Вы находитесь на странице: 1из 4

First colloquium in Pathological Physiology.

1.

Parts of pathological physiology are (3):

a)

The study of the mechanisms underlying disease

b)

Introduction to clinical medicine, is the bridge between the basic sciences and disease

c)

The course of pathological physiology includes general nosology, typical pathological processes and pathophysiology of organs and systems.

2.

Write 4 main stages of illness:

a)

Latent (incubation) period

b)

Prodromal

c)

Period of expressed manifestation

d)

Outcome of the disease.

3.

The results of illness may be (5):

a)

Total resolution

b)

Reconvalescence(healed)

c)

Transformation to chronic form or pathological state

d)

Recidivation (reactivation of the disease)

e)

Death

4.

The main kinds of the treatment of illness are:

a)

Etiologically (infections treated with antibiotics)

b)

Pathogenetic treatmentlo

c)

Symptomatically (the pain)

5.

For the thrombus is typical:

is a clot of blood elements due to endothelial damage in a living organism narrows blood vessels decreased blood supply

6.

Give the definition of emboli:

Is carrying by the blood of various bodies (emboli) to a site distant from the point to the origin(path.physio).

Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin (path. Anatomy).

7.

The white infarction develops in following organs (3):

a)

Heart

b)

Spleen

c)

Brain

8.

The consequences of ischemia may be:

a)

Infarction

b)

The white (anemic) infarction develops in myocardium, brain, spleen

c)

The red (hemorrhagic) infarction develops in lung, kidneys.

9.

The central limb of pathogenesis in case of respiratory hypoxia is:

Disorders of external respiration which can be obstructive, restrictive or regulatory. Changes of oxygen budges indices

10.

The typical deviation of the main constants of oxygenation status is case of circulatory hypoxia are:

a) HbO2A : - Normal

b) HbO2V: Decreased

c) AVD: (AVS?): Increased

d) O2A: Normal, or increased

11.

The rapid and effective compensatory mechanisms of hypoxia are(3):

a) Respiratory: hyperventilation and enlargement of lung surface

b) Tissue mechanisms: anaerobic glycolysis

c) Haemodynamic: increase of cardiac minute volume, Increase of blood vessel tone and

blood circulation, Centralisation of blood circulation, and Mobilization of blood from depot organs

12.

The venous hyperemia is: An increase of organ or tissue blood filling due to inadequate venous drainage.

13.

The ischemia means: Limiting of arterial blood inflow and local deficiency of the blood. Low metabolism, local hypothermia.

14.

The red thrombus consist from: white thrombus (thrombocytes and leukocytes) + erythrocytes and fibrin.

15.

The arterial hyperemia is: Increasing of an organ blood supply due to excessive blood inflow from the arterial vessels and increase of the number of functioning capillaries.

16.

The typical deviations of the main constants of oxygenation status of hystotoxic hypoxia are:

a) HbO2A: Normal

b) HbO2V: Increased

c) AVD: Decreased or 0

d) O2A: Normal

17.

The central limb of pathogenesis in case of hypoxic hypoxia is: Diminishment of partial pressure of oxygen in the inhaled air. In other words, is a result of insufficient oxygen available to the lungs. A blocked airway, drowning, or reduction in partial pressure (higher than 10.000 feets) are examples of how this can occur.

18.

The exogenous ethiological factors of inflammation are:

a)

Physical

b)

Chemical

c)

Mechanical

d)

Biological

19.

SIRS: Definition and main characteristics of pathogenesis: Systemic inflammatory response syndrome is an inflammatory state affecting the whole body, frequently a response of the immune system to infection, but not necessarily so. It is related to sepsis, a condition in which individuals both meet criteria for SIRS and have a known or highly suspected infection.

20.

The physio-chemical changes in the inflammation focus are (6):

a)

Acidosis

b)

Hyperionia

c)

Disionia

d)

Hyperosmia

e)

Hyperoncia

f) Hyperthermia

21. Exudation (definition): Exudation is the movement of fluid part of blood and proteins to inflammation tissue through the change blood vessel wall. Exudation is stimulated by:

increased permeability of blood vessels, decreased in capillary colloidal pressure, increase in focus of inflammation colloidalosmotic pressure, as fluid moves out of the blood vessels, stagnation of flow an clotting of blood occurs at the site of injury, disturbances of lympha retention.

22.

Write the correct values in the table!

 
 

Exudate

Transudate

pH

5,5-7,0

7,4-7,6

Density

1,015 1,027

1,010 1,015

Proteins

>3,0%

< 3%

The kinds of proteins

All possible albumins, globulins, complement, and other

Albumins

Fibrine

is present

Not present

The number of cells/death cells in 1mm3.

>3000/mm3

<3000/mm3

23.

The main kinds of exudation are:

a)

Serous exudates: are watery fluids low in protein content that result from plasma entering the inflammatory site.

b)

Hemorrhagic exudates: occur when there is severe tissue injury that causes damage to blood vessels or when there is significant leakage of red cells from the capillaries.

c)

Fibrinous exudates: contain large amount of fibrinogen and form a thick and sticky meshwork, much like the fibers of a blood clot.

d)

Membranous or pseudomembranous exudates: develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in a fibropurulent exudates.

e)

Purulent or suppurative exudates: contains pus, which is composed of degraded white blood cells, proteins and tissue debris.

24.

The main functions of IL-1 are:

- Form mononuclear phagocytes, fibroblasts, keratinocytes, T and B lymphocytes.

- Cause fever by activating synthesis of PGE in endothelium of hypothalamus blood vessels

- Simulate proliferation of T lymphocytes

 

- Cause excretion of histamine from mast cells in the focus of inflammation

25.

TNF-alpha: functions in case of acute inflammation.

 

a)

Form activated macrophages, monocytes, fibroblasts, mast cells, part of T lymphocytes and NK cells.

b)

Cause fever by directly inducing synthesis of PGE in endothelium of hypothalamus blood vessels, or indirectly by intensifying formation of IL-1.

c)

Stimulate collagenase, formation of PGE in synovial cells by causing damage of joints.

d)

Together with IL-1 activate formation of IL-6.

26.

Inflammation acute phase mediators are:

a)

IL-1

b)

IL-6

c)

TNF-alpha

27.

The main forms of elcosanoids are:

a)prostaglandins

b)prostacyclins

c)thromboxanes

d)leukotrienes

28.

Chronic inflammation is characterized by:

a)

Is self-perpetuating and may last for weeks, months, or even years

b)

It may develop as the result of a recurrent or progressive acute inflammatory process or from low-grade, smoldering response that fail to evoke an acute response.

c)

Infiltration by mononuclear cells and lymphocytes.

d)

Involves the proliferation of fibroblasts instead of exuates.

e)

The risk of scarring and deformity usually is considered greater than in acute inflammation.

29) determine the type of hypoxia:

1)

HbO2- arterial: 95,8%

2)

HbO2- venous: 94,8%

3)

AVD: 1%

4)

Hb: 15 g/dl

Hystohypoxia!

30) cytokines and chronic inflammation:

1)

chemotactix for monocytes for differentiation into macrophages (at site of inflammation)

2)

low level of TNF causes: loss of appetite and weight, tiredness and fever

3)

humoral type reaction (IL-3, IL-5, IL-6, IL-7, IL-9, IL-10, IL-13, TGF-beta)

4)

cellular type reaction (IL-1, IL-2, IL-3, IL-4, IL-7, IL-9, IL-10, IL-12, IFN´s)