49. Fever stages. Fever reactions types.

Stages:

1. Secondary pyrogen IL-1 synthesis and releasing increasing by primary pyrogens.

2. Interleukine-1 influence on thermoregulative center and the center activity reconstruction.

3. Fever clinical expressions (body temperature increasing).

Reactions types:

1. febris intermittens – temperature is coming to norm once or several types during 24 hours (purulent infection, abscesses, tuberculosis);

2. febris remittens – temperature fluctuations are more than 1°C during 24 hours, but it does not come to normal value (majority of viral and many bacterial infections);

3. febris continua – temperature daily fluctuations are less than 1°C (typhus abdominal and exanthematous);

4. febris recurrens (temperature increasing fits are alternated with the periods of its coming to norm (recurrent typhus, malaria).

On one hand, temperature changing dynamics is determined by causative agent life cycle features and peculiarities and, from another hand, by cyrcad(ic) rhythm (near 24 hours) of organism.

50. Fever comparative characteristics with exogenous overheating and hyperthermia other forms.

At fever one can see not disorder but reconstruction of thermoregulation. Organism supports high temperature by itself. If animal in fever state is performed cooling than his temperature will remain high it will not come down.

At hyperthermia or overheating thermoregulation is disturbed. Body temperature is increased although organism is striving for its decreasing. If such animal will be cool by somebody than his temperature will go down.

Hyperthermia other forms or fever-like states (because they are not connected with pyrogens):

1. Neurogenic:

   1. centrogenic – at brain different parts injury (haemorrhagic stroke, tumor, trauma, oedema);

   2. psychogenic – highest nervous activity dysfunctions (neurosis, psychical disorders); significant emotional-mental tension; sometimes – under hypnosis action;

   3. reflexogenic – at urolithiasis or nephrolithiasis (stones in urinary ways or kidney), stones in gallbladder, peritoneum irritation, urethra catheterization; pain syndrome can be present at this; tissues microinjuring can not be excluded leading to primary non-infectious pyrogens formation; usual mechanism of pyrogens action is actual together with reflectory one.

2. Endocrine – at some endocrinopathies; constantly – at hyperthyreoses.

3. Medical – parenteral or eneteral introducing some pharmacological medicines such as: caffeine, ephedrine, methylene blue, hyperosmolaric solutions and others.

50. Edemas. Classification. Oncotic and hydrostatic mechanism.

Edemas – liquid excessive accumulation in organism tissues and serosal cavities.

Types:

1. According to distribution:

   1. general – extracellular hyperhydration expression;

   2. local – are delt with liquid dysbalance in tissue or organ limited part.

2. By aethiology:

   1. cardiac;

   2. renal;

   3. hepatic;

   4. cahectic (at exhaustion);

   5. inflammatory;

   6. allergic;

   7. toxic and others.

3. By developmental mechanisms:

   1. hydrostatic – due to hydrostatic pressure increasing in capillaries – 3 subtypes (by aethiology):

• hypervolemic;

• stagnational;

• microcirculatory;

2. oncotic – due to oncotic pressure changings in capillaries or intersticial liquid:

• hypoproteinic;

• membranogenic;

• lymphogenic;

3. mixedematic or mucosal.

Hydrostatic oedemas main mechanisms:

1. blood volume increasing – hypervolemic;

2. venous pressure increasing – stagnational;

3. microcirculation primary disorders – arterioles dilation and venules spasm – microcirculatory.

Hypervolemic – are observed at extracellular hyperhydration or are delt with sodium ions retardation in organism (cardiac insufficiency, secondary hyperaldosteronism).

Stagnational –due to blood outflow disorder through venous vessels (chronic cardiac insufficiency, venous valves disorders, veins thrombosis).

Microcirculatory – histamine dilates arterioles in parallel to veins constriction.

Oncotic.

They are developed at hypoalbuminemia. Liquid comes from vascular bed to intersticial space.

1. Cahetic – at fasting.

2. Nephrotic- due to proteinuria.

3. Hepatic – due to albumines synthesis disorder in liver.

4. Membranogenic – due to vascular wall permeability increasing which leads to proteins transfer to intersticial space; results – tissular oncotic pressure is increased and water transfers to intersticium; this mechanism is dominant in allergic, inflammatory and toxic oedemas.

5. Lymphogenic – due to lymph production and lymph outflow disorders; removal of proteins with lymph (under norm these proteins are filtrating into the tissue) is disturbed and as a result tissular oncotic pressure is increased; reasons: lymphatic vessels pressure with scar tissue, central venous pressure increasing (cardiac insufficiency) preventing lymph inflow to the blood circulation system.

Mucosal oedemas

The basement of them is tissular colloids hydrophilia increasing. Binded water amount is increased in tissues at this. These oedemas are thyroid hypofunction distinguishing feature.