Introduction of loop diuretics and
glucocorticoids, alkalosis, elevated levels of phosphorus and lower levels of
magnesium.
Main manifestations- hyperreflexia, convulsions, spasmophilia and broncho or
laryngospasm. Vomiting, abdominal pain, pereipheral paresthesia. Chronic
hypocalcemia leads to the development of osteoporosis and bone fractures
Hypercalcemia is observed in in the hyperparathyroidism, hyper vitaminosis D,
malignancy, prolonged immobility orin weightlessness and acidosis including
alcoholism.
Main manifestations- reduces neuromuscular irritability, nausea,vomiting
anorexia, constipation, hypotoncity of muscles, arrhythmia, fatigue, depression
and later coma.
Phosphorus
 Hypophosphatemia occurs in the starvation, malabdorption, vitamin d
deficiency and hyperthyroidism use of antacids, chronic chronic alcoholism and
renal failure
Main manifestations- loss of consciousness, numbness and parasthesisas of the
fingers, toes, cramps, weakness and muscle pain, angina pectoris, hemolytic
anemia
Hyperphosphatemia observed during intoxication with vitamin D, in particular
in the case of UV exposure overdosage and in hypoparathyrosis Main
manifestations- anorexia, nausea, vomiting, hypereflexia, tachycardia and
tetany in children.

13b. Acidosis: definition of the concept, causes, pathogenesis, mechanisms of

compensation.
Ans:- Definition : Acidosis (acidemia) is an excess of acid in the blood that causes the pH to
fall below 7.35 Causes:
Respiratory : Depression of respiratory center in the medulla; Decreased amount of
functioning lung tissue; Airway obstruction; Disorders of the chest wall; Abdominal
distention; Disorders of respiratory muscles : severe hypokalemia, Amyotrophic I ateral
sclerosis, poliomyelitis, myasthenia gravis.

Metabolic : Decreased acid excretion; Excessive acid production; Under production of

bicarbonate (pancreatitis); Excessive loss of bicarbonate (severe diarrhea); Hyperchloremic
acidosis (an increase in the extracellular concentration of chloride, also promotes
bicarbonate loss).
mixed acidosis: is a combination of both metabolic and respiratory acidosis.
Depending on the cause of the ratio of anions and cations of the extracellular
fluid the negative acidosis is divided into excretory, metabolic and exogenous

Pathogenesis:
Respiratory : Rate of respiration is reduced; increased amount of CO2 in the body
(increased HCO3-). The increase in H+ ions reduces pH; hence more acidic.

Metabolic : High amount of H+ ions therefore increased acidity (not due to respiratory
condition), symptoms can be headaches, palpitations, abdominal pain, muscle weakness,
Kussmaul's breathing.

Mechanism of compensation:
 1. Blood buffer. Attached to augmentation of acids in blood, bicarbonate neutralizes
them. Neutralization mechanism is following. Alkaline anion HCO" 3 (mainly sodium
salt) bind hydrogen ion. Carbonic acid is formed. It rapidly dissociates to H2O and CO2.
During acids neutralization amount of bicarbonate diminishes. Diminution of
bicarbonate is very typical index of metabolic acidosis.

2. Respiratory regulation : Accumulation of carbonic acid stimulates respiratory centre.

Breathing becomes deep and frequent. CO2 is the strongest physiological stimulator
of respiratory centre. Heightening of carbonic acid (pCO2) pressure in blood up to 10
mm Hg multiplies pulmonary ventilation in 4 times. Hyperventilation of lungs is the
major compensatory mechanism of metabolic acidosis. It reaches maximum already
in a few hours from acidosis beginning.

3. Renal regulation : Heightening of acidosis and ammoniagenesis, heightened excretion

of acid phosphates.

4. Interchange of ions between blood and cells also has some compensatory importance.
The hydrogen ions come into erythrocytes, osteocytes. Alkaline metals - potassium
calcium ions exit from cells in blood. Thus, there is another typical sign of metabolic
acidosis - hyperpotassemia.

14b. Alkalosis: definition of the concept, causes, pathogenesis, mechanisms

of compensation.
Ans:- Definition : Alkalosis (alkalemia) refers to an excess of base in the blood that causes
the pH to rise above 7.45 Causes:
1) Metabolic: Most common : vomiting and nasogastric (NG) suctioning;
Other: ingestion of bicarbonates, carbonates, acetates, citrates, and I actates found in total
parenteral nutrition solutions, Ringer's lactate, and sodium bicarbonate administration;
rapid administration of stored blood and volume expanders with high citrate and acetate
 levels; excessive inta ke of antacids, which are composed of sodium bicarbonate or calcium
carbonate; loss of acids (gastric fluid loss, diuretic therapy, excessive mineralocorticoid
release); hypercalcemia; diuretic therapy; aldoster one excess.
2) Respiratory : Hyperventilation due to hypoxemia anemia; hypotension; high
altitudes; and pulmonary disease, such as pneumonia, interstitial lung disease, pulmonary
vascular disease, and acute asthma; Direct stimulation of the central respiratory center:
anxiety, pain,fever, sepsis,salicylate ingestion, head trauma, CNS disease
(inflammation, lesions).
Pathogenesis:
1) Metabolic : Low H+ ion levels therefore decreased acidity (not due to respiatory
conditions), symptoms can be abnormal sensations, tachycardia, tetany, abnormal heart
rhythm, sometimes asymptomatic.
2) Respiratory : Rate of respiration is increased; decreased level of CO2 in the body
(decreased HCO3-). Decrease in H+ ions increases pH, hence more alkaline.

Mechanism of compensation:

1) Lung hypoventilation to help balance the pH levels, nephritic mechanisms.

2) Acute respiratory alkalosis is mainly compensated by ion exchange between intra-

and extra-cells and intracellular buffering. Chronic respiratory alkalosis is mainly
compensated by renal regulation.

15b. Changes in total blood volume, classification, characteristic.

Ans:- Normovolemia, hypervolemia, hypovolemia are distinguished, depending on rate of
hematocrite parameter (norm is 0,36-0,48 L/L) as simple, olygocytemic and polycytemic.

♦ Normovolemia :
1. The normal condition of blood, which is characterized by normal volume and normal
hematocrite parameter, is named the simple normovolemia.
2. Olygocytemic normovolemia is characterized by the decrease of hematocrite index
and arises at posthemorrhagic anemia, when blood volume is supplied with
extravascular liquid, and the quantity of erythrocytes is not restored yet; the similar
state arises at massive hemolysis, cachexia.
3. Polycytemic normovolemia can occur in the conditions high- altitude hypoxia, at lungs
emphysema and heart disease, after the transfusion of erythrocyte mass or blood
small quantities.

Hypervolemia : Hypervolemia is a pathological state, which is characterized by the increase

of circulating blood volume.
 1. Simple hypervolemia (hematocrite index is normal) can be the consequence of plenty
blood transfusion, of intensive physical work and heart failure (in those conditions the
deposited blood comes into vessels).
2. Olygocytemic hypervolemia (hematocrite index is lower than norm, and the blood
quantity is increased at the expense of plasma) arises as the result of water excees in
the organism at the disorder of renal function after injections of physiological solution
or blood-substitutes.
3. Polycytemic hypervolemia (hematocrite index is higher than norm, and the blood
quantity is increased at the expense of erythrocytes) occur as the result of deep
hypoxia of the organism at the atmospheric pressure drop, at cardiac defect, at
chronic lungs diseases as the compensatory reaction and also as the result of the
malignant stimulation of erythrocytes growth (erythrismal).

Hypovolemia : Hypovolemia is a pathological state, which is characterized by the volume

circulating blood reduction.
1. The simple hypovolemia (hematocrite index is normal) can be the result of blood
losses, when the blood volume is not restored, of shock states (in this case the
significant part of blood does not participate in the circulation).
2. Olygocytemic hypovolemia (hematocrite index is lower than norm) arises after the
acute bleeding, when the blood volume began to be restored, with the extravessel
liquid, at malignant Addisone-Birmer's anemia (in this case the quantity of plasma is
not changed and the quantity of erythrocytes is much lower than norm).
3. Polycytemic hypovolemia (hematocrite index is higher than norm) is characterized by
the relative increase of the erythrocytes amount in blood. Such state can develop at
dehydratation caused by diarrhea, vomiting, burns, hyperthermia, and also at shock
(the vessels permeability increase and the output of plasma through their limits are
characteristic). At that state blood becomes dense, viscous, and that worsens hemodynamic
processes.

16b. Blood loss types, causes. Immediate and distant compensation

mechanisms and principles of therapy.
Ans:- Blood loss is a pathological state of the organism arising in the reply to the significant
blood loss from vessels and is characterized by the development of number compensatory
and pathological reactions. Types:
♦ Depending on an anatomic type of the damaged vessels there are arterial, venous,
capillary and parenchymal bleedings.
1. Arterial bleeding is when you bleed from an artery. is characterized by massivity and
intensity. The bleedings from big vessels are dangerous, when from the damaged
vessel blood is streaming by a pulsing jet and the irreversible consequences blood loss
can arise within several minutes. The difference between the arterial and venous blood pressure
disappears, the right atrium blood inflow diminishes and blood circulation becomes impossible.
 2. Venous bleeding is characterized by blood outflow from the damaged vessel by a
continuous jet. Venous bleeding more often than arterial ends with independent hemostasis due to the
formation of hematoma and vessel compression, and slowing down of blood flow speed.

3. The capillary bleedings in the condition of normal blood coagulation are the
insignificant and usually stop owing wound filling. The bleeding from capillaries is the
mostly widespread at injuries of skin, muscles, mucous membranes and bones. Blood
follows from smallest capillaries by a thin jet. In such cases the whole wounds surface
bleeds.
4. Parenchymal bleedings are caused by damage of liver, spleen, kidneys and pancreas.
These bleedings can become profuse as the result of plenty microvessels damage of
parenchymal tissue. In the absence of large arteries and veins damage the
spontaneous stop of the bleeding is possible due to blood clot, which is formed in the
area of damaged organ.

Depending on time of occurrence there are primary and secondary bleeding. Primary
bleeding arise at the moment of blood vessels damage;

The secondary bleeding can develop a bit later after a trauma, as the result of wounds
infection development or the repeated trauma of the damaged vessel.

Depending on the localization of bleeding source and the places of blood receipt there are
internal, external and mixed bleedings.

The internal bleeding can be intracavital, intratissual and mixed. Intracavital bleeding
(into abdominal and pleural cavities) are characterized by the violation of clots formation
owing to the defibrination of blood by pleura, peritoneum and synovial joint membrane.
Intratissual bleedings arise in skin, fat tissue, muscles and interfascial spaces. The reason
of the mixed bleedings can be simultaneous damage of abdominal cavity's organs and
retroperitoneal space ones.

The external bleeding arise because of skin and mucous membranes damages. Profuse
external bleedings arise in the result of limbs big vessels damage, at penetrating thorax
wounds and abdominal cavity ones.

The mixed bleeding are characterized by combination of internal and external signs.
First they arise as internal, when blood gets to a hollow body, for example, digestive
tract, bladder uterine cavity, then after some time the signs of external bleeding (bloody
vomiting, hematuria, metrorrhagia) appear.
HEMORRHAGE is also another disorder of blood loss disorder it is a pathological process
that leads to a complex of disorders and compensatory reactions of an organism in
response to reduction of the complete blood volume and hypoxia. It can be caused by
disturbance of blood coagulation and platelet deficiency and also disease of vascular wall
and blood vessel destruction.
 Class 1 hemorrhage: 15% blood loss
Class 2 hemorrhage: 15-30% blood loss
Class 3 hemorrhage 30-40% blood loss
Class 4 hemorrhage: >40% blood loss

Compensation

Compensation : First of all the contraction of vessels smooth muscles of the capacitor department venous system
arise, because these vessels are more sensitive to catecholamines, than the resistance vessels. 10 % of the lost blood without
any change of heart emission can be compensated due to capacitor vessels contraction of skin, lungs and abdominal organs.
The redistribution of blood stream, which is promoted also by the opening of artery-venous anastomosis, increases the blood
supply of vital organs, that is heart and brain due to ischemia of other organs. First vasoconstriction of all the organs, and
then the systems develops. This compensation mechanism is urgent; its main result is the reflectory spasm of peripheral
vessels, which promotes the centralization blood circulation and the maintenance of normal blood pressure level. The
bleeding continuation causes the inclusion of additional adaptation mechanisms - the transition of extravessel liquid into
vessels; it's the so-called hydremic phase of compensation. This is possible due to increase of precapillar resistance under
the influence cateholamines and aldosterone.The precapillar resistance arise due to the contraction of vessels smooth
muscles
(there are two mechanisms: strengthening of basal myogenic tonus due to the vasopressor
nerves activity increase and strengthening of basal myogenic tonus of vessels), and also due
to the short-term increase of blood viscosity. Postcapillar resistance also increases, but to a
lesser degree.

As the result of such changes, the average capillary hydrostatic pressure reduces, and the
colloid-osmotic pressure still remains at a sufficient level, that promotes the amplified
extravessel liquid inflow into the vessels. The consequence of this compensatory mechanism
is the circulating blood volume increase and the maintenance of normal heart and brain
functions.

17b. Hypocoagulation, classification, pathogenesis and clinical manifestations

of vasculitis, thrombocytopathia.
Ans:- Hypocoagulation : Reduced property of blood to form blood clots which results in
spontaneous bleeding or hemorrhage (very often after trivial trauma)

Classification : Inherited( occurs during lifetime, non-inhertiable eg.,body weight) and acquired (present in
gene
, inhertiable eg., blood group )

Etiology:
1. Thrombocytopenia
2. Thrombocytopathy
3. Vasopathy
4. Coagulopathy

Pathogenesis:
1. Decreased amount of thrombocytes in the blood (Injury of the thrombocytes,
Thrombocytes maturation depression, Accelerated usage of thrombocytes.)
2. Haemostasis violation as a result of qualitative thrombocyte's defects or
thrombocyte's dysfunction (which is characterised by vessel-
thrombocyte's hemostasis violation).
3. Violation of thrombocyte's adhesion and aggregation (violated interaction between
thrombocytes and f.Willebrand, fV, fXII)
4. Violated interaction between thrombocytes and f.Willebrand, f. 5,
f. 11 (no interaction between thrombocytes and coagulative plasma factors)
5. Violation of connective tisue development in vessel's subendothelium

Clinical manifestations of vasculitis :

Claudication, aneurysm, purpura, visual disturbance, weight loss, fatigue, irreversible
organ damage

Clinical manifestations of thrombocytopathy:

Skin hemorrhages, nasal bleeding, uterine bleeding, capillary bleeding (particularly during
sex aging and delivery)

18b. Hypercoagulation, etiology, pathogenesis. Disseminated intravascular

coagulation syndrome.
Ans:- Hypercoagulation : Pathological property of the blood which is characterised by
thromboses formation inside the vessels. Examples are thrombosis, DIC-syndrome.
Dessiminative intravascular blood coagulation syndrome (DIC- syndrome).
Etiology:
1. Infection , sepsis (bacteriemia, virusemia)
2. Shock - traumatic, hemorrhagical, anaphylactic, cardiogenic, septic (at septic shock
death occurs in 100 % cases)
 3. Surgical operation
4. Thermal burns and chemical ones
5. Terminal states (stages of the dying), heart stop
6. Acute intravessels hemolysis of the RBC's
7. Obstetrics pathology (20-25 %)
8. Leukemia (33-45 %)
9. Immune diseases
10. Allergy reactions Stages:
1. Hypercoagulation (numerous thrombus's formation because hyperactivity of
coagulative system)
2. Coagulopathy of using (exhaustion of coagulative system, overusing of the
thrombocytes for thrombus's formation)
3. Hypocoagulation (decrease of coagulative system activity,
activation of anticoagulative system and fibrinolysis)
4. Finishing (recovery, complications, death) Pathogenesis:
• Hyperthrombinemia
• Thrombocytes aggregation
• Erythrocyte's damage and hemolysis
• Humoral protease detonating
• Blood coagulative factors exhaustion (causes bleeding)
• Exhaustion of coagulative system (results in thrombosis) Clinical signs:
Hemocoagulative shock (at acute DIC-syndrome)
Haemostasis violation
Thrombocytopenia
Blockage of microcirculation

19b. Anemia: definition of the concept, classification, qualitative changes of

red blood cells.
Ans:- Anemia is decrease of erythrocytes amount and hemoglobin maintenances in unit of
blood volume which is accompanied by qualitative changes of erythrocytes.

Classification:
According to color index :
1. normochromic (the color index is within the limits of 0,85-1,05; for example, acute
posthemorrhagic anemia during firstdays after hemorrhage);
2. hypochromic (the colour index is lower than 0,85; for example, iron deficiency
anemia);
3. hyperchromic (the colour index is higher than 1,05; for example, B12-deficiency
anemia).
Pathogenetic classification:
1. Posthemorrhagic anemias :
 a) acute posthemorrhagic anemia;
B) chronic posthemorrhagic anemia.

2. Hemolytic anemias.
I. Acquired : a) toxic-hemolytic; b) immune; c)mechanical; d) acquired membrane pathy.
II. Hereditary: a) hereditary membraneopathy; b) enzymopathy; Hemoglobinopathy.

3. Anemias as a result of erythropoiesis disorders.

I. : a) irondeficient; b) B12-deficient; c) proteindeficient.

II. Hypo-, aplastic.
III. Metaplastic.
IV. Dysregulative.

Qualitative changes of anemias :

1. Regenerative, but not mature forms of erythrocytes (reticulocytes,
polychromatophils, normocytes);
2. Degenerative changes of erythrocytes (anisocytosis, poikilocytosis, changed in the
staining of the erythrocytes, presence of pathological inclusions);
3. Cells of pathological regeneration (megaloblasts, megalocytes).

20b. Hemolytic anemia. Etiology, pathogenesis, blood picture.

Ans:- Anemias which arise after destruction (hemolysis) of erythrocytes are called
hemolytic.
According to the mechanism of development hemolysis anemias may be : 1.
Anemia with intravascular hemolysis;
2. Anemia with endocellular hemolysis.

Etiology:
Anemia with intravascular hemolysis :
1. factors of physical nature (mechanical trauma, ionizing radiation, ultrasound,
temperature);
2. chemical agents (hemolytic poisons);
3. biological factors ( agents of infectious diseases, toxins, enzymes); immune factors
(antibodies).

Anemia with endocellular hemolysis :

1. occurrence of defective erythrocytes.
 2. occurrence on surface of erythrocytes the chemical groups capable to cooperate
specifically with receptors of macrophages. In this case antibody dependent
phagocytosis of erythrocytes is activated;
3. hypersplenism - increase of phagocytic activity of spleen macrophages.

Pathogenesis : Increased destruction of erythrocytes. It happens before their lifespan (120

days).
There are various reasons for this :
Acquired : Toxic hemolytic anemias, Immune hemolytic anemias, the anemias caused by
mechanical damage of erythrocytes, acquired membranopathy.
Heredity : Membranopathies, Enzymopathies, Hemoglobinopathies.

Blood picture:
1. Reduction of erythrocytes maintenance in unit of blood volume - in men is lower
than 4x1012, in women is lower than 3,7x1012 in IL of blood;
2. Reduction of hemoglobin concentration - in men is lower than 130 g/l, in women is
lower than 120 g/l;
3. Reduction of hematocrit - in men is lower than 0,43 l/l, in women is lower than 0,40
l/l.

21b. Iron deficiency anemia. Etiology, pathogenesis, blood picture.

Iron deficiency anemia (IDA) is a clinical and hematological syndrome caused by iron
deficiency in the body, which leads to impaired hemoglobin synthesis. It leads to a supply of
less oxygen to the body.
Iron deficiency anemia arises as a result of:
1) Insufficient receipt of iron with organism:
а) an alimentary anemia in the infants (feeding with cow or goat milk);
b) disorder of iron absorbtion (resection of stomach, intestines, gastritises, enteritis);
2) Hemorrhage. It is the most widespread reason of iron deficiency in organism;
3) Strengthened use of iron – pregnancy, lactation.
Pathogenesis

Exogenous and endogenous which leads to the disorder of formation of the heme of
hemoglobin in which iron is included. This leads to decrease of the amount of hemoglobin
and decrease of the oxygen transporting function of the blood with subsequent
development of hemic hypoxia
Blood picture: In blood smear the quantity regenerative forms of erythrocytes
(reticulocytes, polychromatophils) decreases and their degenerative forms (anulocytes,
microcytosis, poikilocytosis)
Hypochromic (CI is 0.6 and lower to 0.40) anemia with the erythroblastic type of
hemopoeisis. Hemoglobin is reduced more than red blood cells. Hyporegenrative anemia is
also seen.

22b. B12-deficiency anemia. Etiology, pathogenesis, blood picture.

Vitamin B₁₂ deficiency anemia is a disease in which not enough red blood cells are produced
due to a deficiency of vitamin B₁₂.
ETIOLOGY
1. Exogenous (alimentary) insufficiency – insufficient receipt in an organism with food
stuffs. May develop in small children as a result feeding goat milk or dry dairy mixes.
2. Disorders of vitamin B12 absorbtion:
а) Disorder of formation and secretion of gastro-mucoprotein (internal Castle’s
factor). It happens at hereditary caused disorders, an atrophy of a mucous
membrane of stomach, autoimmune damages of parietal cells of stomach mucous,
due to gastrectomy or removal of more than two thirds of stomach;
b) Disorder of small intestine function: chronic diarrheas (celiac disease, sprue),
resection of the big parts of intestine;
c) Competitive use of vitamin B12 by helmints and microflora of intestines
(diphyllobothriasis).
3. Disorder of transcobalamines formation in liver.
4. Disorder of vitamin B12 deposition in liver.
5. Increased use of vitamin B12 (at pregnancy).

Pathogenesis

Blood picture:
Megaloblast Occurrence in blood and red bone marrow. The color index is increased due to
big saturation of cells by hemoglobin.
The phenomenon of degeneration erythrocytes is typical: anisocytosis (macrocytosis),
poikilocytosis (occurrence of the oval form cells), pathological inclusions (Jolly’s bodies,
Cabot’s rings). The maintenance granulocytes (especially neutrophils) and thrombocytes in
blood is reduced. Huge neutrophils with the hypersegmented nucleus are found out.

Syndromes of B-12 deficiency anemia

1. Hematologic syndrome: а) anemia; b) leukopenia; c) thrombocytopenia.

2. Damages of the digestive tract which are shown by development inflammatory –atrophic changes in mucous membrane.

3. Damages of the central and peripheral nervous system: funicular myelosis, degeneration of peripheral nerves.

23b. Leukocytosis, leukopenia: definition of concept, etiology, pathogenesis. Leukemoid

reactions.
Leukocytosis - an increase in the total number of leukocytes in the blood over
9 g / l (9* 109 / l). Leukocytosis has no independent significance, but is only a symptom that
accompanies the development of many diseases Physiological leukocytosis
Etiology:
Physiological:--food intake, pregnancy, childbirth, menstrual cycles, physical work.
Pathological:--

- inflammatory diseases caused mainly by bacteria (pneumonia, sepsis, meningitis,

pyelonephritis, peritonitis, phlegmon)
- Infectious diseases (salmonellosis, shigellosis, meningococcal infection, plague,
infectious mononucleosis, etc.)
Pathogenesis: There are four mechanisms of leukocytosis:
1. increase in the formation of leukocytes in the hematopoietic organs of reactive
nature, which occurs during infection and tissue necrosis, and tumor character, which
occurs in the case of tumor hyperplasia of leukopoietic tissue, resulting in increased mitotic,
maturation and reserve pool of leukocytes in the bone marrow.
2. acceleration of the release of leukocytes from the bone marrow into the blood due
to increased permeability of the bone marrow barrier under the influence of inflammatory
mediators and glucocorticoids), increased proteolysis of the islet granulocytopoiesis, septic
conditions.
3. redistribution of leukocytes due to their mobilization from the parietal basin to the
circulatory system, which occurs during stress, accompanied by the release of adrenaline
and glucocorticoids, in case of strong emotions, pain, overheating, hypothermia, in case of
endotoxins of microorganisms. shock or collapse.
4. reduction of plasma volume and blood clotting

LEUKOPENIA is a decrease in the total quantity of the leukocytes in the blood less than 4g/l.
Leukopenia can be true (absolute) or false.
Etiology: medicines (sulfonamides), ionizing radiation, infections (hiv, hepatitis, typhus
fever), deficiency of cyanocobalamin and folic acid,protein deficiency, anaphylactic shock,
hypersplenism, hemodialysis, genetic defects etc.
Pathogenesis:

1. decreased leukocyte production in the hematopoietic tissue.

2. decelerated leukocyte release from the bone marrow.
3.excessive loss of leukocyte
4.Redistribution of leukocyte in the vessels.
5.Increased leukocyte destruction in the blood and hematopoietic tissue.

❖ LEUKEMOID REACTION: Leukemoid reaction means changes in the blood and bone
marrow in the form of increased number of immature forms of the white blood cells, as in
leukosis. The pathogenesis of leukemoid reaction is the reactive hyperplasia of the
leukopoietic tissue without its neoplastic transformation.
There are two types of leukemoid reaction namely myeloid and lymphocytic leukemoid
reaction. Etiology: viruses (cytomegalovirus, epstein barr virus, enterovirus,), disorders of
immune system, rhesus incompatibility of mother and fetus.etc.

24b. Haemoblastosis: definition of the concept, classification. Stages of development of

leukemia, clinical manifestations.
The haemoblastosis (hematological malignancy) is a tumor occurring from the
hematopoietic cells. Classification of tumors of the hematopoietic tissue origin is based on
the morphological, cytochemical, immunological, and cyto-and molecular genetic features
of the leukemia. The principal types of the hemoblastosis were distinguished: The leucosis
(leukemia)
The lymphoma In the leukemia pathogenesis there are two stages- monoclonal and
polyclonal
Stages of development of leukemia
• STAGE 1 : lymph nodes are swollen because too many lymphocytes are being made
• STAGE 2 : lymph nodes, spleen, and liver are swollen because too many lymphocytes are
being made
• STAGE 3 : anemia has developed because lymphocytes are crowding out red cells in the
blood
• STAGE 4 : there are too few platelets in the blood
Clinical manifestation of leukemia:- The hematologic syndrome The immunological
insufficiency syndrome and reduced antimicrobial resistance due to depression of the
normal granulo-, mono-, cyto-, and lymphocytopoiesis in the leukemia and also the
functional inferiority of the leukemic lymphocytes and granulocytes promote disorders of
the phagocytosis, inhibition of the humoral and cellular immune reactions.
The extramedullary syndrome of the leukemic manifestation is associated with damage of
various organs by the leukemic infiltrates, and also by secretion of toxic substances by the
tumor cells, which in large quantities are released during their decay.

25b. Acute and chronic leukemia, etiology, pathogenesis, blood picture.

 Acute leukemia/leucosis is characterized disorder of blood forming cells differentiation, do
not go further IV classes. According to modern conception all acute leucosis divide on two
groups - myeloblast and lymphoblast.
Acute myeloblastic leucosis differentiate on five cytochemical signs - presence or absence
in leucosis cells of the following substances : peroxidase, acid phosphatase, unspecific
esterase, lipids and glycogen.
1. MO - acute undifferentiated leucosis
2. Ml - acute myeloblastic leucosis without signs of maturing (worse 3 % of
promyelocytes)
3. M2 - acute myeloblastic leucosis with signs of maturing (over 3 % of promyelocytes)
4. M3 - acute promyelocytic leucosis (over 30 % of promyelocytes)
5. M4 - acute myelomonoblastic leucosis - over 20 % of promyelocytes
6. M5 - acute monoblastic leucosis
7. M6 - acute erythroblastic leucosis
8. M7 - acute megacaryoblastic leucosis

Classification of acute lymphoblastic leucosis :

1. Acute leucosis of general type (from cells-
predecessors of B lymphocytes)
2. T-lymphoblastic leucosis 3. B-lymphoblastic leucosis.

Blood picture : Acute leukemia/leucosis is characterized disorder of blood forming cells

differentiation, do not go further IV classes. The growth up of cells, which do not mature,
lead to accumulation blast cells II, III and IV classes. They more and more take part of bone
marrow at the expense of volume, which should be occupied normal hemopoietic
elements.

Chronic leukemia : Chronic leucosis differ from acute, that the cells bone marrow mature
normally (up to VI class), but proliferate in very plenty.
Classification of chronic myeloid leukemia
1. Chronic myeloleucosis
2. Chronic monocytic leucosis
3. Chronic erythromyelosis
4. Chronic megacaryocytic leucosis
5. Eosinophilic leucosis
Classification of chronic lymphoid leukemia :
1. B - cell leucosis
2. 2. T - cell leucosis
3. 3. Haircell leucosis Blood picture:
In the blood present as the maturing cells as an abundance cells of all classes - young,
transition and mature. Hiatus leukemicus is absent. In particular, in blood of chronic
myelocytic leucosis will be the next cells - predecessor II and III classes, myeloblasts (IV
classes), cell V classes - promyelocytes myelocytes metamyelocytes stick nucleus
neutrophils and mature cells of the VI class (neutrophils). The picture of peripheral blood
 of chronic lymphocytic leucosis is characterized by the following features: there are a lot
of mature lymphocytes, there are prolymphocytes and lymphoblasts, and also desroyed
lymphoid cells (Gumprecht's bodies or shadows of lymphocytes).

26b. Heart failure related to myocardial damage: etiology, compensatory mechanisms.

Heart failure is defined as the pathophysiologic state in which impaired cardiac function is
unable to maintain an adequate circulation for the metabolic needs of the tissues of the
body. It may be acute or chronic
Acute heart failure (AHF), also known as acute decompensated heart failure or cardiac
failure, is not a single disease entity, but rather a syndrome of the worsening of signs and
symptoms reflecting an inability of the heart to pump blood at a rate commensurate to the
needs of the body at normal filling pressure
Chronic heart failure, known as congestive heart failure or heart failure, is an ongoing
inability of the heart to pump enough blood through the body to ensure a sufficient supply
of oxygen.
Cardiac insufficiency, also known as heart failure, develops due to discordance between
heart load and ability to perform work. Cardiac insufficiency occurs when the heart muscle is
weakened and cannot pump enough blood to meet the body needs for blood and oxygen.
Heart Failure due to Myocardium Damage:
- Myocardial hypoxia or ischaemia
- Metabolic disorder
- Infectional myocardial damage
- Toxic myocardial damage
- Nervous-trophical and hormonal influence
- It can be the consequence of genetic defects, infections, intoxication and diseases
which cause myocardial hypoxia or lead to the disturbance of protein, lipid, mineral
metabolism as well as metabolism of trace elements and vitamins.
The inflammatory dystrophic, immune and autoimmune pathological processes can underlie
the pathogenesis of myocardial injuries.
COMPENSATORY MECHANISMS
- In order to maintain normal cardiac output, several compensatory mechanisms play
a role as under:
- Compensatory enlargement in the form of cardiac hypertrophy, cardiac dilatation, or
both.
–
- Tachycardia (i.e. increased heart rate) due to activation of neurohumoral system e.g.
release of norepinephrine and atrial natrouretic peptide, activation of renin
angiotensinaldosterone mechanism.
- Increase blood volume.

27b. Heart failure associated with volume overload: etiology, compensatory mechanisms.

Definition:- Volume overload refers to the state of one of the chambers of the heart in
which too large a volume of blood exists within it for it to function efficiently. Ventricular
volume overload is approximately equivalent to an excessively high preload.
It is a cause of cardiac failure. This results from elevated left and/or right ventricular filling
pressures
Etiology:- Causes of heart failure include coronary artery disease, heart attacks, high blood
pressure and faulty heart valves. Heart failure can disturb the normal functioning of the
kidney, weakening its ability to excrete • sodium from the body and triggering mechanisms
that cause water retention resulting in volume overload. Compensatory Mechanisms:-
heart can quickly adapt itself of an increased loading by compensating any possible
circulatory Disorder.
Depending on the type of load, one or the other compensatory mechanism is Activated.
In the case of blood volume overloading the heterometric compensatory mechanism
(FrankStarling mechanism) appears to be effective. Blood filling of heart chambers during
the diastole Is increased leading to an intensive distension of the muscle fibers.
Such stretching makes the Enchanced heart contraction during the systole. Within the
known load limits there is a linear Relation between inflowing blood volume and force of
myocardial contraction.

28b. Coronargenic and non-coronary-genic lesions of the myocardium: types,

pathogenesis.

Coronargenic lesions :- Coronarogenic Heart Damage, Ischemic Heart Disease, Myocardial

Infarction. It was mentioned earlier that functioning, metabolism and blood supply of the
heart make it extremely sensitive in the case when myocardial oxygen needs are
incongruous with the level of blood inflow through coronary vessels.
Pathogenesis:-.The diseases and pathological conditions accompanying disorders of the
myocardial blood Supply due to the damage of coronary arteries predominantly of the
artherosclerotc character Are combined into specific nosological unit “ischemic heart
disease” (IHD). It may manifest itself Predominantly by the functional disorders and pain
syndrome or condition necrotic changes in The myocardium.
Non-Coronarygenic lesions:-. If the myocardium disorder is not directly linked with the
Disturbance of its blood supply by the coronary vessels, such disorder is called noncoronary-
Genic. There exist many clinical reasons the development of which is not related with the
Pathology of heart vessels.
Pathogenesis:-the hypoxic necrosis of the myocardium can be reproduced by various kinds
of hypoxia. Necrosis occurrence during hypoxia is caused by additional • physical or
emotional loading with an activation of the sympatheticadrenal system

Types : Classification of coronary lesions is a system use to classify coronary arterial calcific
plaque burden. It is classified as Type A B C

1) Type A
-discrete (<10 mm)
-concentric
-nonangulated segment <45^
-smooth contour
-little or no calcification
-less than totally occlusive
-not ostial in location
-no major branch involvement
-absence of thrombus

2) TypeB
-tubular (10-20 mm)
-eccentric
-moderate tortuosity of proximal segment
-moderately angulated, 45-90^
-irregular contour
-moderate to heavy calcification
-ostial in location
-bifurcation lesions requiring double guidewires
-some thrombus present
-this can be sub classified into two sub categories

-Type Bl: having one of the above characteristics

-Type B2 : having two or more of the above characteristics

3) Type C
-diffuse
 -excessive tortuosity of proximal segment
-extremely angulated, >90^
-inability to protect major side branch
-degenerated vein graft with friable lesions

There are also:

1) Bifurcation lesions- This type of lesion arises at or adjacent to the separation of a
major coronary artery.
2) Calcified lesions- Vascular calcification of the coronary arteries is a common process
that is active, regulated and involves atherosclerotic as well as inflammatory and hormonal
disease processes.
3) Chronic total occlusions- This is the complete obstruction of a coronary artery.
4) Left main coronary artery (LMCA) disease- Left main coronary artery disease can be
problematic given that it is the origin of the majority of the left ventricular coronary supply.
5) Ostial lesion- An ostial lesion is one that starts within 3mm of the origin of a major
coronary artery.

29b. Myocardial infarction: etiology, risk factors, pathogenesis, principles of prevention.

The concept of myocardial hypernation, reperfusion complications.
Ischemic heart disease occurs when there is a partial blockage of blood flow to the heart.
When the heart does not get enough blood it has to work harder and it becomes starved for
oxygen. If the blood flow is completely blocked then a myocardial infarction (heart attack)
occurs.
Etiology:
1) Atherosclerosis of the coronary arteries (in 90-95 % died people at section was found)
2) Trombosis of the coronary arteries :
-at the 4 stage of atherosclerosis
-arterial hypertension (because it causes blood coagulation hyperactivity)
3) Trombembolism (septic endocarditis, thrombus lyses)
4) Spasm of the coronary arteries

Risk factors:
1. Stress (at trauma, operation, cold, negative emotions) BECAUSE IT CAUSES : Increase
of the heart activity, Stimulation of the heart metabolism, Increase of 02 using.
2. Age (most often appears in 40 - 59 years old person).
3. Hypokinesia (activation of the sympathetic-adrenal system)
 4. Obesity (hypercholesterolemia)
5. Sex : Males are more prone
6. Heredity
7. Arterial hypertension
8. Diabetes mellitus
9. Infection (chlamydia pneumonia) Pathogenesis:
1. Initial mechanisms : As a result of atherosclerotic disease of the coronary arteries;
Increase of the atherosclerotical plaque size; Increase of injured vessel sensitivity to
vasospastic effects; Thrombosis

2. Mechanisms of the cardiomyocites necrosis : As a result of cardiomyocytes ischemia;

ATP deficit; Acidosis; Ca accumulation; lipid triad.

Principles of prevention : Healthy diet, exercise, no smoking, no alcohol, Strophanthin

(plant extract).

Hibernal myocardium : A condition of the heart which is characterized by the sharply

decreased pump function of the heart (at human absolute rest) without cardiomyocytes
cytolysis as a result of blood supply reducing.

Sings : Decreased left ventricle output at increased 02 need of the organism (physical
activity, fever, hyperthyroidism); Decreased using of ATP; Retardation of the
cardiomyocytes necrosis; Renewal of H+ concentration, creatinphosphate level, pC02
(during 1-3 hour).

Reperfusion complications : Include both local ( swelling of limb, muscle infarction/

rhabdomyolysis) and general (acidosis, hypercalcemia, hypovolemic shock, arrhythmias).

30b. Cardiac rhythm automatism disorders: types, causes of development, pathogenesis.

Automatism violations are of 2 types : normotropic and heterotropic

1. Normotropic : Includes sinus tachycardia, sinus bradycardia and sinus arrhythmia.
Sinus tachycardia refers to a rapid heart rate (> 100 to 180 beats per minute) that has the
origin in the SA node. The main reasons are physical or emotional stress, myocardial
ischemia or infarction, myocardial dystrophy, congestive heart failure, fever,
hyperthyroidism, pharmacological agents (atropine, isoproterenol, adrenalin),
compensatory response to decreased cardiac output.
ECG sings: all waves have normal configuration and priority, P wave and PR interval (0.12 to
0.20 second) precedes each QRS complex (sinus rhythm), all R-R are shortened.
Sinus bradycardia describes a slow heart rate (< 60 to 40 beats per minute) that has the
origin in the SA node. It may be normal in trained athletes who maintain a large stroke
volume, during sleep; in pathological condition after influenza or typhoid, intracranium
pressure rise, irritation of the n. Vagus nucleases, may be an indicator of poor prognosis in
patient with acute myocardial infarction that is associated with hypotension.
ECG sings: all waves have normal configuration and priority, normal P wave and PR interval
precedes each QRS complex (sinus rhythm), all R-R are lengthened. This arrhythmia may
cause heart output decrease and leads to cerebral or coronary blood flow insufficiency, in
that condition ectopic pacemaker could be activated.
Sinus (respiratory) arrhythmia is characterized by gradually lengthening (at expiration) and
shortening (at inspiration) R-R intervals and is the result of intrathoracic pressure changes
during respiration. It is the normal for the children and can occur in adult after influenza, at
neurocirculative dystone, hypertension, congestive heart failure, diabetes mellitus. ECG
sings: sinus rhythm, difference of all R-R is more than 0.15 second (at norm difference of all
R-R is less than 0,15 sec).
2. Heterotropic : They are the result of ectopic automatism driver activation that is localized
out SA node because SA node failure (reasons - digitalis toxicity, myocardial infarction, acute
myocarditis, excessive vagal tone, hyper- or hypokalemia).
This includes :
Tardy ectopic rhythm (vicarious, passive) arises at the SA node arrest.

ECG sings: heart beats not more 60 per minute. If ectopic pacemaker is localized in atrium
on ECG inverted P wave is observed before QRS. If ectopic pacemaker is localized in AV node
on ECG inverted P wave is observed after normal QRS, or hidden in QRS (atrial-ventricular
rhythm). If ectopic pacemaker is localized in ventricle heart rate is less then 40 per minute,
QRS is deformed (wide, distorted), it is so called idioventricular rhythm.
Unparoxismal tachycardia begins and ends gradually, heart rate is 90 – 130/min. Ectopic
driver may be localized in atrium, in AV node or in ventricle. So, complex PQRST has sings of
nonsinus rhythm (alteration of configuration, duration and succession waves)
Migration of supraventricular rhythm driver is characterized by the gradual removal of
rhythm driver from SA node to AV one.
ECG sings: violation of P wave configuration and lasting, dysrtythmia.

31b. Cardiac rhythm conduction disorders: types, causes of development, pathogenesis.

Conductions violation are:

- Heart block
- Pre excitation ventricular syndrome

A. Heart block : sinus atrial, SA node arrest, intra atrial, atrioventricular, ventricular
1. Sinoatrial block has such sings: impulses are not transmitted out the SA node, so on
ECG waves P, QRS, and T are absent, pause is equal 2 (R- R). Some time occurs sinus arrest
and on ECG no 3 or 4 (sequence) cardiac complex, it may result irregular pulse, prolonged
period of asystole.

2. Atrial block : ECG sings P waves are deformed and their duration is more than 0.11
second.

3. Atrium-ventricular block has three degrees :

First-degree AV block is characterized only by the prolonged P-Q interval (< 0.2 second) in
the result of retardation impulses conduction from atria to ventricles through AV node.
Isolated first-degree AV block is never symptomatic.

Second-degree AV block is divided into two types.

Type-first (Mobitz type I or Wenkebach phenomenon) is characterized by progressive

lengthening of the PQ interval until an impulse is blocked, one cardiac cycle falls and then
the cycle repeats again. After the fall of ventricle contraction P-Q interval is restored, gradually becoming
longer with each heart contraction. R-R are different, rhythm is irregular and there are more P waves than QRS
complexes.

Type II (Mobitz type II) is usually associated with organic cardiac disease. It is the
intermittent block of atrial impulses conduction with a constant PR interval (normal or
long), but QRS complexes fall more frequently, may be such correlations: 2:1; 3:1; 4:1. This type is complicated by
cardiac output decrease.

Third- degree AV block, or complete AV block, occurs when the conduction link between
the atria and ventricles is lost. The atria continue to beat at a normal rate and the ventricles
develop their own rate, which normally is slow (30- 40/min, idioventricular rhythm). The atria
and ventricles rates are regular but dissociated (on ECG P waves and QRS complexes occur independently, count of P waves
more than QRG. It causes periods of syncope, known as a Stokes-Adams attack (sings: asystole more than 10-20 sec, a
decrease of cardiac output, insensibility, convulsions, is possible death).

4. Ventricle block : Interruption of impulse conduction through the bundle branches is called
bundle branch block. Bundle branch block interrupts the normal progression of
depolarization, causing the ventricles to depolarize one after the other because the impulses
must travel through muscle tissue rather than through the specialized conductive
tissue. It cause the QRS deformation, it is wide (normal is 0.08 to 0.12 second) and distorted. The left bundle branch
bifurcates into left anterior and posterior fascicles. An interruption of one of these fascicles is referred to as a hemiblock.
Their ECG sings are very difference, but the main sing is QRS complex deformation.

B. Pre excitation ventricular syndrome : Pre-excitation or Wolff- Parkinson-White (WPW) syndrome

exists when atrial impulses are transmitted directly to the ventricles through shortcut conduction
pathways. The impulses do not travel through the AV node but through accessory brunch (bungle of
Kent).
This connects the conduction system of the atria to either ventricle, bypassing the AV node. Impulses
go down the accessory pathways and return by the normal conduction system to set up a re-entry
system, it can cause supraventricular tachycardia.

The ECG is characterized by a short P-R (less than 0.12 sec), a slurred upstoke on the QRS (delta
wave), a wide QRS (more than 0.10 sec), secondary ST and T waves are changed (repolarization is
altered).

Another preexcitation pattern is the Lown- Ganong-Levine syndrome, characterized by a short PR

interval without a delta wave. These syndromes are dangerous because may cause electricity
unstabilized myocardium, activation of ectopic driver and extrasistoles or paroxysmal ventricular
tachycardia beginning.

32b. Cardiac rhythm automatism and conduction disorders: types, causes of development,
pathogenesis.

Combined heart properties violations include disorders of automatism, conduction and

irritability.
Extrasystole is the extraordinary systole in the result of ectopic pacemaker activation. New
pacemaker (out sinus node) causes beginning excitation wave, which spreads in altered
direction. Dependency on cell localization, where the extraordinary impulse isformed,
distinguishes such types of extrasystole: sinus, atrial, atria-ventricular and ventricular.
Sinus extrasystole or premature atrial contraction is a beat initiated by an ectopic atrial
focus that appears early in the cycle (before the next expected sinus beat). An excitation
wave is usually conducted through the ventricular pathway in the normal manner not
changes the shape of the QRS. A pause will follow the beat, and the SA node will start a new
cycle.
Atrial extrasystole is the result of ectopic pacemaker activation in different parts of atria. It
ischaracterized by Р wave distortion(depressed, dysphasic, negative) because excitation
wave goes retrograde, by partial compensatory pause.
Atrio-ventricular extrasystole is observed at beginning ectopic pacemaker in AV node (top
and middle part). Excitation wave spreads in two directions: in ventricles — innormal,
inatria–in retrograde. So, Р-wave is negative and indicates or after normal QRS complex or
can be coincide with QRS. Ventricular extrasystole or premature ventricular contraction (it is
caused by a ventricular ectopic pacemaker) is more dangerous than sinus or atrial because
violates the pumping action of the heart. After such extrasystole the ventricle usually is not
able to repolarise sufficiently to respond to the next impulse that arises in the SA node
(compensatory pause arises), diastolic volume is usually insufficient for ejection of blood.
On the ECG: extrasystole complex is registered early in the cycle, is not usually preceded by
P wave, QRS is distorted and wide, large looping ST segment opposite in direction to that of
the QRS, full compensatory pause (interval between the R waves before and after the
extrasystole complex is twice that of the normal R-R) Paroxysmal tachycardia. Extraordinary
contractions can arise one by one or by groups.
Paroxysmal tachycardia develops in case of numerous extrasystoles, with a rapid heart rate
(in measure 140-250 beats per min, averaging about 170), which sudden onset and offset
and couses physiological rhythm break. Duration of paroxysm can be different – from
(some) seconds to (some) minutes, after that it similarly suddenly ends and adjusts normal
rhythm.
Atrial paroxysmal tachycardia The patient frequently complains of a sudden pounding or
fluttering in the chest associated with weakness or breathlessness. The fast rate stresses
then heart and increases its need for oxygen. The tachycardia may also diminish cardiac
output because of shortened ventricular filling tame. The heart is beating so rapidly that the
ventricle doesn’t have time to fill completely, each beat pumps out less blood. If this
tachycardia persists, the usual treatment is stimulation of the n.Vagus by carotid sinus or
eyes massage, which slows the heart rate. Since this can produce dangerous slowing or
cardiac arrest, the patient should be monitored.
Atrial flutter is a rapid and regular atrial ectopic tachycardia, with a rate that ranges from
240 to 450 beats per minute. There two types of atrial flutter.
Type I flutter is the result of re-entry mechanism in the right atrium and the rate frequency
may be 240- 350/min. The mechanism of type II is unknown. The atrial rate ranges between
350 and 450 beats in minute.
On the ECG are defined regular and rapid F-waves (sawtooth pattern). Not all of the
impulses are conduced, so the ventricular rate is usually slower. Because the impulses are
coming so rapidly, the AV node cannot accept and conduct each one and ventricle response
may be regular or irregular (some degree of block occurs at the node).
Atrial fibrillation is the result of chaotic current flow within the atria. When the atrial cells
cannot repolarize in time for the next incoming stimulus, the ectopic current is rejected by
the refractory cells and sent in another direction.
On ECG: atrial electrical activity is disorganized and indicated by f-waves with frequency
350-700/min. Conduction through the AV node is disorganized, so complexes QRS appear
irregular; the peripheral pulse is grossly irregular, and a pulse deficit can be observed.
Ventricle flutter (ventricular tachycardia) is the result of ventricle frequency excitement by
permanently circulation impulses (re-entry mechanism). A rate usually is 150-200/min. On
ECG: rate is fast, QRS is wide, and P waves may sometime be visible in the complex QRS. It is
very dangerous arrhythmia because it leads to reduced cardiac output, and many times, to
ventricular fibrillation. Inventricularfibrillation,the ventricle quivers but doesn’t contract, so
there is no cardiac output, and there are no palpable or audible pulses. The classic ECG
pattern of ventricular fibrillation is that of gross disorganization without identifiable
waveforms or intervals (frequency 200-500/min)

33b. Hypertonic disease (primary arterial hypertension): etiology and pathogenesis,

consequences, principles of prevention.

Primary hypertension is the elevated blood pressure in the absence of any underlying
disease.It is also called essential hypertension. Arterial blood pressure is increased because
of increased peripheral resistance, which occurs due to some unknown cause.
Primary hypertension is of two types:
i. Benign hypertension ii. Malignant hypertension.
Etiology:- increase blood volume and cardiac output, increased activity of sympathetic
nervous system, renal dysfunction, increased peripheral resistance and hereditary
predisposition
Pathogenesis - Increase circulatory blood volume: Na retention in blood increases its
osmotic pressure leading to hypervolemia which causes increase in cardiac output and BP. -
increase cardiac output: sympathetic nervous system activation, adrenalin excretion lead to
increase cardiac contractility/ heart rate which causes an increase in cardiac output and BP -
Kidney function violation: long time spasm of kidneys causes decrease or arterial pressurein
renal capillaries which activates juxtaglomerular apparats to secrete renin which converts to
angiotensin to and BP increases.
Principle of Prevention:- Primary hypertension can be controlled but cannot be cured.
antihypertensive drugs to control primary hypertension:
1. Beta adrenoceptor blockers
2. Alpha adrenoceptor blockers
3. Calcium channel blockers
4. Vasodilators
5. Diuretics
6. Angiotensin II receptor blockers
7. Inhibitors of angiotensin-converting enzyme (ACE inhibitors)

34b. Secondary arterial hypertension: etiology, pathogenesis, consequences.

Secondary arterial hypertension: etiology, pathogenesis, consequences. Secondary
hypertension is the high blood pressure due to some underlying disorders.
The different forms of secondary hypertension are:
i. Cardiovascular hypertension
ii. Endocrine hypertension iii.
Renal hypertension IV.
neurogenic hypertension
v. Hypertension during pregnancy
Etiology: - Renal: glomerulonephritis, diabetic nephropathy, atherosclerosis of kidney
artery, traumaof kidney vessels and amyloidosis - Endocrine: phaeochromocytoma,
acromegaly, connd syndrome, cushings disease - Haemodynamic: atherosclerosis of aorta,
regurgitation of aorta - Neurogenic: encephalitis, brain tumour, brain ischemia ortrauma.
Pathogenesis Depending on the cause of the disease for example hyperthyroidism due to
increased work of the heart under the influence of thyroid hormones consequently
increased Q corresponds to the hyperkinetic type. Hyperthyroidism is accompanied by the
deposoition of mucopolysaccharides in the walls of arterioles.
Consequences:- atherosclerosis, heart attack, stroke, heat failure, myocardial infaction

35b. Obstructive and restrictive respiratory insufficiency: etiology, pathogenesis, effects

on the body.

Obstructive respiratory disease is the abnormal respiratory condition characterized by

difficulty in expiration: Obstruction of respiratory ways is narrowing their lumen and
increase of resistance to movement of air. The damage can be located as in upper
respiratory ways (with diameter of 2 mm and more), and in lower respiratory ways
(diameter – up to 2 mm).
Etiology:-trouble getting enough oxygen into your lungs.
Pathogenesis:- Obstructive respiratory insufficiency arises also for want of chronic
unspecific diseases lung – chronic bronchitis, emphysema, bronchoectasis, bronchial astma.
Emphysema is an illness, in which rupture interalveolar septums and lungs capillaries. By
basis it is considered degraded collagen and elastic fibres of proteolytic enzymes, which
thrown out from phagocytes under influences of the external factors – microorganisms, dust
particles, tobacco smoke.
Restrictive insufficiency. This form of respiratory insufficiency arises, when the extensibility
lung is reduced, that is when they be not capable easily to be straightened.
Etiology:- - рneumothorax, - deformation of thorax, - paralysis of respiratory muscles
Pathogenesis:- Restrictive insufficiency arises in case inflammation and edema lung. Owing
to arterial both venous hyperemia and swelling of interstitial tissue the alveoles is
compressed from the outside and completely are not straightened. The deficiency of
surfactant can arise in case of insufficient synthesis or excessive remove from a surface of
alveoles.
Effects of these on the body: They cause hypoventilation of the alveoli. The lungs become
rigid and poorly expanded in restrictive processes. These processes are accompanied by
increased work of the respiratory muscles, increasing energy expenditure on breathing.
They cause prolonged overload of respiratory muscles which can lead to fatigue and an
increase of respiratory failure.

36b. Disregulatory ventilative insufficiency: causes, pathogenesis, classification of dyspnea

in depth and frequency of breathing. Apnea. Periodic breathing.

The main causes of Disregulative ventilatory respiratory failure are disorders of the
nervous regulation of the respiratory muscles of the thorax and diaphragm providing their
periodic contractions. This may be due to mechanisms such as dysfunction of the respiratory
center and impaired transmission of efferent influences of the respiratory center on the
respiratory muscles.
Dysfunction of respiratory centers can cause the rhythm of the breath, it’s depth and rate
to change. And dyspnea develop. These changes may be manifestations of the
compensatory reactions of the organism aimed at maintaining the constancy of the gas
composition of the blood, or experience disorders of regulation of breathing and cause
disturbance of alveolar ventilation and as a consequence, respiratory failure.Changes of
breathing rate and depth cause either hypoventilation or hyperventilation.
Hypoventilation causes hypoxi development, hypercapnia and respiratory acidosis.

Hyperventilation which occurs as an adaptive response during physical load and is not
accompanied by the corresponding increase of the MHV leads to decreased partial pressure
of the carbon dioxide (PCO2) in the blood(hypocapnia) and development of respiratory
alkalosis. In turn it can cause decrease of blood supply to the brain and heart by increasing
the vascular Tony’s, changes of the electrolyte composition of the blood (
hypocalcemia,hypokalemia), deterioration of the dissociation of oxyhemoglobin and slowing
down the utilization of oxygen by the tissues and other changes.
Dysfunction of the respiratory center may be due to such factors: hypoxia, hypoglycemia,
intoxication ( drug, harmful products of metabolism in haptic and Renal failure, etc.) Types
of breathing in disorders of nervous regulation:
bradypnea. is an abnormally slow breathing rate. Is the infrequent breathing which is
caused by changing of nature of the nervous impulses coming from various receptors to the
respiratory center or primary disorders of the respiratory neurons.
Tachypnea: is quick shallow breathing. In such cases there is ventilation of mainly dead
spaces if the lungs as supply to the alveoli is decreased (hypoventilation)
Hyperpnea: is the deep infrequent breathing under physiological conditions, the hyperpnea
develops as a reaction of the respiratory system aimed at strengthening the lung ventilation
and bringing it in line with the needs of metabolism, which increases. Hyperpnea develops
as a result of the enhanced irritation of chemoreceptors of the carotid sinus and aortic arch,
due to emotional excitation, irritation of the skin exteroreceptors( pain, temperature).
Hiccups: is the appearance of the diaphragm, during which air is drawn into the lungs. It
develops in stimulation of the afferrent endings in the diaphragm and abdominal organs.
The persistent hiccup is observed after an operation on these organs and can significantly
disrupt the rhythm of breathing and decrease of the alveolar ventilation.
TYPES OF DYSPNEA
Orthopnea - it is the sensation of dyspnoea in the recumbent position, relieved by sitting or
standing.
Paroxysmal nocturnal dyspnea (PND) - it is a sensation of dyspnoea that awakens the
patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.
Trepopnea - it is a sensation of dyspnoea that occurs in one lateral decubitus position as
opposed to the other.
Platypnea - it is a sensation of dyspnoea that occurs in the upright position and is relieved
with recumbency.
Apnea: means the lack of breath. It is a temporary standstill in breathing. Apnea can cause
disruption of gas exchange in the body, the severity of which depends on the frequency of
occurrence and duration of the apnea. Temporary stopping of breathing may be associated
with the weakening of reflex or direct chemical stimulation of the respiratory center. Apnea
is more common in dysfunction of the respiratory center, particularly in development of the
periodic breathing.
Periodic breathing: the periodic breathing is alternating periods of breathing with period of
its absence (apnea). There are two types of periodic breathing: cheyne- stokes and biot’s
respiration.
37b. Asphyxia: definition, stage of development.
Asphyxia or asphyxiation is a condition of deficient supply of oxygen to the body that arises
from abnormal breathing. It develops if the respiratory failure occurs acutely or sub acutely
and reaches such a degree, when oxygen is no longer in the blood, and carbon dioxide is not
released from the blood.
Most frequently, asphyxia occurs in the case of choking, closing their orifices, presence of
fluid in the airways and alveoli( caused by drowning, pulmonary edema or vomit), and
bilateral pneumothorax.
In addition, asphyxia can be caused by the sharp inhibition of the respiratory center, spinal
motor neurons, conducting disorders of the nerve impulses to the respiratory muscles, and
significant limitation of the chest movement.
Effects of asphyxia develop in three stages:
1. Stage of Hyperpnea Hyperpnea is the first stage of asphyxia. It extends for about 1
minute. In this stage, breathing becomes deep and rapid. It is due to the powerful
stimulation of respiratory centers by excess of carbon dioxide. Hyperpnea is followed by
dyspnea and cyanosis. Eyes become more prominent.
2. Stage of Convulsions Stage of convulsions is characterized mainly by convulsions
(uncontrolled involuntary muscular contractions). Duration of this stage is less than 1
minute.
Hypercapnea acts on brain and produces the following effects: i. Violent expiratory efforts ii.
Generalized convulsions iii. Increase in heart rate iv. Increase in arterial blood pressure v.
Loss of consciousness.
3. Stage of Collapse Stage of collapse lasts for about 3 minutes. Severe hypoxia
produces the followingeffects during this stage:
i. Dilatation of pupils ii. Decrease in heart rate iii. Loss of all reflexes

38b. Hypoxia: types, etiology, pathogenesis, compensatory reactions, consequences.

Hypoxia is a condition in which the body or a region of the body is deprived of adequate
oxygen supply at the tissue level. Hypoxia may be classified as either generalized, affecting
the whole body, or local, affecting a region of the body.
Types:- hypoxic, hypemic, stagnant, histotoxic
Hypoxic Hypoxia

This is the most common form of hypoxia encountered in aviation and occurs at the lung
level. This type of hypoxia is commonly called altitude hypoxia.
Hypemic Hypoxia

This type of hypoxia is caused by the reduced ability of the blood to carry oxygen. Anemia,
hemorrhage, hemoglobin abnormalities, sulfa drugs, nitrites, and carbon monoxide interfere
with the ability of the blood to carry oxygen, reducing the amount of oxygen the blood can
carry to the cells.
Stagnant Hypoxia

This type of hypoxia occurs at the circulatory level. If the blood flow is compromised for any
reason, then sufficient oxygen cannot get to the body tissues.
Histotoxic hypoxia
This type of hypoxia happens at the cell level. This means that the cell expecting and
needing the oxygen is impaired and cannot use the oxygen to support metabolism. Alcohol,
narcotics, and cyanide are three primary factors that can cause histoxic hypoxia.
Compensatory mechanism

-Respiratory: dyspnea
-Haemodynamic: tachycardia, increase stoke blood volume, increase cardiac output,
increase blood flow acceleration, peripheral vessels narrowing. -Blood: erythrocytosis,
increase hemoglobin charge in erythrocytes, increase hemoglobin to oxygen in lung,
decrease hemoglobin to oxygen in tissues. -Tissue: decrease metabolism, activation of
glycolysis, activation of respiratory chain enzymes.

Consequences:- Brain cells are extremely sensitive to oxygen deprivation and can begin to
die within five minutes after oxygen supply has been cut off. When hypoxia lasts for longer
periods of time, it can cause coma, seizures, and even brain death.

39b. Violation of the secretory and motor function of the stomach, clinical manifestations.

Violation of secretory functions:

A/C to quantity of gastric juice and its quality there are gastric hyperand hyposecretion.
Gastric hypersecretion is characteristed by:

- hyperaciditas and hyperchlorhydria - increase of the common acidity and

maintenance of the free hydrochloric acid in gastric juice
- increase of the quantity of gastric juice as after reception of food, and also on the
empty stomach;
 - increase of digestive ability of gastric juice
Gastric hypo-secretions is characterised by:--

- reduction of quantity of gastric juice on an empty stomach and after reception of

food;
- reduction of digesting ability of gastric juice due to achylia (the full stop formation of
hydrochloric acid and enzymes).
- decreased or zero acidity of gastric juice (hypo-or unacidity), reduction of the
contents in it or absence of free hydrochloric acid (hypo- or achlorhydria);
Clinical manifestations:
1) small guantity of contents go into intestine, that results in reduction of guts
peristaltics and to development of constipations;
2) in the stomach processes of fermentation and formation gases increase. It causes
appearance of an eructation and a heartburn;
3) motor activity of stomach is increased, what leads to hypertonus and hyperkinesis of
smooth muscles.

Violation of stomach motor function is called gastric diskinesia.

There are two kinds of gastric diskinesia: hypertonic and hypotonic.
Hypertonic kind is characterised by strengthening of peristaltics(hyperkinesia) and
increasing of stomach muscles tone (hypertonia). The hypotonic kind, on the contrary, is
characterized by hypotonia and hypokinesia. The reasons of motor gastric disturbance of
hypertonic type may be:

- some food factors (rough food, alcohol);

- Increased vagal tone - Increased gastric secretion - GIT hormones like
motilin.
Clinical manifestations:-

• long delay of food in stomach that promotes increase of gastric secretion and
development of ulcers on mucous membrane;
• development of anti-peristaltics of stomach that results in development of dispeptic
disturbances (eructation, nausea, vomitting).
Reduction of motor activity of stomach may be caused by:

- Alimentary factors (food)

- Reduction of gastric secretion
- Reduction of vagal tone
- GIT hormones (gastro-inhibiting hormones and secretins)
 - Absence of pyloric part of stomach
- weakening of organism, an exhaustion, gastroptosis.

Clinical manifestations: --At hypotonic diskinesias time of food staying in the stomach is
shortened that conducts to disturbance of its digestion. Action of the undigested
components of food on receptors of guts mucous membrane causes the increase of
peristaltics and diarrhea.

40b. Stomach ulcer and duodenal ulcer, etiology and pathogenesis.

etiology

• Psychoemotional negative overstrains (negative emotions, disputed situations, feeling

of constant alarm, strain etc.).
• Stress.
• Hereditary predisposition. Value of this factor proves to be true concerning high (40-50
%) frequency of disease in parents and relatives of the patients, especially of the young
age. It is established, that patients with the burdened heredity mucous membrane of
stomach have 1.5-2 times bigger of parietal cells than in healthy person. Characters of
genetic predisposition are also 0(1) group of blood, deficiency of al-antitripsin and
fucoglycoproteins.
• Errors in nutrition: eating of rough or spicy (hot) food, bad chewing , fast meal,
absence of the teeth, the insufficient maintenance(contents) in food of proteins and
vitamins.
• Chronic gastritis and duodenitis with increased secretion of glands of mucus
membrane.
• Microbic factor - Helicobacter pylori.
• Harmful habits - smoking, overindulge of alcohol

Pathogenesis of stomach ulcer

-contamination of mucous membrane by helicobacter is accompanied by development of

Superficial anthral gastritis and duodenitis, lead to increase gastrin and HCL secretion. -
excess HCL enter duodenum lumen in conditions of deficiency of pancreatic bicarbonates
Which promotes development of duodenitis which are

• contaminated by H.pylori and causes ulcers in duodenum. Or acid in duodenum causes

ulcer.
-psychoemotional strain, hereditary predisposition, alcohol, smoking e.t.c. in area of
Metaplased mucous membrane forms ulcers.

41b. Digestive disorders associated with disturbance of secretion of bile and pancreatic
juice.

Absence of bile (acholia) or its reduced formation (hypocholia) with insufficient receipt in a
duodenum is a consequence of disturbance of functions of formation and allocation of bile.
bile helps in emulsification of fat in the duodenum. If there is any disturbance in bile
secretion then digestion of fat will be disturbed. Chylomicrons will not be able to produce so
absorption will also be hindered. And many pancreatic enzymes help in digestion like for
proteins trypsin, chymotrypsin, carboxypeptidase, for carbohydrates pancreatic amylase, for
fat lipase etc. So disturbance in their digestion occurs.
Violation of bile secretion causes: jaundice, steatorrhea, indigestion, cholemia, decreased
cholesterol formation, decreased fat digestion, decreased fat hormone synthesis. It occurs
due to blockage of pancreatic or bile ducts, pancreatic cancer, pancreatitis, tumour blocking
ducts.
Dietry fats stimulate pancreatic juice secretion but due to violation of pancreatic juice
secretion, indigestion of carbohydrates, fats and proteins occur which leads to malnutrition.
Steatorea is a syndrome, which is based on the violation of digestion and fats absorption.
Fats are excreted with feces. The fat-like vitamins are being lost together with fats.

Violation of the secretion of pancreatic juice is observed in the case of obstruction or

compression of the duct of the pancreas when there is-

• cystic fibrosis (bone fibrosis of the pancreas • acute and chronic

pancreatitis or duodenitis.
• Violation of neuro-humoral mechanisms of regulation of
pancreatic secretion
In the case of pancreatic juice deficiency, a significant portion of fat is not digested and
excreted in the feces (steatorrhea). Disorders of protein digestion occur due to insufficient
production of peptidases by the pancreas, as well as in case of violation of their activation.
Thus, trypsinogen is activated by intestinal juice enterokinase and auto catalytically, the
remaining proteolytic enzymes and phospholipase A are activated by trypsin. In the case of a
decrease in pancreatic secretion, the hydrolysis of food nucleic acids is disrupted and, to a
lesser extent, the starch is broken down.
42b. Violation of digestive, suction and motor functions of the intestines: causes, clinical
manifestations

Disturbance of digestion in intestine

The syndrome of maldigestion is disturbances of primary digestion, caused by insufficient

receiption of digestive enzymes into guts in particular in case of pancreatic hyposecretion.
Syndrome is presented by:--

- disturbance of digestion of fats (absence of lipase and phospholipase). About 60- 80

% of fat that gets into intestines is deduced with feaces – steatorrhea (fat in feaces)
- disturbance of absorbtion of fat-soluble vitamins – causes the development of
hypovitaminosis A, E and K;
- disturbance of proteins digestion (absence of digestive proteases). In feaces there is
a plenty of muscular fibres;
- disturbance of decomposition of nucleinic acids (absence of nucleases) -
disturbance of digestion of carbohydrates (absence of amylases)

Disturbance of absorbtion in guts may be caused by disturbances that appear on three

levels:

• Pre-enterocytic disturbance. Develop as a result of disturbances of digestion

processes before absorbtion
• enterocytic from disturbance of intestinal mucous membrane epithelial cells activity.
It is caused by decreased absorbtion area, hereditary factors, disturbed functioning
of ion pumps, less energy.
• postenterocytic disturbance
Disturbances of motor function of guts refer to intestinal dyskinesia.

There are two types of intestinal dyskinesia: hyperkinetic and hypokinetic.

Hyperkinetic is characterized by strengthening of the peristaltics, segmentary and
pendulum-like movements, and is manifastatied as diarrheas.
Clinical manifestations:

o secretory non gas acidosis (loss of hydrocarbonates) o

Dehydration
o disturbances of digestion (digestion, absorption)
Hypokinetic is characterized by weakening of motor activity of guts which result to
development of constipations.
Clinical manifestations:--

- Intestinal dyskinesias of hypokinetic type are manifestated by reduction intestinal

peristaltics. That results in appearance of constipations
 - Development of intestinal auto-intoxication
- Occurance of meteorism
- Formation of feces stones
- in extreme cases intestinal obstruction may develop.

43b. Disorder of the metabolic function of the liver, causes, pathogenesis.

Carbohydrates metabolism defect:-

The slowing-down of glycogen synthesis leads to the simultaneous limitation of glucuronic

acid formation. The slowing-down of glycogen splitting in liver is conditioned by
corresponding enzymes defect or their total absence. These diseases are called
glycogenosises. They are manifested by glycogen accumulation in liver, by hepatomegalia
and hypoglycemia. Several forms are distinguished among them, depending which enzymes
is not synthesized.
Glycogenosis of type I is caused by the defect of glucose-6-phosphatase (Hirke disease).
Glycogen storage disease type II, also called Pompe disease, is an autosomal recessive
metabolic disorder which damages muscle and nerve cells throughout the body. It is caused
by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid
alpha-glucosidase enzyme.
Glycogenosis of type III (Korri disease, Forbs disease, so called debrancher enzyme defect) is
the deficit of amilo-l,6-glucosidase, the enzymes, which breaks the connections in the places
of glycogen molecule branching.
Glycogenosis of type VI (Gers's disease) is conditioned by the deficit of liver phosphorilasis
complex - proteinkinasa, phosphorilasa kinasa and phosphorilasa.
The galactose-l-phosphaturidiltranspherasa deficit causes galactozemia and hepatomegalia.
Fat metabolism disorder:-
At pathologic conditions, liver stores mainly fats. That phenomenon is called the fatty liver
infiltration.
Liver fats infiltration becomes possible in such cases:
a) The increased lipolysis in the fat tissue, most often - at the decompensated diabetes
mellitus. The lipidic predecessors of lipoproteides (fatty acids) are so high at diabetes patients, that they have no time to
start to participate in triglycerides synthesis and the last-in lipoproteides synthesis.

b) Hypoglycemia (at starvation or glycogenosis) can provoke the liver fats infiltration. In
the
conditions of glucose deficit, the insulin production secondarily decreases and lipolysis is activated. The excess of free fat
acids, which come into the liver, can exceed the abilities to join triglycerides into lipoproteides. The incompatibility
between the delivery and synthesis processes provokes the fats infiltration.
c) Lipoproteides production and fats expelling from the liver decrease in the conditions,
when sources of aminoacids are restricted (e.g., at albumin starvation), thus apoproteines
synthesis is decreased. Lipides, as raw material for lipoproteides synthesis, remain unused because the deficit of
protein component.

d) The fatty infiltration can be caused by the lipotropic aminoacids deficit (choline and
metionine) in food.

e) The same picture can be caused by B12 - hypovitaminosis and folic acid deficit,
because it is caused by endogenic choline deficit.

f) The fatty infiltration can be also conditioned by toxins influences, for example
amanitotoxine, which blockes R-oxidixation of fatty acids in mitochondrias.

Protein metabolism disturbsnce:-

The main consequences of albumin metabolism infringement at the liver affection are as
follows:
• Hypoproteinemia is the result of blood level decrease of albumins, a- and |3- globulins,
which are synthesized by hepatocytes. It leads to hypooncia and as the result edema
develops.

• Hyper-gamma-globulinemiais the result of gamma-globulines synthesize increase by

Kuffer's cells and plasmocytes.

• Dysproteinemia is the result of macroglobulins and crioglobulins accumulation.

• Hemorrhagic syndrome in the result of the decreased synthesis of blood coagulation

factors (besides YLU factor).

• The increase of blood RN (retarded nitrogen) in the result of the decreased urea
synthesis and ammonia accumulation. That happens at 80% parenchyma affection.

• increase of enxymes level in blood (aminotranspherases). Microelements metabolism

disorder
example is Wilsons disease, when copper deposits in hepatocytes. In this disease, the
deposited copper enters the metal-containing enzymes, or is withdrawn with bile. In case
when metall-thionein protein is very high in relation to copper. That shifts of copper liver
pool balance in such a way, that leads to the drop of its secretion with bile and to the
decrease of its joining the ceruloplasmin, an albumin, that transports copper in blood. At the
long-term copper accumulation by abnormal metall- thionein, the binding centres satiate,
and copper excess is absorbed by liver lysosomes. The metal is accumulated in hepatocytes
and leads to hepatomegalia.

44b. Insufficiency of the liver detoxificative function, mechanism of the main clinical
symptoms. Pathogenesis of the hepatic coma.
The antitoxic liver function aggravation is connected to the violation of certain reactions
directed to rendering harmless the toxic substances, which are formed in an organism or
come from outside:
a) Urea synthesis disorder resulting in ammonia accumulations.
b) Conjugation disorder, i.e. the formation of pair compounds with glucuronic acid,
glycin, cystine, taurine. In such way unconjugated bilirubin, scatol, indol, phenol, kadaverin,
thyramin, etc. become harmless.
c) Acetylization disorder leading to sulphamides accumulation at their long-term usage.

d) Oxidization disorder leading to the accumulation of aromatic carbons.

Deep disorders of the antitoxic liver function bring forward liver encephalopathy and liver
coma.

Hepatocerebral coma
The hepatocerebral coma is a syndrome developing in the result of the liver insufficiency. It
is characterized by the deep affection of the central nervous system (consciousness loss,
reflexes loss, cramps, blood flowand breathing disorders).
The reasons are as follows: viral hepatitis, toxic liver dystrophy, cirrhosis, portal hypertensia.

45b. Jaundice (icterus): types, causes and mechanisms of development, clinical signs.

jaundice is yellowishing of skin, mucous membranes and sclera in the result of bile pigments
depositing in them.
There are three types of jaundice:- prehepatic, hepatic, posthepatic
Hemolytic jaundice:- ( prehepatic jaundice) due to increased hemolysis of erythrocytes. The
special features of bile pigments exchange at this jaundice are as follows: in the blood - high
level of unconjugated bilirubin; in the feces - stercobilin concentration is increased; in the
urine - stercobilin concentration is increased too, and no cholemia.
Parenchymatous jaundice:- ( hepatic jaundice) conditioned by endogenic (inheritable) and
outside influences. The basis of inheritable hepatic jaundice is the violations of the
unconjugated bilirubin capture by hepatocytes, its insufficient conjugation or its insufficient
isolation of the conjugated bilirubin from the hepatocyte.
Parenchymatous jaundice is characterized by the following violations of bile pigments
metabolism: in the blood - the unconjugated bilirubin concentration is increased and the
conjugated bilirub appears; in the feces - stercobilin drops; in the urine- stercobilin drops,
the appearance of urobilin and conjugated bilirubin.
Obstructive jaundice (post hepatic jaundice) is connected with the obstruction for bile
outflow (tumour, cholelithiasis).
Clinically: in the blood - the increase of the unconjugated bilirubin and the appearance of
the conjugated bilirubin; in the feces - the absence or the drop of stercobilin; in the urine -
the absence or the drop of stercobilin, the appearance of the conjugated bilirubin.
Cholemic syndrome appears at obstructive and parenchimatous jaundices, when bile comes
into blood. It is caused by bile acids and the main symptoms are the next: bradycardia,
hypotension, excitability, skin itch.

46b. Glomerulonephritis: classification, etiology, pathogenesis.

Glomerulonephritis is a pathological process characterized by bilateral
immunoinflammatory damage to the glomeruli with involvement in the pathological process
of partially tubules, interstitial tissue and blood vessels.
Classification: acute, chronic, rapidly progressive
The acute (diffuse) glomerulonephritis is the renal disease of the infectious-allergic nature
with the primary damage of the capillaries of the glomeruli.
Etiology. The acute glomerulonephritis occurs after streptococcal infection. Streptococcus
of the group A. Other infectious agents (viri, parasites) are of great importance. In the
glomerulonephritis development the etiological role of the hypothermia, burn, diffuse
lesions of the connective tissue (the systemic lupus erythematosus, rheumatoid arthritis,
and polyarteritis nodosa).
Pathogenesis.

There are two main mechanism of destruction of the glomeruli:

• The defeat of the basal membrane of the glomeruli by the antibodies to its anti gens
- the cytotoxic (nephrotoxic) glomerulonephritis, which is characterized by the rapid
progressive course. The carrier of the antigenic properties of the basal membrane
isglycoprotein:

• The development of the inflammatory process in the glomeruli as a result

of fixing of theimmune complexes on the basal membrane and inside
of it -- the immune glomerulonephritis.
 Clinical and pathophysiological manifestations of the acute glomerulonephritis reflect changes of the
renal and extrarenal functions. The leading signs of the classic course of the disease are the fast onset,
oliguria, proteinuria, azotemia, hypertension, edema.

The chronic (diffuse) glomerulonephritis is the prolonged progressive disease

characterized by the diffuse bilateral inflammatory damage of the kidneys of the
allergic nature, heterogenous by origin, clinical manifestations, and pathogenesis.
Etiology. The chronic glomerulonephritis can occur after acute
glomerulonephritis. There are the following forms of the chronic
glomerulonephritis: Infectious (poststreptococcal, in the case of the prolonged
bacterial endocarditis, malaria, syphilis, tuberculosis, and other infections);

• Non-infectious (scrum, post-vaccination, medicinal, traumatic. poisoning

with various poisons, the hypothermia, renal vein thrombosis, diffuse
connective tissue diseases - the rheumatoid arthritis, systemic lupus
erythematosus, hemorrhagic vasculitis,etc.); • Special (posteclampsic,
radiation, hereditary, etc.)

Pathogenesis.

The disease course develops by both the immune-pathological and non- immune
mechanisms of pathogenesis.

The first include the autoimmune mechanisms of the renal damage, the cellular
immunity with the appearance of T- lymphocytes sensitized to the renal antigens.

The non immune mechanisms of the kidney damage include the proteinuria in
damage of the glomeruli with subsequent accumulation of filtered protein in the
proximal tubules, their destruction is caused by activation of the POL and lysosomal
enzymes.
Clinical manifestations of the glomerulonephritis include all renal syndromes: urinary, edematous, nephrotic,
hypertensive, anemic, and also of the blood coagulation, tubular acidosis and, ultimately, the renal
insufficiency.

In the decompensatory phase due to the significant sclerotic changes and decreased number of the
functioning nephrons the chronic glomerulonephritis converts into chronic renal failure.

47b. Acute and chronic renal insufficiency: causes, pathogenesis, stages.

Acute renal insufficiency is characterized by such disorder renal functions when diuresis is
reduced to 500 ml. This state is called as oliguria. If daily urine does not exceed 100 ml,
takes place anuria.
Etiology:- prerenal, renal and postrenal.
Prerenal factors include: circulating liquid decrease (traumatic shock, blood loss, burns,
vomitis, diarrhea), dilatation of vessels and vessels capacity increase (sepsis, anaphylaxia),
heart insufficiency (infarction of myocardium).
Renal factors include: ischemia kidneys, action nephrotoxical (antibiotics, heavy metals,
organic solvents, X-ray contrast substances), intravessels erythrocytes hemolysis,
glomerulonephritis, states assosiated to pregnancy(septic abortion, eclampsia in pregnant,
bleeding).
Postrenal factors include: ureters obstruction ureters (calculus, blood clots, tumour) and
urinal channel obstruction (prostat hypertrophy, carcinoma).

The clinical course of acute renal insufficiency can be presented in four phases.
Initial phase - is a period, which courses from lesion of kidneys untill, oliguria development.
It takes several hours (ischemia) up to about one week (after action nephrotoxine). Oliguric
phase is characterized by acute decrease of GFS. It duration course last several days up to
several weeks (two weeks in average ). The patients perish just in this phase.
Diuretic phase is characterized by gradual increase of urine volume.
Phase of recovery - period, during which renal function completely are restored, though
easy or moderate GFS decrease can be saved in some patients.

Chronic renal insufficiency:-

Etiology:-The main reasons: primary glomerulus diseases (chronic glomerulonephritis), the
primary canaliculus diseases (chronic pielonephritis tuberculosis), vescular diseases
(hypertonic illness, thrombosis, embolism), diffuse connective tissue diseases (sclerodermia,
nodular periarteriitis), illness metabolism (gout, diabetes mellitus), obstructive nephropathia
(urolithiasis, hydronephrosis), hereditary anomalies ( kidneys polycystic).
The manifestations of chronic renal failure represent the inability of the kidney to perform
its normal functions in terms of regulating fluid and electrolyte balance, controlling blood
pressure through fluid volume and the reninangiotensin system, eliminating nitrogenous
and other waste products, governing the red blood cell count through erythropoietin
synthesis, and directing parathyroid and skeletal function through phosphate elimination
and activation of vitamin D. This all happens due to decrease to nephron amount.

Stages 5 stages on basis of glomerular filtration rate.

Stage 1 with normal or high GFR (GFR > 90 mL/min)
Stage 2 Mild CKD (GFR = 60-89 mL/min)
Stage 3A Moderate CKD (GFR = 45-59 mL/min)
Stage 3B Moderate CKD (GFR = 30-44 mL/min)
Stage 4 Severe CKD (GFR = 15-29 mL/min)
Stage 5 End Stage CKD (GFR <15 mL/min)

48b. Pathogenesis of manifestations of renal insufficiency: edema, arterial hypertension,

anemia, acidosis, uremia.

edematous syndrome :- the renal pathology is often accompanied by the swelling ,which
first are manifested by swollen eyelids and further leads to accumulation of fluids in the
pleura, pericardium etc. The increase of the total amount of fluid in the body as especially in
the extra cellular space, develops as a result of the increase sodium and then water
reabsorption.
Syndrome of the arterial hypertension:- it develop due to activation of RAS and formation
of the potent vasoconstriction- angiotensin 2 that is capable to influence on the systemic
circulation or inhibit the production of vasodilatory prostaglandins and kinins in the renal
medulla and papillae in the case of the chronic pyelonephritis.
Anemic syndrome:- in the renal disease cause by dysfunction of the gromuli and tubules,
the anemia often develops.as a role it can be normocytes, normochromic, and
hyporegenerative. Pathogeneticaly the occurence off such types of the anemia is Associated
primarily with inhibition of the erythropoietin production on the backgroundof enhanced
secreation of the erythropoiesis inhibitor.
Uremic syndrome:- it occurs as a result of the significantly decreased CFR and accumulation
of toxic products of metabolism in the blood .the uremia is primarily due to accumulation of
the uria, uric acid , creatinin, and to a later extent , amino acids and toxic products in the
blood , which are the result of putrefaction in the intestine.

49b. Hyperfunction of adenohypophysis and neurohypophysis, etiology, pathogenesis,

clinical manifestations.

HYPERFUNCTION OF ADENOHYPOPHYSIS
The main reason of hyperpituitarism is development of benign tumor – adenoma of
endocrine cells.
There are two groups of adenomas.
1. Eosinophilic adenoma, develops from acidophilic cells of adenohypophysis forming
STH. Clinically hyperproduction of Somatotropic hormone (STH) appears by giantism (if
adenoma develops in children and young people before closing of epiphysar cartilages) and
acromegalia (in adult).
Giantism is characterized by the proportional increase of all body components. Acromegalia
appears by increased growth of hands, legs, chin, nose, tongue, liver, kyphoscoliosis. Besides
that increased metabolic activity of STH -hyperglycemia, insulin resistanse, even to
development of metahypophysar diabetes, fatty infiltration of liver develop.

2. Basophilic adenoma, grows from basophilic cells of adenohypophysis which more

often produce ACTH. During this the Itsenko-Cushing disease develops.
It is characterized by:
а) secondary hypercorticism;
b) strengthened pigmentation of skin.
There are tumors which produce other hormones of adenohypophysis less often:
Thyrotropic hormone, gonadotropic hormones, prolactin, MSH.
The increased level of ACTH during this disease is combined with increase of level of other
products of proopiomelanocortin.

HYPERFUNCTION OF NEUROHYPOPHYSIS

Their main effects:

Vasopressine (antidiuretic hormone) renders the following influence through V1 and V2
receptors:

✓ 1. Act on tubulus contortus distalis and collective tubules of kidneys,

strengthens reabsorption of water;

✓ 2. Causes contraction of smooth muscles of blood vessels;

✓ 3. Strengthens glycogenolysis and gluconeogenesis in liver;

✓ 4. Stimulates consolidation of memory traces and mobilization of saved

information (hormone of memory); ✓ 5. Endogenic analgetic
(depresses pain).
Oxytocin has the functions:
1. Stimulates secretion of milk (lactation) causing contraction of myoepithelial cells of
smallsized ducts of mammary glands;
2. Initiates and strengthens contractions of uterus of pregnant woman;
3. Worsens storing and mobilization of information (amnestic hormone).
Redundant secretion of vasopressin arises in tumors of different tissues forming
vasopressin, and also in disorders of hypothalamic endocrine function regulation. Its main
manifestation is hypervolemia leading to development of stable arterial hypertension
50b. Hypofunction of adenohypophysis and neurohypophysis, etiology, pathogenesis,
clinical manifestations.

HYPERFUNCTION OF ADENOHYPOPHYSIS (hyperpituitarism)

There are panhypopituitarity and partial hypopituitarity.

Panhypopituitarity – is decrease of formation of all adenohypophysis hormones.
Clinical forms of panhypopituitarity:
1. Hypophysar Simond’s cachexia ;
2. Postpartal necrosis of hypophysis – syndrome of Schegan;
3. Chromophobe hypophysis adenomas, i.e. tumors, which grow from chromophobe cells.
Clinical manifestations of panhypopituitarity are connected with deficiency of
adenohypophysis hormones and disorders of peripheral endocrine glands activity (thyroid
gland, cortex of adrenal, sexual glands).
Partial hypopituitarity is the disorder of formation of separate hormones of
adenohypophysis (not all). The following variants of partial hypopituitarity are described:
1) Hypophysar nanism (dwarfishness) - deficiency of STH;
2) Secondary hypogonadism - deficiency of FSH and LH;
3) Secondary hypothyrosis - deficiency of TTH;
4) Secondary hypocorticism - deficiency of ACTH
The insufficiency of STH results to development of hypophysar dwarfishness, or nanism and
appears by such disorders:
1) decrease of intensity of protein synthesis that leads to delay and stop of growth (more
than 30 % from average) and development of bones, internal organs, muscles.
3) fallout of fat mobilizing action with tendency to obesity
The insufficiency of ACTH leads to secondary partial insufficiency of adrenal cortex. The
glucocorticoid function suffers mainly. Mineralocorticoid function practically does not vary.
Insufficiency of TTH causes secondary decrease function of thyroid gland and development
of secondary hypothyrosis symptoms. In case of primary hypofunction of thyroid gland the
introduction of TTH can restore its function.
Insufficiency of gonadotropic hormones results in decrease of ability of Sertoli cells to
accumulate androgens and oppression of spermatogenesis and ability to impregnation in
men. In case of defect of LG hormone the function of Leidig’s cells is infringed, the formation
of androgens ceases and develops eunuchoidism with preservation of partial ability to
impregnation, as the process of spermatozoids maturing does not stop.

HYPOFUNCTION OF NEUROHYPOPHYSIS

Insufficient production of vasopressin results to development of diabetes insipidus.

There are two pathogenetic variants:

✓ Central (neurogenic) during which will a little quantity of vasopressine is formed

✓ Nephrogenic during which the sensitivity of epithelial cells receptors of distal nephron
to vasopressin is reduced. The decreasing of water reabsorption in kidneys results to
poliuria and decreasing of circulatting blood volume (hypovolemia), falling of arterial
pressure and hypoxia.
The decrease of oxytocin production appears by disorders of lactation, weakness of labor
activity.

51b. Hyperfunction of the thyroid gland: etiology, pathogenesis, clinical manifestations.

Hyperfunction of thyroid gland is designated by the term “thyrotoxicosis” or

“hyperthyrosis”.
ETIOLOGY:
1. Central disturbances – increase of thyroliberin and thyrotropic hormone (ТТH)
secretion.
2. Strictly glandular disturbances (primary hyperthyrosis). The most widespread clinical
forms of primaryhyperthyrosis are:
а) Diffuse toxic goiter (Bazed’s disease, Graves’ disease, Parri’s disease);
b) Toxic adenoma of thyroid gland;
c) Nodular goiter. The most often reason of development hyperthyrosis is diffuse
toxic goiter. diffuse toxic goiter is autoimmune disease.
3. Peripheral disorders :
а) Increase of cell sensitivity to action of Т3 and Т4;
b) Decrease of binding of thyroid hormonees by transport proteins;
c) Decrease of thyroid hormonees’ metabolism in liver in its insufficiency.
Main manifestations of diffuse toxic goiter: а) goiter (increase of thyroid gland); b)
Tachycardia, arrhythmia, cardiac insufficiency; c) increase of basic metabolism more than 10
%; d) increase of temperature; e) weigth loss; f) muscular weakness; g) exophtalmus;
disorders of nervous system –– irritability, instability of mood, inconsistency of acts, tremor.

In pathogenesis of hyperthyrosis manifestations the following mechanisms are important:

1. Anabolic effects. They are high-dose effects of thyroid hormones. They are:
а) delay of growth; b)
atrophy of muscles and weakness; c) weight loss; d) negative nitrogen balance; e) increase of nitrogen leading out,
phosphorum, potassium, ammonia; f) increase in blood of residual nitrogen and nitrogen-containing aminoacids.

2. Strengthening heat-forming action of thyroid hormonees. It appears: a) by

increase of basic metabolism;

b) by increase heat formation and increase of body temperature; c) by good adaptation to cold and bad – to high
temperature;

d) hyperphagia – increased consumption of energy.Triiodthyronine separates oxidation and phosphorilation in cell

mitochondria, therefore the energy of oxidationof NADPH2 is not accumulated in ATP. The decrease of ATP synthesis
increases concentration of its precursors – organic phosphate. The carry of ADP in mitochondria is changed also, as Т3
contacts to a carrier of ADP tarnslocase that in turn strengthens oxidizing processes and by that dispersion of energy,
causing increase of basic metabolism.

3. Increase of functional activity of excitable tissues. It is connected with increase of activity

of Na-K-pumps in cell membranes and increase of cell sensitivity to catecholamines. It
stipulates the following manifestations of hyperthyrosis: a) disorders of activity of central nervous system – acceleration of
mental processes, anxiety, excitation, insomnia; b) constant spontaneous contractive activity of skeletal muscles – fibrillar
twitching, tremor. It is connectedwith muscular weakness, tiredness; c) Changes of activity the increase of heart minute
volume, arterial pressure in cardiovascular system –tachycardia; d) Increase contractive activity of smooth intestinal
muscles – diarrhea; e) Increase of absorbtive and excretive processes intensity. It is connected with hyperglycemia and
hypocholesterinemia.

4.Catecholamine effects are stipulated by increase of cells sensitivity to action of

catecholamins. In clinic of hyperthyreosis the greatest significance have the functional
effects of catecholamins, in particular, their influence on heart – vassel system and
metabolic changes. In tissue the utilization of glucose is increased. There is activated phosphorylase of liver and
muscles, therefore glucogenolis amplifies and there is no glycogen in these tissue. Increase activity of hexokinase and
glucose absorbtion in intestines, is accompanied with alimentary hyperglicaemia.

5. Disturbance with unstablished mechanisms of development – orbitopathy and two-sided

exophtalm.

52b. Hypofunction of the thyroid gland, etiology, pathogenesis, clinical manifestations.

Hypofuction of thyroid gland is the decreased activity of thyroid gland.
ETIOLOGY
1. Central disorders: decrease of formation both secretion of thyreoliberine and
thyreotropic hormone (ТТH).
2. Gland disorders , which result in development primary hypothyrosis:
a) destruction of a gland tissue, for example, radioactive iod;
b) deficiency of iod drinking water and food – endemic goiter;
c) autoimmune damage of gland cells – autoimmune thyroiditis of Chaschimoto;
d) inherent disorders – hypo- and aplasia of thyroid gland, enzymopathy.
3. Peripheral disorders:
а) nonsensitivity of peripheral cells for action of thyroid hormones;
b) increased binding of thyroid hormones with plasma proteins of blood;
c) strengthened metabolism in liver.

PATHOGENEIS
1. Disturbances of growth and defferenciation of tissue. in conditions of hypothyreosis
the growth of bones in length is decreased. The complex of changes of a skeleton –
hyperthyroid dwarfism develops. Along side with it the mental development – gradually is
developed also arises cretinism.
2. The decrease heat formation of action thyroid hormones, which appears:
а) decrease of base metabolism (falling on 20-40 of %);

b) by decrease of heat production, in this connection temperature falls;

c) bad adaptation to a cold for want of preservation of adaptation to high temperature.

3. Decrease of functional activity of exitated tissues. This is connected with falling of activity
Nа-К-АТPаs and changes of processes of ions active transport. Besides that decrease sensitivity
of tissues to catecholamins, has significance that is stipulated by decrease of an amount
βadrenoreceptors on cells. The functional changes of exitated organs and tissues are:
а) disorders of the central nervous system activity – decrease of mental activity, slackness, lethargy,sleepiness etc.;

b) decrease of functional activity of skeletal muscles – weakness, decrease tone, fast tiredness;

c) by disorders of heart activity – vessel system – bradycardia, decrease of heart minute volume, decrease of
arterial pressure;

d) decrease of contraction of the of smooth muscles function of intestines – constipation;

e) disturbance of processes absorbtion and excretion. The decrease glucose absorbtion in intestin couse
hypoglycemia and disorders of excretion of cholesterine in structure of bile to hypocholesterinemia and hereinafter to
atherosclerosis.

4. Disturbances with the unknown mechanisms of development. They are mucous edema –
mixedema. Thisis characterized by increasing tissues the quantity glycosaminglycans,
connecting water; by a thickening of a skin, puffy face. It is admited mixedema is consiquence of action
thyrotropic hormone on connective tissue, amount it is increased on glandular and peripheral forms of hypothyrosis vitally
increase
53b. Hypofunction of the cortex and medulla substances of the adrenal glands: causes,
mechanism of the main manifestations. The notion of acute and chronic adrenal
insufficiency.

There are primary and secondary kinds of adrenal cortex insufficiency. Primary insufficiency
arises as a result of adrenals injury, secondary is connected with the defeat of hypotalamus
(deficiency of corticoliberin), or with hypofunction of adenohypophysis (deficiency of ACTH).
Insufficiency of adrenal cortex can be acute and chronic.
Examples of acute insufficiency are:а) state after removal of adrenals; b) hemorrhage in
adrenals which arises during sepsis, meningococci infection (syndrome
WaterhouseFriderixan); c) syndrome of cancellation of glucocorticoides after prolonged use
their in large dose
Fast falling of the adrenals function causes development of collaps and the patients can die
during the first day.
The chronic insufficiency of adrenals cortex is characterized Adison’s disease (bronzed
disease). The most often reasons of it are: а) tuberculose destruction of adrenals; b)
autoimmune process.
MANIFESTATIONS OF INSUFFICIENT MINERALOCORTICOIDS

1) dehydration develops owing to loss of sodium ions (decreases

rearbsortion) with the loss of water (poliuria);
2) arterial hypotension is stipulated by decrease of circulating blood
volume;
3) hemoconcentration (condensation of blood) is connected with liquid
loss, results to disorders of microcirculation and hypoxia;
4) decreasing of kidney blood circulation is stipulated by increase of
arterial pressure with disturbances of glomerular filtration and development
of intoxication (nitrogenemia);
5) hyperpotassiumemia is stipulated by decrease of canales secretion of
potassium ions and their output from the damaged cells. It causes disorders
of function of arousing tissues;
6) distal canales acidosis. It is connected with disorders of acidogenesis
in distal nephron canales;
7) gastro-intestinal disorders (nausea,vomiting, diarrhea). Loss of sodium
(osmotic diarrhea) and intoxication have significant meaning. This disorders
without appropriate correction result to death.
MANIFESTATIONS OF INSUFFICIENT GLUCOCORTICOIDS

1) hypoglycemia;
2) arterial hypotension (permissive reaction on catecholamines);
3) decrease of response of fat tissue on lipotropic stimules;
4) decrease resistance of an organism on action of different pathogenic
factors;
5) decrease of ability to remove water during water load (water
poisoning);
6) muscular weakness and fast tiredness;
7) emotional disorders (depression);
8) delay of growth and development of children;
9) sensor disorders - loss of ability to distinguish separate shades
gustatory osmetic acoustical sensations;
10) distress-syndrome of a newborn (hyalinic membranosis). It is
stipulated by disorders of surfactant formation in lungs owing to what lungs
are not straightened after birth of a child.

54b. Hyperfunction of the cortex and medulla substances of the adrenal glands: causes,
mechanism of the main manifestations.

Hyperaldosteronism. Arises during hyperfunction of glomerular zone of adrenals cortex,

which produce mineralcorticoides.
There are primary and secondary hyperaldosteronism.
Primary hyperaldosteronism (Conn syndrome) arises in adenoma of zone glomerular,
which secretes high quantity of aldosteron.
Main manifestations of this disease:

1) arterial hypertension. It is connected with increase of sodium contents in blood and

in wall of blood vessels, after what the sensitivity of their smooth muscles to action of
pressor factors, particularly catecholamines increases.
2) hypopotassiumaemia (result of hypersecretion of potassium ions in canaliculas of
kidneys). It causes disorders of arousing organs and tissues (disorders of heart activity,
miostenia, pareses);
3) ungas alcalosis. It is connected with amplification of acidogenesis in distall nephron
canaliculas;
4) polyuria arises as a consequence sensitivity of kineys canales epithelium loss to
action of vasopressin. It explains absence of volume increase of circulatting blood and
edema.

Secondary hyperaldosteronism is a result of renin-angiotensin system activation. This state

appears by: a) arterial hypertension; b) edema; c) hypopotassiumaemia; d) ungas alcalosis.
Hypercorticism with hyperproduction of glucocorticoides:

✓ 1. Cushing’s disease – basophil adenoma of anterior part of hypophysis.

✓ 2. Cushing’s syndrome:
а) tumor – adenoma of zona fasticulata of adrenal cortex;
b) ectopic production of АCТH by some malignant tumors (pulmonar cancer);
c) iatrogenic – introduction of glucocorticoides in an organism with the medical
purpose.
HYPER FUNCTION OF ADRENAL MEDULLA

✓ Hyperfunction of adrenal medulla arises in tumors of chromaphine cells –

pheochromocytome.

✓ It appears by arterial hypertension, tachycardia, extrasystole, flatering of atriums,

hyperglycaemia, hyperlipidemia, hyperthermia. In time of paroxizm vertigo,
headache, hallucinations, increased excitability of the nervous system, cramps
appear.

Depending on the level of blockade of cortisole synthesis there are three variants of androgenital syndrome.

І. Disorders of early stages of synthesis – deficiency of glucocorticoides, mineralcorticoides and androgens

hyperproduction. Manifestations: signs of insufficiency of gluco- and mineralocorticoidal functions of adrenal
cortex features of early sexual maturing in males, virilization in women (appearance of man's sexual features).

ІІ. Disorders of intermediate stages – deficiency of glucocorticoides, surplus of androgens, formation of

mineralocorticoides is not disordered (classical androgenic syndrome). Manifestations are the same, as in the
first case, only without signs of insufficiency of mineralocorticoidal function.

ІІІ. Disorders at final stages of cortizol synthesis – deficiency of glucocorticoides, hyperproduction of androgens
and mineralocorticoides. Features of hyperaldosteronism are connected with manifestations of classical
androgenital syndrome.
55b. Violation of the function of parathyroid glands: causes, mechanisms of development,
clinical manifestations.

HYPER-PARATHYROIDISM
ETIOLOGY
1) Tumor – adenoma of parathyroid gland;
2) Hyperfunction of parathyroid glands stipulated by decrease of endocrine cells
sensitivity to calcium ions asa result of regulation disorders by a principle of negative
feedback.
Hyperparathyrosis appears by two groups of the connected among themselves changes.
1. Disturbance of bone tissue – generalized fibrose osteodystrophy. It is known as
Reklinhausen’s disease. It is stipulated by increase of osteoklasts activity and suppression of
the osteoblasts function.
It appears by pain in bones and joints, softening of bones, acute deformation of a skeleton.
Develops demineralization of bone tissue (osteomalation) which results in increase of the
contents of calcium ions in blood plasma – hypercalciemia.
2. Hypercalciemia. It leads to:
а) Calcification of soft tissues (kidneys, vessels, lungs). In severe cases develops renal
insufficiency;
b) Formation of calcium stones in kidneys:
c) Disorder of excitability of the nervous system and muscles – muscular
weakness, depression, disturbancesof memory;
d) Arterial hypertension;
e) Disturbances of gastric secretion and occurrence of ulcers in stomach.
Secondary hyperthyrosis arises as response on hypocalcaemia during syndrome
malabsorption, Fancony’ssyndrome, chronic renal insufficiency, during hemodialysis.
Hyperplasia of parathyroid glands frequently is transformed in adenoma

HYPO-PARATHYROIDISM
ETIOLOGY
1) Accidental damage or deleting of parathyroid glands during operations on thyroid gland
2) Damage of parathyroid glands during treatment with radioactive iodine of thyroid gland
diseases
3) Autoimmune damage of parathyroid glands
4) Inherent hypoplasia of parathyroid glands
5) Nonsensitivity of cells targets to action of parathyrin – pseudohypoparathyrosis.
Main manifestation of hypoparathyrosis is hypocalciemia. It causes development
parathyroid tetania which appears by acute increase of nervous – muscular excitability,
multiple fibrillar twitching of muscles of all body. Then occur attacks of clonic cramps which
transform into tonic.
The convulsive twitching can be distributed also to internal bodies (pilorospasm,
laryngospasm).
During one of such attacks the death can occur. During chronic hypoparathyrosis in animal
the clinical picture of parathyrotropic cachexia develops. It is characterized by weight loss,
anorexia, increased nervous –muscular excitability, dyspepsia and diverse trophicdisorders

56b. Violation of the function of parathyroid glands: causes, mechanisms of development,

clinical manifestations.

HYPER-PARATHYROIDISM
ETIOLOGY
1) Tumor – adenoma of parathyroid gland;
2) Hyperfunction of parathyroid glands stipulated by decrease of endocrine cells
sensitivity to calcium ions asa result of regulation disorders by a principle of negative
feedback.
Hyperparathyrosis appears by two groups of the connected among themselves changes.
1. Disturbance of bone tissue – generalized fibrose osteodystrophy. It is known as
Reklinhausen’s disease. It is stipulated by increase of osteoklasts activity and suppression of
the osteoblasts function.
It appears by pain in bones and joints, softening of bones, acute deformation of a skeleton.
Develops demineralization of bone tissue (osteomalation) which results in increase of the
contents of calcium ions in blood plasma – hypercalciemia.
2. Hypercalciemia. It leads to:
а) Calcification of soft tissues (kidneys, vessels, lungs). In severe cases develops renal
insufficiency;
b) Formation of calcium stones in kidneys:
c) Disorder of excitability of the nervous system and muscles – muscular
weakness, depression, disturbancesof memory;
d) Arterial hypertension;
e) Disturbances of gastric secretion and occurrence of ulcers in stomach.
Secondary hyperthyrosis arises as response on hypocalcaemia during syndrome
malabsorption, Fancony’ssyndrome, chronic renal insufficiency, during hemodialysis.
Hyperplasia of parathyroid glands frequently is transformed in adenoma

HYPO-PARATHYROIDISM
ETIOLOGY
1) Accidental damage or deleting of parathyroid glands during operations on thyroid
gland
2) Damage of parathyroid glands during treatment with radioactive iodine of thyroid
gland diseases
3) Autoimmune damage of parathyroid glands
4) Inherent hypoplasia of parathyroid glands
5) Nonsensitivity of cells targets to action of parathyrin – pseudohypoparathyrosis.
Main manifestation of hypoparathyrosis is hypocalciemia. It causes development
parathyroid tetania which appears by acute increase of nervous – muscular excitability,
multiple fibrillar twitching of muscles of all body. Then occur attacks of clonic cramps which
transform into tonic.
The convulsive twitching can be distributed also to internal bodies (pilorospasm,
laryngospasm).
During one of such attacks the death can occur. During chronic hypoparathyrosis in animal
the clinical picture of parathyrotropic cachexia develops. It is characterized by weight loss,
anorexia, increased nervous –muscular excitability, dyspepsia and diverse trophicdisorders

57b. Violation of motor function of the nervous system: etiology, pathogenesis.

Hyperkinesis.

Upper motor neuron dysfunction reflects an interruption in the pyramidal tract and
consequent decreased activation of the lower motor neurons innervating one or more areas
of the body. Upper motor neuron dysfunction usually affects more than one muscle group,
and generally affects distal muscle groups more severely than proximal groups.
Lower motor neurons dysfunction: are of two basic types: large (alpha) and small (gamma).
Dysfunction of the large motor neurons of the anterior horn of the spinal cord, the motor
nuclei of the brainstem, and their axons causes impairment of voluntary and involuntary
movement.
Causes: Mechanical nerve damage, Poisons and toxins (botulinum toxin, alpha
bungarotoxin, curare-extract, insecticides, organophosphorus chemical warfare agents)
Pharmacological agents Hereditary factors (myastenia gravis)
Pathogenesis:

Hypokinesia: this disorder is manifested by paralysis( loss of movement) and

pareses(weakening of movement). The paralysis of half of the body is called hemiplegia,
paralysis of either the upper or lower part of the body is called paraplegia and the paralysis
of all limbs is called tetraplegia or quadriplegia. depending on the pathogenesis of the
paralysis, the tonus of the affected muscle may either be lost(flaccid paralysis) or
increased(spastic paralysis).
There are also peripheral and central paralysis and also reflex paralysis.
The central paralysis is characterized with the intentional motions loss; tendonal and
periostal reflexes (hyperreflexia) activation, pathological reflexes appearance, for example,
the extension of the first ringer in case of the external foot-side irritation (Babinsky reflex) or
the crus frontal surface (Openhame reflex).
Peripheral (flabby) paralysis is observed in fact of spinal cord column. anterior horns,
anterior radicles, plexuses and nerves. For peripheral paralysis the total movements loss
characteristic – intentional and reflectory. Muscular tonus is absent (atonia). Tendonal
reflexes disappear (areflexia

Hyperkineses– are the unintentional forcible motions, pyramidally or extrapyramidally

caused.

• Pyramidal hyperkineses get shown with the convulsive state. Long lasting
unintentional are called tonic convulsions (cramps). If muscular contractions
alternate with relaxations, such cramps are called clonic. For example epilepsy. They
include two phases – tonic ant clonic. Tonic phase lasts about one minute and reflects the total
muscular spasm – tetanus. clonic phase lasts longer – up to 2-3 minutes. During this phase biting of tongue and
lips, unintentional defecation and uresis are possible. If cramp attacks come one by one in short time periods,
that is called epileptic status.. Known causes of epilepsy include:Head Injury/Trauma, Brain Infection, such as
meningitis, Brain Tumor, Stroke, Lead Poisoning, High Fever, Poor Nution,rit Heredity
• Extrapyramidal caused hyperkinesis include tremor, myoclonia, chorea, atetosis
• Types of hemiplegia: atethosis, ballism, chorea, intentional cerebral tremor,
myoclonus, parkinsonian tremor.
1. Motor disorders due to the cerebellum dysfunctions: etiology, pathogenesis,
clinical manifestations. Acute cerebellar ataxia (ACA) is a disorder that occurs when
the cerebellum becomes inflamed or damaged.
ETIOLOGY: These can be vascular (due to stroke, hemorrhage), idiopathic, iatrogenic (drug),
traumatic, autoimmune, metabolic, infective, inflammatory, neoplastic, toxic
CLINICAL MANIFESTATION Dysdiadochokinesia/ dysmetria Ataxia Nystagmus Intention
tremor Speech - slurred or scanning Hypotonia

58b. Motor disorders due to the cerebellum dysfunctions: etiology, pathogenesis, clinical
manifestations.
The cerebellum is a highly organized center, which regulates the functions of the muscles. It
received the flow of impulses from the receptors of the muscles, joints, tendons, skin, and
also of the organs of the sight, hearing, and balance.
Cerebellar dysfunction causes balance problems and gait disorders along with difficulties in
coordination resulting in ataxia, uncoordinated movements, imbalance, speech
problems(dysarthria), visual problems (nystagmus) and vertigo as a part of the
vestibulocerebellar system.
Causes:-- vascular (due to stroke, hemorrhage), idiopathic, iatrogenic, traumatic,
autoimmune, metabolic, infectious, inflammatory, neoplastic, and some rare genetic
disorders. An etiological evaluation is necessary for the diagnosis of cerebellar dysfunction
and the treatment of cerebellar disorders.
Gaze-evoked nystagmus is the most common form of nystagmus encountered in disorders
of the cerebellum.
Ataxic speech tends to become slow with slurring
Cerebellar damage typically results in impairment of performance of limb movements.
Ataxia of limbs includes: dysmetria, decomposition of movement, dysdiadochokinesia,
cerebellar tremor, isometrataxia, disorders of muscle tone (both hypotonia and cerebellar
fits), loss of check and rebound, abnormal handwriting, and megalographia.
Tremor in cerebellar diseases is mainly composed of low frequency oscillations, usually with
a kinetic component. Kinetic tremor is often associated with a concomitant postural tremor.
Cerebellar patients have increased body sway and a broad-based stance due to the inability
to maintain the body in a stationary position (ataxia of stance).

59b. Pain: definition, etiology, pathogenesis, pain classification, pain syndromes.

Pain is a typical process that emerged during evolution, which occurs when exposed to body
pain (nociceptive) stimulus or the weakening analgesic (antinociceptive) systems
Component of pain reactions

1. Perception, transmitting and awareness of pain

2. The formation of autonomic, emotional and behavioral reactions

3. Mobilization of analgesic systems

ETIOLOGY

1. Mechanical stimuli (> 40 g / mm2)

2. Thermal stimuli (<15oC i >45oC)
 3. Chemical compounds (bradykinin, serotonin, histamine, pH <6, K +> 20 mmol
/ L, acetylcholine, proteolytic enzymes). Prostaglandins, substance P - increased pain
sensitivity of nerve endings
4. Damage to nerve conductors (neuropathic pain).
PATHOGENESIS

І. Peripheral mechanisms

- chemical irritation
- compression of nerves
- regeneration of nerves (neuroma)
- demyelination of nerves
II. Peripheral-central mechanisms

- pathological reflexes
- imbalance of afferent inputs
- reduce the inhibitory effect of the reticular formation
- denervation hypersensitivity
ІІІ. The central mechanisms

- generating of pathological enhance excitement

- removal of inhibitory influence of the cortex to thalamic nucleus
- deafferentation of neurons
- changes in the quality of pain
- dissociation of pain and external pain stimulus
- conditioned reflex mechanism

CLASSIFICATION

A/c to clinical characteristics

• Sharp and dull pain

• Localized and diffuse pain

• Tingling, tingling, hot flashes, etc.

A/c to value for the body
• Physiological pain

• Pathological pain
A/c to the duration of pain sensation

• Acute pain

• Chronic pain : Neuralgia, Causalgia, Phantom pain, Thalamic pain

A/c to For a place of painful stimuli
Somatic: Surface, fast (early), slow (late), deep, slow (late)
Visceral: own visceral, parietal
A/c to localization
Local; Projection; Reflective (Irradiated, reflex)
A/c to speed of development
Fast pain (early); Slow pain (late)

PAIN SYNDROME: A form of chronic pain that usually affects an arm or a leg. It might
develop after an injury, a surgery, a stroke or a heart attack. The pain is out of proportion to
the severity of initial injury. The symptoms include low back pain, headaches, joint pain,
muscle aches, burning or tingling pain, jolts of sharp pain. Mostly it is triggered by nerve
trauma or injury to the affected limb that damages the thinnest sensory and autonomic
nerve fibers.

60b. Antinociceptive systems. Violation of pain perception, anesthesia, analgesia. of pain,

anesthesia, analgesia.

Antinociceptive system: This system includes two levels of painful information control:
central – at level of brain and segmented – at level of spinal cord. The control is carried out
with the help of biologically active substa nces. Depending on the mechanism analgesia is
selected four antinociceptive system
The neuronal opiate system: These substances extracted from brain, have determined their
chemical structure and have named encephalins. Except for brain, them have found in
cerebrospinal of liquid and blood.
The neuronal neoopiate system: Antipainful action of this system will be realized through
noradrenaline,serotonin, dofaminum.Noradrenaline oppresses realization painful of
impulses cord and at level of trunk brain.Serotonin causes antipainful action only for want of
significant excess. Manu of serotoninergic neurons is found in gelatinous substance of dorsal
horns of spinal cord, medulla oblongata, Varolii pons, medial thalamus. To serotonin the
exclusive role in genesis of headache belongs. Before painful attack the contents
serotoninsharply increases and develops vasoconstriction.
The hormonal opiate system: It is hypophysis. Adenohypophysis synthesizes substance
proopiomelanocortin. Farther with removal peptide of fragments from it will be derivated
adrenocorticotropic, melanocytostimulating and β-lipotropic hormones. All these hormones
cause anaesthetic action. Besides from β-lipotropic hormone content substance – β-
endorphine.
The hormones of neopiate system: It is represented vasopressin. This hormone is formed in
supraoptic andparaventricular nucleuses hypothalamus and is secreted in blood by dorsal
part of hypophysis. The appearance of a pain quite often is combined with of bloodloss.
Vasopressin in these cases influence double action – it detains liquid and reduces pain.
The loss ofsensitivity is called anesthesia, the loss of algesic sensitivity is called analgesia,
the loss of themperatural sensitivity thermoanesthesia. The loss of proprioceptive (deep
located) sensitivity is also available. The sensitivity increase is called hyperesthesia, and the
appearance of unusual feelings (tingling, anttickling) – paresthesia.

6b. Disorders of the trophic function of the nervous system. Disorders of autonomic
nervous system functions.
DISORDER OF TROPHIC FUNCTION

These disorders involve hemocoagulation, angiopathic, and chronic inflammatory processes in the
derma, that lead to necrosis and sclerosis of dermal connective tissue.

Diabetic ulcers are one example of neuropathic ulcers. They always occur on the foot. They occur
either as perforating ulcers on the sole of the foot beneath the heads of the metatarsals or at other
bony prominences (e.g. the toes, the ball of the great toe, the malleoli).

Typically a diabetic ulcer is deep, painless, and infected and has a 'punched out' appearance. These
ulcers are known as 'perforating ulcers'. Tissue surrounding the ulcer is generally well perfused.
Peripheral pulses are often palpable. In the case of neuropathic ulcers, there is generalised sensory
impairment. There is often a history of minor trauma that precedes the development of the ulcer.
Note that infection may spread quickly and may lead to extensive limb-threatening necrosis and
septicaemia.

62b. Violation of behavioral and emotional reactions. Neurosis.

Emotions are always accompanied by the autonomic, endocrine and motor responses. It
explain by the fact that any emotional excitation is closely connected with the
hypothalamus. It is known that the hypothalamus is , first, the highest autonomic centre,
which organizes all the autonomic component of emotions and secondary, it independently
an together with the pituitary gland controls many endocrine glands; it leads the emergency
of the endocrine component of emotions.
The essence of these reaction is to prepare the body for the upcoming muscular work
associated with looking for food , escaping the predator etc. In norm all emotional
responses have a certain degree of manifestation, adequate to those life situations, in which
there is the body. The processes of the excitation the the emotional centers are
characterized by the certain strength and duration.
They are controlled and accurately suppress by the corresponding inhibitory structures. If
for some reasons the excessive stimulation of the emotional centers occurs, the persistent
dysfunction of the central nervous system is possible.
Clinically its manifested with the neurosis:A sharp increase of the excitation processes is
observed in the stimulation of the neurosis of disappear , for ex: when animal during
experiments are deprived of the ability to avoid form repeated shock with electric current.
The neurosis is manifested by different somatic dissorder. The functioning of the
uncontrolled focus in the centra central nervous system via the autonomic nervous and
hypothalamic-pitutary system leads to the disruption of the internal organs amd endocrine
glands, occurence of the resistance arterial hypertension, ischemic heart disease, ulcerative
lesion of the alimentary canal, diabetes, hyperthyroidism etc
63b. Shock: classification, mechanisms of development. The role of biologically active
substances in the development of organ failure.

Shock is grave pathological process accompanying with an exhaustion of the vital

functions of an organism and resulting it on a side of life and death because of
critical decrease of capillary blood circulation in lesion organs.
CLASSIFICATION:
Depending on the reasons of occurrence there are following kinds of shock:

• traumatic;
• hemorrhagic;
• burn;
• turnicate (develops after removal of jute after four hours and more after
imposing);
• anhydremic (dehydrative);
• cardiogenic;
• pancreatic;
• septic;
• infectional-toxic;
• Anaphylactic.
Depending on the initial mechanisms underlying in pathogenesis of shock there are:

• hypovolemic shock (hemorrhagic, anhydremic);

• shock connected with disturbances of pump function of heart (cardiogenic);
• forms of shock (anaphylactic, pancreatic);
• pain shock at which the central regulation of blood circulation
(traumatic, after burning) is damaged.
MECHANISM OF DEVELOPMENT:
Irrespective of the reasons of occurrence the shock is shown by a complex
of infringements of hemodynamics which are:
 • reduction of arterial pressure;
• reduction of circulating blood volume ;
• decrease of volumetric speed of organ circulation;
• infringement of reologic properties of blood (aggregation of form elements,
increase of blood viscosity).
In basis of development of blood circulation disorders at shock the
following mechanisms may lay.

A. Reduction of volume of circulating blood:

• blood loss (hemorrhagic shock);2) loss of blood plasma at massive exudative

inflammation (burn shock);
• an exit of fluid from blood vessels (anaphylactic shock);
• dehydration (anhydremic shock);
• redistribution of blood in vascular system (thrombosis and embolism of main
veins).
B. Reduction of minute volume of heart:

• infringement of contractive functions of heart (heart attack of myocardium); •

tamponade of heart (heart break, exudative pericarditis);
• arrhythmias (fibrillation of ventricles).
C. Reduction of the general peripheral resistance in result of generalized dilation of
vessels:

• fall of neurogenic tone of arterioles (pain forms of shock);

• reduction of basal tone of vessels under action of biologicaly active substances
(anaphylactic, pancreatic shock) or toxic products (traumatic, turnicate,
infection- toxic shock). D. Infringements of reologic properties of blood:

• syndrome of intravascular disseminated coagulation of blood (pancreatic

shock);
• aggregation of form elements of blood (septic, infection-toxic shock);
• concentration of blood – hemoconcentration (anhydremic shock).
ROLE OF BIOLOGICALLY ACTIVE SUBSTANCES:
Extreme conditions are usually accompanied by the strengthened liberation and
formation of histamine, serotonin, kinins, lysosomal enzymes and other biologically
active substances. Therefore to extreme conditions disturbances of microcirculation
are peculiar: infringement of perfusion of microvessels, dilatation and decrease of
their sensitivity to vasopressing influences, increase of permeability of vascular walls
and their structural infringements even to necrobiosis. Pathological aggregation of
erythrocytes, ‘sludg-syndrome’, hypercoagulation of blood, disseminated
intravascular coagulation of blood and microthrombosis of vessels.
64b. Features of hypovolemic and cardiogenic shock development, pathogenesis of
disorders. Principles of antishock therapy.

Cardiogenic shock is observed at decrease of pump function of cardiac muscle (heart

infarction, myocarditis), at heard disorders of heart rhythm (paroxysmal tachycardia), at
tamponade heart (thrombosis of cavities, exudation or bleeding in pericardium), at massive
embolia of lungs arteries (tromboembolia of lungs).
Main mechanism cardiogenic a shock is reduction of stroke and minute volume of blood,
arterial pressure and increase of heart filling pressure. As well as at anhydremic shock,
owing to sympathoadrenergic reactions, the tachycardia, increase of peripheral resistance
of vessels is observed. hypovolemic shock (hemorrhagic, anhydremic)
Hemorrhagic shock appears during external (knife, bullet wound erosion bleedings of
stomach at stomach ulcer, tumors, from lung at tuberculosis etc.) or internal (hemothorax,
hemoperitonium) bleedings in conditions of tissues traumation.
Anhydremic shock appears owing to significant dehydratation at loss of liquid and
electrolytes. During the exudative pleurities, intestinal obturation, peritonitis liquid comes
from vascular system into cavities. During the unrestrained vomitting and strong diarrhea
the liquid is lost outside. Develops hypovolemia which plays a role of main pathogenetic
link.
PRINCIPLE OF ANTISHOCK THERAPY

For hypovolemic:

- Maintain or increase the intravascular volume

- Decrease fluid loss
- Supplematary O2 therapy
For Cardiogenic

- O2 therapy
- Administration of cardiac drugs
- Increase heart pumping action through medications.

65b. Septic and traumatic shock: causes, pathogenesis of being abnormalities,

crashsyndrome.

SEPTIC SHOCK: Septic (endotoxin) shock appears as complication of sepsis. Main damaging
(injuring) factor are endotoxins of microorganisms. The most often reason ofsepsis are
gramm negative microorganisms, and also streptococci, staphylococci, pneumococci and
many others.
Main pathogenetic parts of septic shock: Increase of requirement of an organism in oxygen
owing to amplification of exchange processes, tachypnoe, tachycardia, fever. Then decrease
of the general peripheral resistance of vessels is observed; Decrease of blood oxygenation in
lungs and insufficient extraction of oxygen from blood by tissues. Oxygenation is decreased
in connection due to circulation infringements in asmall circle, aggregation of trombocytes
on walls of vessels; Activation by endotoxins of proteolytic systems in biological liquids
(kallikrein-kinin’s, complement, fibrinolytic).
TRAUMATIC SHOCK: Traumatic shock develops owing to large damages of tissues. In its
clinic two stages are distinguished: 1) excitation (erectile); 2) inhibition (torpid).
The stage of excitation is short-term, is characterized by excitation of the central nervous
system owing to reception of pain impulses from the injured tissues.
The stage of inhibition is more long (from several hours to about day) and is characterized
by development inhibition processes in the central nervous system. General inhibition seizes
also the centres of the vital functions (blood circulation, breath), they are broken, owing to
what oxygen starvation develops. Hypoxia, in turn, aggravates infringements in
cardiovascular and respiratory centres. Disorders of haemodynamic and external breath
progress vice circle becomes isolated.
CRASH SYNDROME: CRASH syndrome” is the syndrome of Corpus callosum hypoplasia,
Retardation, Adducted thumbs, Spastic paraplegia and Hydrocephalus. It is a rare,
congenital X-linked developmental disorder

66b. Collapse: definition of the concept, types, mechanisms of development.

Collapse is an acute vascular insufficiency which is characterized by fall of a vascular tone,

and also acute reduction of circulating blood volume . It is shown in clinics by short-term
loss of consciousness, general weakness, features of acute vascular insufficiency with
infringements hemodynamics practically in all organs and tissues.
The infectious collapse develops as complication of acute infectious diseases:
meningoencephalitis, and typhoid fever typhus fever, acute dysentery, pneumonia,
botulism, the Siberian ulcer, virus hepatites, toxic influenza.
Hypoxic collapse may appear in conditions of reduced partial pressure of oxygen in air.
Ortostatic collapse appears at fast transition from horizontal position in vertical, and also at
longtime of standing.
Hemorrhagic collapse develops at massive blood loss as a result of fast reduction
of circulating blood. two basic mechanisms in pathogenesis:
1) fall of veinis and arteriols tone as a result of action of infectious, toxic, physical,
allergic and other factors directly on a vascular wall, vasomotoric centre and on vascular
receptors (sinocarotid zones, arches of an aorta);
2) fast reduction of circulating blood volume (blood loss,plasma loss).

67b. Coma: definition of the concept, types, mechanisms of development.

Cоmа is a pathological state that is characterized with deep oppression of functions of the
central nervous system and it is shown by loss of consciousness, absence of reflexes on
external irritators and disorders of the vital functions regulation of an organism.
CLASSIFICATION, ETIOLOGY AND PATHOGENESIS

• 1. Cоmas at initial injury and diseases of the central nervous system (insult,
craniocerebral trauma).

• 2. Cоmas in the endocrine diseases that apper as at insufficiency of some glands of

internal secretion (diabetic, hypocorticoid, hypopituitary, hypothyreoid), and at their
hyperfunction (thyreotoxic, hypoglycemic).

• 3. Toxic cоmas are observed at endogenic ( uraemia, hepatic insufficiency,

toxicoinfections, pancreatitis) and exogenic intoxications (alcoholic poisonings,
barbiturate poisoning, phosphororganic poisoning.
4. Cоmas caused by infringements of gas exchange at various kinds of hypoxias.

• 5. Cоmas caused by loss of electrolytes, water and energetic substances

The main pathogenetic mechanisms

1. Disorder of cellular breath and an exchange of energy in brain. A basis of them is

hypoxia, anemia, disorders of brain blood circulation, blockade of respiratory enzymes by
cytotoxic poisons, acidosis (at diabetic and uraemic cоma), deficiency of power substances
or blockade of their recycling (starvation, hypoglycemis coma). In development of brain
hypoxia disorders of microcirculation play role. Owing to hypoxia it is broken oxidizing
phosphorelation, the content and use АТP and creatinphosphate decreases
2. Disorder of synaptic transmission in the central nervous system. It may be
connected with:
a) disorder of synthesis, transport, deposition and secretion of neuromediators;
b) replacement of neuromediators by pseudomediators;
c) excessive activation of inhibition postsynaptic receptors;
 d) blockade stimulating postsynaptic receptors.
3. Disorder of electrolyte balance with changes of cellular potentials and process of
polarization of neurons membranes, and also infringement of osmotic pressure.
4. Changes of physical properties and structures of brain and intracranial formations.
Pathogenetic value has swelling and edema of brain and brain membrane, increase of
intracranial pressure which strengthen infringement of hemodynamics and liquordynamic,
make hypoxia of nervous cells heavier and oppress their physiological activity. Mechanical
damage of brain matters cells at a craniocerebral trauma, tumours, hemorrhage in brain.

THIRD PART

1c. Alpinists slowly climb on south side of Everest. It was sixth hours of ascending. General
weakness was present. Breath became more difficult. There was palpitation. Pulse rate
achieved to 100 beats for a minute. Dizziness, headache lowering of mood and appetite,
and meteorism were observed.
1. How this symptomatic complex is called?
Hypobaropathy of mountain disease also known as acute mountain sickness (AMS), altitude illness,
Acosta disease, puna, and soroche

2. What height were alpinists on?

About 5000-6000 ( Mount Everest peak 8849 m)

3. What etiology of these disorders in the alpinists?

Increase in altitude causes decrease in atmospheric pressure which in turn results in Lowering of
partial oxygen pressure (hypoxia)

Hypoxia and decreased atmospheric pressure accompanied brings about signs and symptoms seen
here in the alipinist ( syndrome of compensation)
2c. As a result of damage to one of the reactor units spewed radioactive products. In the
area of high radiation activity were three persons. Tentatively they received by 2.5-3.0
Gray. They were immediately taken to the hospital.
1. What consequences can be expected in the victims?
Bone marrow form of radiation sickness. It develops when irradiated at doses of 1-10
Grey

2. What distinguished periods in the development of radiation sickness?

3. Describe the mechanism of action of ionizing radiation?

3c. Woman is heterozygous on phenylketonuria gene, and her husband is homozygous on

normal alleles of this gene.
1. What is probability in this family of giving birth to a child sick with phenylketonuria?
2. Define probability of phenylketonuria display, if wife is heterozygous on given gene/
3. Describe pathogenesis of phenylketonuria disease?
4c. In the family was born a healthy boy. At a child developed normally. The 25-year-old
age he set Huntington's chorea. His mother and maternal grandfather suffered from
Huntington's chorea.
1. Determine the type of inheritance?
2. If in the family had other children, or they would be sick chorea?
3. Describe pathogenesis of Huntington's chorea disease?
5c. Reputed French surgeon Larey somehow said: “The wounds in victors heal quick” 1.
How you understand this phrase from organism reactivity position? 2. What is role of
cerebral cortex, limbic system and hypothalamus in reactivity? 3. Explain role of
autonomic nervous system in reactivity and organism adaptation?
6c. The patient was hospitalized with complaints on cough, rise of temperature to 38-39º
C, general weakness, and headache. Illness was related to super cooling. After clinical
research pneumonia was diagnosed. 1. What was an immediate disease cause? 2. What
reactivity mechanisms lead to decreasing of resistance to a given disease? 3. What are
your propositions to promote rising of organism resistance to catarrhal diseases?
7c. In the patients is diagnosed sepsis with liver, lungs and kidneys abscesses. A week ago
he cut a finger with knife. Prior to this the patient was getting treatment with
glucocorticoids on extent of 20 days due to the chronic eczema of the right leg. 1. What
was the cause of decreasing of patient’s resistance towards infection? 2. What protective
mechanisms were depressed? 3. Why (describe pathogenesis of decreasing patient’s
resistance)?
8c. The patient 45 years old was hospitalized in pulmonological department with
complaints on cough, weakness, raised body temperature (38-39 °С). She was frequently
ill with respiratory diseases. During last five years suffers from rheumatoid arthritis. There
was established a diagnosis: bronchopneumonia. Disease badly responded to treatment
by antibiotics. Blood test: Leucocytes - 15×10^9/l, Basophils - 1 %, Metamyelocytes – 0,1
%, Stab Neutrophils - 4 %, Segmented Neutrophils - 68 %, Lymphocytes - 17 %, Monocytes
- 2 %. Т-lymphocytes – 0,8x109/l; Тh, Ts, Тk – within of norm. B-lymphocytes – 0,2x10^9/l;
Ig A – 0,18 mcmol/l; Ig М – 1,1 mcmol/l; Ig G – 87,5 mcmol/l. 1. What desease can be in
patient? 2. Why do the respiratory diseases frequently intensify in patient? 3. Explain
their pathogenesis?
9c. The patient 57 years old was hospitalized in pulmonological department with
diagnosis: inferior lobar right side pneumonia. A month ago was sick a flu. He was rarely
sick with acute respiratory diseases. Blood test: Leucocytes - 4,7×10^9/l, Basophils - 1 %,
Eosynophils – 3 %, Stab Neutrophils - 1 %, Segmented Neutrophils - 69 %,
Lymphocytes - 10 %, Monocytes - 16 %. Т-lymphocytes – 0,4×10^9/l, Тh – 16 %, Ts –
14 %, Тk – 58 %. B-lymphocytes– 0,18×10^9/l, Ig A – 1,2 mcmol/l, Ig М – 1,2 mcmol/l, Ig G
– 62,5 mcmol/l. 1. What desease can be in patient? 2. What blood indexes do relate
directly to pneumonia development? 2. Explain pathogenesis?
10c. The boy 8 years old was repeatedly hospitalized in children's department with
pleuropneumonia. On skin of neck and upper half of trunk there are large purulent
eruptions a few furuncles was established, that he annually 3-4 times a year gets sick with
acute respiratory diseases with bronchi spasm. Blood test: Leucocytes - 16,2×10^9/l,
Basophils - 2 %, Eosynophils – 4 %, Stab Neutrophils - 3 %, Segmented Neutrophils - 80 %,
Lymphocytes - 9 %, Monocytes - 2 %. Т-lymphocytes – 0,95×10^9/l, Тh – 20%, Ts –
20 %, Тk – 60 %. B-lymphocytes– 0,02×10^9/l, Ig A – 0,125 mcmol/I, Ig М – 0,1 mcmol/I, Ig
G – 0,63 mcmol/l. 1. What indexes of immune system are different from norm? 2. What
is the type of immunodeficiency? 3. Explain its origin and pathogenesis?
11c. The girl 4 years old from the first life days is ill with pneumonia, gastroenteritis,
purulent angina, pyodermia. Blood test: erythrocytes – 3,0×10^12/l, Нb – 91 g/I,
leucocytes – 20,0×10^9/l. Granulocytes – 80 %, lymphocytes – 14 % (Т-lymphocytes –
0,88×10^9/I, B-lymphocytes – 0,05×10^9/l). Ig A – 0,003 mcmol/l, Ig G – 1,2 mcmol/l, Ig М
– 0,2 mcmol/l. Activity of complement system is normal. Reaction of lymphocytes with
phytohemaglutinin is positive. 1. What desease can be in patient? 2. Explain the causes
of raised child sensitivity to infections? 3. What disorders in immune system can promote
their development?
12c. The child 3 years old from first life days is frequently ill with bronchitis and
pneumonia. Diseases are accompanied standing out of vesicles on lips, and nose, carried
the measles, chicken-pox. The child falls behind in growth. Blood test: erythrocytes –
2,8×10^12/l, leucocytes – 4,9×10^9/l, granulocytes – 80 %, lymphocytes – 11 %,
monocytes – 7 %, Т-lymphocytes – 0,2×10^9/I. Т-lymphocytes ability to form sockets is
decreased. B-lymphocytes – 0,03×10^9/l). Ig A – 13,8 mcmol/l, Ig G – 81 mcmol/l, Ig М –
1,2mcmol/l. Uric acid in blood – 0,03 mmol/l, in urine – 0,5 mmol/l. 1. What desease can
be in patient? 2. Why did arise raised sensitivity to infection in the child? 3. Explain
pathogenesis of this disturbance.
13c. The child 3 months old was hospitalized in children's department due to pustule
defects of skin and lungs. Fungus Candida was found. Blood test: Leucocytes - 4×10^9/l,
Basophils - 1 %, Stab Neutrophils - 1 %, Segmented Neutrophils - 87 %,
Lymphocytes - 7 %, Monocytes - 4 %. Т-lymphocytes – 0,03×10^9/l, Blymphocytes–
0,24×10^9/l. Reaction with phytohemaglutinins is very weak. Ig A – 14 mcmol/I, Ig М –
2,0 mcmol/I, Ig G – 60 mcmol/l. Lymph nodules aren’t palpated. 1. What desease can be
in patient? 2. What disturbance of immune system is observed in the child? 3. Explain
pathogenesis of raised child’s organism sensitivity to infection?
14c. A patient 46 years, soloist of the theater, appealed to the doctor with complaints of
frequent occurrence of common cold, headache, swelling of the face, fever. The disease is
exacerbated after staying in the country. He was treated for acute respiratory illness.
Recently medications not only help, but also strengthened headache, runny nose. Doctor
suspected allergies. 1. What kind of allergie reaction can be? 2. Explain the mechanism of
these disorders? 3. What do you recommend to the patient?
15c. The 35 year old patient, trained nurse, complains on eczematous damage of hands
skin. She noticed that after injections of streptomycin to patients the itch becomes
stronger, the vesicles appear on hands skin. Liquid exudes from the vesicles. Symptoms
disappear at vocation. 1. What is the nature of nurse’s illness? 2. Explain the mechanism
of skin damage? 3. What recommendations will you give for prevention of this illness?
16c. In work time the metal worker suddenly felt pain in the left eye. Doctor found a
foreign body in external eye corner at examination. Conjunctiva is bright red. Conjunctiva
of right eye also has red color, but less brightly expressed. 1. What disorder of the blood
circulation does take place in given case? 2. Explain mechanism of vascular changes in
conjunctiva of left and right eyes? 3. What is the cause of red color of conjunctiva (explain
pathogenesis)?
17c. The man 42 occasional numbness, tingling and pain in the lower extremities, pale and
cooling them, weakening pulse in the arteries of the foot. 1. Why is this phenomenon? 2.
What factors can provoke them? 3. Write down possible consequences?
18c. The victim with a fractured of right shoulder got a gypsum bandage. The next day
there was swelling, cyanosis and cold of injured hand. 1. What kind of circulatory disorder
show these signs? 2. Explain the mechanism of swelling? 3. What caused cyanotic color?
19c. The patient had headache. Then temperature increased up to 37,6 ˚C. In the evening
the patient felt strong heat. Temperature increased up to 40,2 ˚C. The doctor diagnosed
influenza. 1. Explain reason of the fever, trace the stage of fever in stages? 2. Explain the
mechanism of temperature increase, how you can explain the chill? 3. Do you consider
that body temperature of the patients would be reduced?
20c. In the result of burn of a shoulder an inflammation developed with sharply expressed
pain. 1. Why did the pain appear? 2. Enumerate other possible displays of inflammatory
reaction? 3. What is their pathogenesis?
21c. A patient addressed to doctor with complains on the pain and noise in the left ear,
lowering of hearing. During the examination of the tympanic membrane the dense net of
dilated vessels is revealed. Upper part of tympanic membrane is dark red, the lower ones
is brighter. 1. What pathological process did develop in the ear? 2. Why different parts of
the tympanic membrane do have different color? 3. What is the mechanism of the found
vessel disturbances?
22c. From pleural cavity of the patient doctor got exudate of such composition: protein 58
g/l, leucocytes – 6200/mcl, prevail neutrophiles, much wholes and destroyed cells, рН 6,6.
1. What exudate did doctor get in the patient? Explain mechanism of exudate formation in
pleural cavity? 2. What is the origin of found cells? 3. What is the positive and negative
role of exudate in inflammation?
23c. The 54 years old woman was hospitalized in regional oncological clinic for
investigation. At examination doctor revealed the tumor of dense consistence, knobby,
painless, and soldered with surround tissue. Axillar lymphatic nodes were increased. On
the base of clinical and hystological researche cancer of mammaliar gland was diagnosed.
At operation gland, region lymphatic nodes, and ovaries were removed. Started
radiotherapy. 1. Why doctor did do conclusion, that this is malignant tumor? 2. Why in
the patient were increased axillar lymphatic nodes? What purpose their remove with? 3.
Why ovaries are removed in the patient? What is the expediency of application radiation
therapy?
24c. After chemical burns in the patient developed stenosis of esophagus that impede
swallowing. There came to the weight loss - weight decreased on 16 %. These studies of
blood test: red blood cells - 3,1x10^12 / L, white blood cells - 5,2x10^9 / l, hemoglobin -
113 g / L glucose concentration - 3.7 mmol / L, protein - 57 g / l. 1. What type of fasting in
patient? Possible effects hypoproteinemia? How to normalize the protein content in the
blood? 2. How do you explain the decrease of formed elements and hemoglobin in the
blood? 3. How to supported blood sugar in starving person? How will the resistance to
the action of infectious agents?
25c. Weight of the body is 65 kg, hematocrit - 0,52 l/l, sodium level in the blood is 138
mmol/l, potassium - 3,6 mmol/l. 1. What disorder of water-electrolyte balance has the
patient? 2. What reason can be in patient? 3. Calculate an amount of water and
electrolytes for the correction of their deficiency?
26c. The activation of two endocrine glands play the part in immediate mechanisms of
blood loss compensation. 1. Name these glands? 2. What hormones of these glands take
part in the compensation of blood loss? 3. What is a mechanism of action of these
hormones?
27c. The patient lost 20 % of blood after crash. 1. What is a quantity of hematocrit
parameter (normal, lower or the highest) in 10 minutes, in 3 hour, and in 1 month after
blood loss? 2. Ground your opinion? 3. Explain patogenesis of this?
28c. The patient lost 50 % of blood. 1. Is such blood loss dangerous to his life? 2. What
disorders arise after massive blood loss? 3. Explain patogenesis of this?
29c. Victim is delivered in receiving branch of hospital by the casual transport through 8
minutes after traffic incident. Complains on pain in stomach with irradiation into the
right shoulder. The skin is pale, is covered with cold sweat. Arterial pressure - 95/70 mm
Hg, pulse – 102 beats for 1 minute, breath - 28 for 1 minute. The blood was taken
immediately on analysis an amount of erythrocytes - 4,2x10^12/l, hemoglobin content -
126 g/l. 1. Analyse these data. What parameters deviate from norm? What it is possible
to think about in this case? 2. How does it explained painless of skin? What does it mean
this reaction? 3. How do you evaluate the increase of rate pulse and breath?
30c. In a patient with thyrotoxicosis following blood parameters are: number of
erythrocytes - 5,6x10^12/l, hemoglobin - 170 g/l, color index - 0.91. 1. What is the name
of these changes? 2. Explain pathogenesis of this? 3. What reason of this can be?
31c. Hemorrhagic syndrome arose in the patient after operation on pancreas. 1. What
mechanism of hemostasis does damage? 2. What is the pathogenesis of this syndrome?
3. What consequences can be at this patient?
32c. At inspection of the patient with atherosclerosis doctor determined increase of blood
coagulation property. 1. Explain the mechanism of this phenomenon? 2. What
consequences can be at this patient? 3. How to prevent it?
33c. The patient suffers from hereditary coagulophathy because deficit of the factor ХІІ
(Hageman). 1. What phase of blood coagulation does change in this case? 2. How does
fibrinolysis change in the patient? 3. What is the connection between the factor ХІІ
(Hageman) and fibrinolysis?
34c. In order to identify the type of hemophilia to three servings examined blood were
added 3 samples of plasma, without VIII, IX, XI coagulation factors. The normal clotting
time was observed in vitro, which was added testplasma with severe deficiency of factors
VIII and XI. 1. What type of hemophilia is in the patient? 2. A deficit of what clotting
factor is? 3. Describe pathogenesis of this disease?
35c. In a sick child 2 years with severe hemorrhagic syndrome found no antihemophilic
globulin (factor VIII) in blood plasma. 1. What disease suffering child? 2. At what stage
clotting primary hemostatic disorders arise in this case? 3. Which of the mechanisms of
formation prothrombin activity - internal or external - will be defective?
36c. Blood test result: Total amount of leucocytes 12,0x10^9/l, Basophiles 1%,
Eosinophiles 2%, Metamyelocytes 2%, Stabnucleonic Neutrophiles 15%, Segmental
Neutrophiles 56%, Lymphocytes 20%, Monocytes 4% 1. Analyze above mentioned
leukocytes formulas and indicate, what changes of total leukocytes and separate forms
are present in each of them? 2. What is the name of these changes? 3. What pathological
processes and disease are characterized for? Give examples?
37c. Blood test result: Total amount of leucocytes 13,0x10^9/l, Basophiles 1%,
Eosinophiles 14%, Stabnucleonic Neutrophiles 5%, Segmental Neutrophiles 52%,
Lymphocytes 24%, Monocytes 4% 1. Analyze above mentioned leukocytes formulas and
indicate, what changes of total leukocytes and separate forms are present in each of
them? 2. What pathological processes and disease are characterized for? 3. Give
examples?
38c. Blood test result: Total amount of leucocytes 96,0x10^9/l, Basophiles 1%,
Eosinophiles 2%, Stabnucleonic Neutrophiles 4%, Segmental Neutrophiles 9%,
Lymphoblasts 2%, Lymphocytes 78%, Monocytes 4% 1. Determine which of the above
parameters deviate from the norm? 2. How named this changes? 2. For what form of
leukemia characterized this leucogram?
39c. Blood test result: Total amount of leucocytes 186,0x10^9/l, Basophiles 1%,
Eosinophiles 1%, Metamyeloblasts 72%, Stabnucleonic Neutrophiles 4%, Segmental
Neutrophiles 3%, Lymphocytes 16%, Monocytes 3% 1. Determine which of the above
parameters deviate from the norm? 2. How named this changes? 3. For what form of
leukemia characterized this leucogram?
40c. Patient C., 24 years old, appealed to the clinic with complaints of headache, back
pain, facial swelling, general weakness. All previous years felt healthy. A month before
hospitalization suffered from tonsillitis. Observing data: the number of erythrocytes is
3,1x10^12 / L, white blood cell is 12,6x10^9 / L, erythrocyte sedimentation rate is 28 mm /
h. In urine: severe proteinuria, microhematuria, leukocyturia. In discussing of the studing
patient's results answer on the questions: 1. What form of hypertension patient suffers?
2. Give opinion. 3. Explain the cause and mechanism of hypertension in this case?
41c. In the history of the patient, who entered the observation, proved long and stable
increase in blood pressure. The patient analysis showed a reduction of renin in blood
plasma, increasing the volume of extracellular fluid, increased content of sodium and
potassium decrease in saliva. Treatment with diuretics (medication that eliminate sodium
and water from the human body) gave a positive result. In discussing of patient's results
answer on the questions: 1. Analyze clinical and biochemical data of patient? 2. What
mechanism of hypertension development they suggest - the strengthening of the
formation of angiotensin II or increased secretion of mineralocorticoids? 3. Describe the
mechanism?
42c. Three months ago patient R. had tonsillitis. Now patient began to disturb
breathlessness, heaviness in the right hypochondrium area, and fits of hard breathing.
There swelling of the lower extremities is present. These objective examination data: the
skin with shade icteric, cyanotic lips, legs swollen. Neck veins are pulsating. Borders of the
heart expanded to both ventricles, but more left one. Blood pressure is 90/60 mm Hg,
respiratory rate is 26 / min. Diagnosed myocarditis, cardiovascular failure in the stage of
compensation. 1. What is the cause of myocardial damage in a patient? 2. What
disorders indicate heart failure? 3. Explain their pathogenesis.
43c. In the person’ blood was identified 9.2 mmol / l of cholesterol, 1.50 mmol / l of
phospholipids, 63 g / L of LDL. References (performance standards in adults): Cholesterol
overall - 3,5-8,0 mmol / l, Phospholipids comon - 1,52-3,62 mmol / l, LDL - 3,0-4,5 g / l 1.
What does these data suggest? 2. What is the role of LDL in atherosclerosis? 3. What is
the role of phospholipids in cholesterol metabolism?
44c. Patient G., 50 years old, long time suffering from arterial hypertension, which caused
the development of heart failure. At the moment of examination claims that his condition
worsens. With the physical and emotional stress occur dyspnea, palpitations, disturbed
the pain in the right upper quadrant. An objective examination revealed acrocyanosis,
swelling of the lower extremities. 1. What pathophysiological variant of heart failure
developed in the patient? 2. What is the most likely cause of pain in the right upper
quadrant of the patient? 3. What is the mechanism of compensation work under these
conditions? Describe it.
45c. A patient with transmural myocardial infarction, sudden developed shortness of
breath, wheezing wet in lung, indicating the development of acute heart failure. 1. What
pathophysiological version of heart failure developed in the patient? 2. What is the
pathogenesis of heart failure in this case? 3. What consequences can be at this patient?
46c. The patient, who was on the operating table under anesthesia, appears sharp
respiratory depression. Pulse became rare and weak. Cyanosis appears. Emergency
measures taken anesthesiologist, eliminated these violations. 1. What can be associated
respiratory depression by? 2. How, in your opinion, has changed the patient oxygen
content and carbon dioxide content in arterial blood? 3. Explain the appearance of
cyanosis?
47c. In the man 22-nd years old on the background irregular nutrition, smoking, long
nervous overstrain appeared the pains in epigastric area. They arise fasting and
strengthen through 2-3 hours after eat period and night. At the altitude be of pain occurs
heartburn and vomiting acidic contents. Roentgenological it is exposure the plenty of
liquid in stomach fasting, accelerated of evacuating of stomach, spastic reductions of the
head duodenum is marked. The inspection it is difficult because of the expressed edema
mucous. 1. What parts of gastrointestinal сhannel take place of disorder functions in the
patient? 2. What role of irregular nutrition smoking and nervous overstrain in the
development of disease? 3. Why acute attack of pain for 2-3 hours after eat period and
night?
48c. Experimental animal was fixed on the fixing tool and left without nutrition for day.
After dissecting in stomach the ulcers are found. 1. How the experimental ulcers obtained
by such way are called? 2. What hormone promotes their formation? Where does it
derivate? 3. What mechanisms of it ulcerogenic acting?
49c. The patient complain on dermal itch , irritebleness, disorders of sleep, fast
weakening. The skin and mucous icteric colour. The pulse rate - 56/mines, arterial
pressure - 100/75 mm Hg. The feces is acholic. The urine is darkcolour. 1.What type of an
icterus? 2.What did it can be cause by? 3.Why patient has the irritability of skin?
50c. In the patient appeared on dermal itch , irritebleness, disorders of sleep, fast
weakening after fatty food intake. The skin and mucous acquired icteric colour. The pulse
rate decreased to 60/min, arterial pressure - 105/65 mm Hg. The feces got acholic. The
urine - darkcolour. 1.What type of icterus? 2.Likely cause of icterus? 3.Why in the
patient appearted the irritability of skin itch?
51c. In the patient with chronic glomerulonephritis the pains in muscles and joints, itch of
skin, ammoniacal odor from a mouth have appeared. The filtrate nitrogen of a blood was
increased from 82 to 216 mmol/l. The specific gravity of the urine within a week was
retained at a level 1,005-1,007. 1. Estimate dynamic of disease? 2. What substances
cause the increasing of filtrate nitrogen in a blood? 3. Explane the values of specific
gravity of the urine?
52c. The patient is hospitalized in a clinic in a comatose condition. Breathing is rarely and
deep, pupils are narrow. Skin is yellowish and dry, with many hemorrhagic rash. The body
temperature is 38,8º C. Sharp smell of urine from the mouth. AP is 145/105 mm Hg. The
contents of the urea and creatinine are increased. Erythrocytes amount in the blood - 2,0 x
10^12/l, hemoglobin content - 50 g/l, thrombocytes amount - 70 x10^9/l. 1. What
complication of kidney disorder is characterized by these changes? 2. Which proofs of this
state are in this patient? 3. Describe pathogenesis of this complication?
53c. pН – 7,25, pСО2 – 75 mm Hg, SВ – 27 mmole/l, ВВ – 49 mmole/l, ВЕ – (+ 2,0) mmole/l.
The patient has the operation with usage of artificial ventilation of the lungs. 1. What
type of violation of acid-base balance of the patient: acidosis or аlkalosis, metabolic or
respiratory, compensated or not compensated, pure or mixed? 2. What is the cause of the
disorder of acid-base balance in each case? 3. Describe pathogenesis of this violation?
54c. pН – 7,36, pСО2 – 36 mm Hg, SВ – 19,5 mmole/l, ВВ – 39 mmole/l, ВЕ – (-5) mmole/l,
keton bodies of blood – 1,3 mmole/l (norm – 0,1 mmole/l), titre acidity of urine – 37
mmole/day (norm – 20-40 mmole/day). 1. What type of violation of acid-base balance of
the patient: acidosis or аlkalosis, metabolic or respiratory, compensated or not
compensated, pure or mixed? 2. What is the cause of the disorder of acid-base balance in
each case? 3. Describe pathogenesis of this violation?
55c. pН – 7,28, pСО2 – 35 mm Hg, SВ – 16,5 mmole/l, ВВ – 35 mole/l, ВЕ – (-9) mmole/l,
titre acidity of urine – 8 mmole/day, ammonium of urine – 17 mmole/l (norm – 20-50
mmole/l). 1. What type of violation of acid-base balance of the patient: acidosis or
аlkalosis, metabolic or respiratory, compensated or not compensated, pure or mixed? 2.
What is the cause of the disorder of acid-base balance in each case? 3. Describe
pathogenesis of this violation?
56c. Bodies temperature of the patient with thyreotoxicosis is 37,9 dgr C. 1. Is it typical for
the patients with thyreotoxicosis? 2. Explain the mechanism of temperatures increase in
the patient? 3. Is this hypertermia the fever?
57c. Parathyroid gland are removed during the operation on thyroid gland. 1. What
pathological state will be the consequence of this operation? 2. How will the level of
calcium in blood be change in this case? 3. How will the muscle tone be change ? Why?
58c. The examined has the following results of glucose-tolerance test: level of sugar in
blood fasting is 7.0 mmol/l, in 1 hour after reception of glucose it equals to 8,8 mmol/l, in
2 hours after reception of glucose – 7.2 mmol/l. 1. What do these results testify about? 2.
Draw the curve of change of sugar level in blood of the healthy person within two hours
after sugar load? 3. What is the differense in test result in healthy person and this
patient?
59c. The experimental models of diabetes mellitus are received by the way of pancreas
removal, introduction of allocsan, somatotropic hormone, glucagon. 1. In what cases does
absolute insulin insufficiency is occured in what - relative? 2. Explain the mechanism of
insulin insufficiency in each case? 3. What other hormones we can use for modeling of
diabetes?
60c. Last year, five years old boy had polyomyelitis. Now he is not able to work. The
movements by his right leg are completely absent. Right crus and right thigh are atrophic.
Muscles tone of the right leg is reduced. Tendinous- periosteal reflexes are absent. 1.
What form of disturbance of motor activity is observed in the child? 2. Explain the reason
of appearance of muscles atrophic of the right leg? 3. Explain the reason of
disappearance of reflexes?
61c. In the patient, who was delivered to clinic with heavy trauma of backbone paraplegia
of lower extremities is observed. Muscle tone is increased. Tendinous reflexes are
strengthened. 1. What type of paralysis is present in patient? 2. Why does muscle tone is
saved ? 3. Explain mechanisms of strengthening of tondinous reflexes?
62c. The patient was brought to the clinic in coma. Breathing is noisy, deep. In exhaled air
the smell of acetone. The content of glucose in blood is 16,1 mmol/l. There is sugar in
urine. Urine reaction on acetone is sharply positive. 1. What types of coma is present in
this case? 2. What disease are such disorders characterized? 3. Evaluate the level of
glucose in blood?