Pathophysiology Exam Questions

1. The disease: definition, stage. The etiology. Pathogenesis.

2. Terminal states: preahoniya, agony, clinical death, biological death. The most important methods of resuscitation.
3. Pathogenic effect of thermal factors, hyper- and hypothermia, frostbite and burns, cold. Using high and low
temperatures in medicine.
4. Types of ionizing radiation. The primary mechanism of action of ionizing radiation.
Mutagenic, carcinogenic and somatic effect of ionizing radiation.
5. The forms of acute radiation sickness. Stage bone-marrow form of acute radiation disease.
6. Pathogenic action of chemical factors. Exogenous and endogenous poisons. The addiction to toxins, alcoholism, drug
addiction, substance abuse.
7. Pathogenic effect of biological factors to species. Ways generalization of infection.
The interaction of micro- and macro- organisms.
8. Types of mutations. The most important mutagens.
9. Methods of diagnosis of hereditary diseases.
10. Type the transmission of hereditary diseases.
11. Chromosomal diseases: Down syndrome, Klainfelter, Turner, trisomy X.
12. The principles of prevention and treatment of hereditary diseases.
13. Individual reactivity. Its dependence on age, gender, heredity, environmental factors.
14. Age reactivity. Violation of the nervous, endocrine and immune system with aging.
15. Phagocytosis: definition, stages and mechanisms.
16. The system of mononuclear phagocytes.
17. Immunodeficiency disease. Classification, examples.
18. Immunosuppressive conditions. AIDS.

Q19. Allergies, Definition, causes and classification of allergic reactions by Coombs and Gel?

Allergy is a damaging immune response by the body to substances (Allergens) in the environment that are harmless to
most people

Allergens include:

 Domestic allergen: mainly domestic dust which include particles, bed cloth, furniture and bacteria
 Epidermal allergens: causes sensitization of epidermis e.g. scurf, wool, bird, fish, scales
 Officinal allergens: due to medicines and their metabolites usually haptens
 Pollen allergens: due to pollen
 Food allergens: due to foods such as milk, eggs, fish, peanuts
 Industrial allergens: mostly haptens e.g. resin, glue, latex
 Allergens of infectious origin: includes fungi and bacteria that cause chronic diseases such as tuberculosis

Classification of Allergic reaction

Type 1 Type 2 Type 3 Type 4

 Other names Immediate/ Cytotoxic Immune-complex Delayed/ T cell
Anaphylactic mediated
Antigen Free, foreign Fixed, Free endogenous
antigen endogenous (self) or free exogenous
antigen antigen
Antibody IgE fixed on mast IgG/ IgM – free in IgG/ IgM – free in NO Antibody,
cells in connective circulation circulation instead T Cells
tissues or and Antigen
basophils in presenting cells
circulation
Immune response Antigen bound IgE IgM or IgG binds The antigen and Macrophages
activates the to host cell antibody react presents antigens.
release of surface activating together and Activating T cells
histamines and complement and circulate in the and producing
other mediators producing MAC blood the lymphokine
from mast cells mediated cell antibody-antigen mediated tissue
and basophils destruction complex eventually destrution
gets deposited in
various tissues
causing damage
Examples Anaphylaxis, Hemolytic Serum sickness, Leprosy,
Atopic allergy, anemia, Glomerulonephritis Tuberculosis, PPD
food allergy Erythroblastosis tuberculin test
pollen

Q20. Stages of allergic Reaction?

Entering into an organism the antigen/allergen causes sensitization which is an immunological rising of an organism’s
sensitiveness to the antigen/allergen which can be exogenous or endogenous. There are 3 stages of allergic reactions:

1. Immunological stage: all the changes In the immune system during the oenetration of an allergen into the
organism, formation of antibodies or sensitized lymphocytes and their binding with the repeatedly entering
antigen
2. Pathochemical Stage: formation of biological active substances. The stimulus to their formation is the binding of
an allergen to antibodies or sensitized lymphocytes at the end of immunological stage
3. Pathophysiology stage: the pathogenic action of formed mediators on cells, organs and tissues of organisms
with clinical display

Q21. Autoallergy, Mechanism of formation?

Autoallergy is due to altered reactivity in which antibodies are produced against an individual’s own tissues causing a
destructive rather that a protective effect. It’s an obsolete term

Autoimmune disease is a condition arising from an abnormal response to a normal body part e.g. diabetes 1, Graves
disease and multiple sclerosis

Autoimmune disease occurs when our immune system loses its natural immunological tolerance to healthy self-cells.
Possible causes of autoimmune disease are:

 Genetic mutations: on DNA coding for MHC – hence self-antigen can’t be displayed on MHC of healthy cells due
to a defect
  Infections: if the displayed pathogenic antigen on an MHC of an infected cell is similar to a displayed self-antigen
of a healthy cell. The produced antibodies might bind to both of them marking them for destruction by white
blood cells e.g. rheumatic heart disease
 Damage to immunological privileged sites: the privileged contain no blood vessels or lymph vessels hence they
are out of reach for white blood cells e.g. cornea and brain. Physical damage to these privileged places can
release self-antigens that have not yet been encountered by our immune system leading to an immune
response that can destroy those areas

Q22. Basic principle in prevention and treatment of allergic reactions in medical practice during anesthetic
procedure?

Use epinephrine shot as it causes:

 Vasoconstriction – hence it reduces swelling and increases blood pressure

 Relaxes muscles around the airways in the lungs helping the airways to open up
 Increases heart contraction and heart rate which can help to prevent cardiovascular collapse
 Prevent the release of additional allergic chemicals which aids in stopping further progression of the reaction

Q23. Arterial and venous congestion (hyperemia)?

Hemodynamic disorders that have to do with blood flow into and out of the blood vessel

Hyperemia: increase blood flow to an organ, it’s an active process that occurs due to a physiological response e.g.
exercising or a pathophysiological response e.g. inflammation

Congestion: results from decreased outflow due to obstruction, congestive heart failure (i.e. the ventricle is not
pumping properly hence backup of blood in atria and vena cava) or thrombosis (i.e. intra-vascular mass). Congestion
leads to cyanosis (i.e. blue blood) and hypoxia. It’s a passive process.

Congestion will lead to blood backing up which causes pressure to rise and which may force fluid out of the vessels
resulting in Edema

Prolonged hypoxia will lead to necrosis i.e. infarction

Q24. Ischemia/ Stasis?

Ischemia is the reduction of blood flow to an organ or tissue and since blood carries oxygen there is also a reduction of
oxygen supply to the tissue/organ which leads to hypoxia.

Ischemia could be due to:

1. Something blocking the flow of blood from the inside the blood vessel e.g. thrombus (blood clot made from
platelets and fibrin)
2. Due to blood vessels being compressed from the outside e.g. inflammation and swelling that physically applies
external pressure to the blood vessel, it compresses the blood vessel and restrict blood flow

Stasis: stagnation of blood flow, it can be caused by:

1. Hyper viscosity syndromes: polycythemia increases resistance to flow and can cause small vessel stasis and
deformed red cells in sickle cell anemia causes vascular occlusion
2. Ulcerated atherosclerotic: Exposed sub endothelial ECM and cause turbulence
3. Abnormal Aortic and arterial dilations: can lead to aneurasim
4. Mitral valve stenosis (e.g. after rheumatic heart disease): results in left arterial dilation
5.
Q25. Thrombosis?

Thrombosis: A process of forming a solid mass in circulation from constituents of flowing blood, the mass itself is called
a thrombi. The harmful effect of thrombi include ischemic injury and thromboembolism

Blood clot: blood coagulate in vitro

Hematoma: extravascular accumulated blood clot e.g. in tissues

Virchow’s triad: the 3 events which predispose thrombus formation

1. Endothelial Injury: results in exposure of sub endothelial

collagen and release of coagulation hemostasis mediators
as well as endothelial cells themselves releasing mediators
of hemostasis. Endothelial injury can be caused by viruses
such as herpes, septicemia, nematodes and focal tissue
injury such as trauma
2. Hypercoagulability: this is disruption of primary and
secondary hemostasis as well as fibrinolysis. This can be
due to inflammation, cancer, endocrine disease such as
Cushing’s disease and decrease in antithrombin
3. Altered blood flow/stasis: this can be due to stasis (blood
flow decreased hence more contact time with endothelium hence the platelets are more likely activated) and
aneurysm (dilation within blood vessels resulting in turbulent blood flow after aneurysm) and cardiac diseases

Q26. Embolism?

Embolism is the process of partial or complete obstruction of some part of the cardiovascular system by any mass
carried in the circulation.

Emboli is the transported intravascular mass detached from its site of origin

Classification of Emboli:

1. Depending upon material of emboli

a. Solid – detached thrombi (thromboembolism), tumor cell clumps, bacteria clumps
b. Liquid – Fat, bone marrow
c. Gaseous – air
2. Depending upon whether infected or not
a. Bland – when sterile
b. Septic – when infected
3. Depending upon source of emboli
a. Cardia emboli
b. Arterial emboli
c. Venous emboli
d. Lymphatic emboli
4. Depending upon the flow of blood
a. Paradoxical embolus – carried from venous side to arterial side or vice versa
b. Retrograde embolus – Embolus travels against flow of blood

27. Inflammation: definition, main components of the inflammatory response, local

Signs?
Definition: Inflammation is a defense reaction of the organism and its tissues to injurious stimuli with the aim to repair
the damage or at least limit it.

Signs of acute inflammation:

1. Dolor/pain
2. Tumor/Swelling
3. Rubor/reddening: caused by vasoldilation
4. Calor/warmth
5. Loss of function

Causes of local inflammation:

1. Microorganisms: bacteria, fungi, virus and parasite

2. Foreign body: foreign protein e.g. pollen
3. Tissue destruction: with formation of tissue debris e.g. cuts, chemical compounds and physical influences such
as colds

Main components of inflammation:

1. Vascular
2. Cellular
3. chemical

28. Mediators of inflammation?

Mediators are substances that initiate and regulate inflammatory reactions. They are cell derived or plasma protein
derived and they include:

 vasoactive amines
 Lipid products
 Cytokines
 Products of complement activation
 Cell derived mediator Sources Action
Histamine Mast cells, Basophils, Vasodilation, increased vascular permeability, endothelial
platelets activation
Serotonin Platelets Vasoconstriction
Prostaglandins Mast cells, Vasodilation, pain, fever
leukocytes
Leukotrienes Mast cells, Increased vascular permeability, chemotaxis, leukocytes,
leukocytes adhesion and activation
Platelet activating factor Leukocytes, mast Vasodilation, increased vascular permeability, leukocyte
cells adhesion, chemotaxis, degranulation, oxidative burst
Reactive Oxygen Species Leukocytes Killing of microbes, tissue damage
Nitric oxide Endothelium, Vascular smooth muscle relaxation, killing of microbes
macrophages
Cytokines (TNF, IL-1, IL-6) Macrophages, Local: endothelial activation (Expression of adhesion molecules)
endothelial cells, Systemic: Metabolic abnormalities, hypotension (shock)
mast cells
Chemokines Leukocytes, activated Chemotaxis, leukocyte activation
macrophages

Plasma protein derived Sources Action

Complement Plasma produced in liver Leukocyte chemotaxis and activation, direct target killing
MAC, vasodilation (mast cell stimulation)
Kinins Plasma produced in liver Increased vascular permeability, smooth muscle contraction,
vasodilation, pain
Proteases activated during Plasma produced in liver Endothelial activation, leukocyte recruitment
coagulation

29. Alteration during inflammation. Physical and chemical changes in the inflammation?

30. Violation of local circulation during inflammation. Conhaym’s experiment?

31. Exudation during inflammation. Types of exudates?

Types of exudates

Serous exudate Usually seen in mild inflammation, with relatively low protein. Its consistency resembles that
of serum, and can usually be seen in certain disease states like tuberculosis.
Cattarhal exudate Seen in the nose and throat and is characterized by a high content of mucus.
Hemorrhagic Exudate Damage to blood vessels occur, RBC’s present in exudate
Fibrinous exudate Composed mainly of fibrinogen and fibrin. It is characteristic of rheumatic carditis, but is
seen in all severe injuries such as strep throat and bacterial pneumonia. Fibrinous
inflammation is often difficult to resolve due to blood vessels growing into the exudate and
 filling space that was occupied by fibrin. Often, large amounts of antibiotics are necessary for
resolution
Purulent or Consists of plasma with both active and dead neutrophils, fibrinogen, and necrotic
suppurative exudate
parenchymal cells. This kind of exudate is consistent with more severe infections, and is
commonly referred to as pus
Malignant (or Is effusion where cancer cells are present
cancerous) pleural
effusion

Exudate vs transudate

Exudate Transudate
Cause Inflammation increased vascular ↑ Hydrostatic pressure and ↓
permeability Colloid osmotic pressure
Specific gravity 1.02 1.012
Content Rich in protein especially fibrinogen Low in protein
hence it coagulates No inflammatory cells
Contains inflammatory cells
Occurs in Late inflammation Early inflammation

Types of exudates Content Disorders

Serous Promotes washing of microorganisms and their toxins Serous exudate in brain can squeeze
from the damaged surface brain and create brain disorders
Serous infiltration of lung alveolar
septs can cause the development of
acute respiratory insufficiency
syndrome
Fibrinous Fibrinogen which forms clots of fibrin in tissues Occurs when organism is affected by
Corynebacterium diphtheria,
pneumococcus, streptococcus,
mycobacterium tuberculosis
Purulent Viable leukocytes Causes are streptococcus,
Purulent bodies (perishing leukocytes) staphylococcus, gonococcus,
Proteins especially globulin meningococcus and frenkels
diplococcus
Hemorrhagic Erythrocyte in exudate Siberian ulcer, natural small pox,
influenza
combination More than 1 type of exudate

32. Emigration during inflammation. Stage emigration. Sequence output leukocytes. Their role in the inflammation?

Cellular changes in response to an acute inflammatory response: Under inflammation a blood vessel will dilate mainly
because of histamine binding with endothelial cells hence increasing vessel permeability

1. Margination: leukocytes accumulating near but do not touch the blood vessel wall
2. Leukocyte rolling: is associated with selectins hence selectin molecules stimulate white blood cells to roll along
the vessel wall
3. Firm adhesion: is associated with interactions with integrans. Leukocytes are firmly stuck to blood vessel wall
4. Diapedesis: leukocytes are squeezing through endothelial cells of blood vessel wall into the surrounding tissue
 5. Chemotaxis: it occurs after leukocyte leaves the blood circulation and it travels through the surrounding tissue
via a chemical gradient

Q33 & Q34. Fever, definition, types of fever by origin, role of pyrogens? And stages?

Pyrogen: substance that causes fever, this can be

endogenous e.g. cytokines or exogenous e.g. LPS
of gram negative bacteria

Fever: is an increase in body temperature due to

an increase in the hypothalamic set-point

Stages of pathogenesis of fever:

1. Stage 1: Production of cytokines and their

release: when macrophages interact with a
pyrogen they release:
a. Pyretic cytokines which cause
fever: Interleukin-1, 6, 8,
Macrophage inflammatory
response 1 beta, interferon-
gamma
b. Antipyretic cytokines which limit
occurrence of fever: interleukin-10, Arginine vasopressin, alpha- melanocyte stimulating hormone,
glucocorticoids, Tumor necrosis factor alpha

2. Stage 2: cytokines involved in the thermoregulatory center i.e. hypothalamus

a. acts on organum vasculosum of lamina terminalis
b. activate pre optic region and alter set point by activating phospholipases – inducing the production of
prostaglandin E
c. alter set point by increasing cAMP
3. Stage 3: initiation of effector mechanism and temperature rise:
a. once set point is elevated
b. thermoregulatory mechanisms activated to increase or lose heat e.g. vasocontriction, shivering,
increased metabolism, piloerection

Types of fever:

1. Continuous fever: temperature remains normal throughout the day and does not fluctuate more than 10C e.g.
typhoid
2. Intermittent fever: Temperature elevation is present only for a period later cycling back to normal
3. Quotidian fever: with periodicity pf 24 hours e.g. plasmodium falciparum
4. Tertian fever: 48 hour periodicity e.g. plasmodium vivax
5. Quartan fever: 72 hours periodicity e.g. plasmodium malaria
6. Remittent fever: temperature remain elevated throughout te day and fluctuate more than 1oC in 24 hour e.g.
infective endocarditis
7. Neutropenic fever AKA febrile neutropenia: fever with absence of normal immune system function, typical for
people receiving immune suppressing chemotherapy
Type of fever based on temperature:

 Subfebrile Fever: >38oC

 Relative fever: 38-39oC
 High Fever: 39-41oC
 Hyperpyretic Fever: <41oC

Temperature measurements:

 Rectal temperature: is at or over 37.5-38.3oC

 Oral temperature: is at or over 37.7oC
 Axillary or tympanic temperature: is at or over 37.2oC

Advantages of fever:

 Increased mobility of leukocytes

 Enhanced leukocyte phagocytosis
 Endotoxin effects decreased
 Increased proliferation of T cells
 Hindering of pathogens with certain temperature preferences

35. Tumours: definition, types of anaplasia?

Neoplasm is abnormal growth of tissues in which it forms a mass commonly referred to as a tumor.
Anaplasia is structural differentiation loss within a cell or group of cells. Anaplasia refers to a lack of differentiation in
neoplastic cells. Well-differentiated tumors resemble their tissue of origin, whereas poorly-differentiated or
undifferentiated (anaplastic) tumor cells appear primitive and lack specialization along any particular cell line. In general,
benign tumors tend to be well-differentiated. Malignant tumors run the gamut from well-differentiated to
undifferentiated.

-plasia and -trophy

Anaplasia Structural differentiation loss within a Metaplasia Conversion in cell type
cell or group of cells.
Aplasia Organ or part of organ is missing Prosoplasia Development of new cell function
Hypoplasia Congenital below average number of Desmoplasia Connective tissue growth
cells
Hyperplasia Proliferation of cells Atrophy Decreased number/volume of cells
Neoplasia Abnormal proliferation Hyper/Hypo Increased/ decreased volume of
trophy cells
Dysplasia Change in cell or tissue phenotype Abiotrophy Loss in vitality of organ or tissue
 Dystrophy Degenerative disorder from improper
nutrition

Abiotrophy (loss in vitality of organ or tissue)

Dystrophy (any degenerative disorder resulting from improper or faulty nutrition)

36. Morphological anaplasia of tumor tissue?

Anaplastic cells have certain characteristics (the list below is adapted from Robbins).
1. Pleomorphism (variation in size and shape).
2. Abnormal nuclear morphology, such as hyperchromatism (very dark nuclei), irregular nuclear contours, an
increased nuclear:cytoplasmic ratio, coarse chromatin, and nucleoli.
3. Mitoses (tons of them – or, more importantly, abnormal ones, like the ones at the tips of the arrows above).
4. Loss of polarity (disrupted orientation of cells; loss of architecture and organization)
5. Other things: tumor giant cells, ischemic necrosis (from tumor cells outgrowing their blood supply

37. Biochemical anaplasia of tumor cells?

38. Carcinogens, their classification. Examples?

A carcinogen is any substance that promotes carcinogenesis, the formation of cancer. This may be due to the ability to
damage the genome or to the disruption of cellular metabolic processes.
Classification of carcinogens:
1. Chemical Carcinogens:
a. Polycyclic aromatic hydrocarbons: has 3 or more benzene rings
b. Aromatic amine and amides: azo dyes such as benzidine
c. Nitrosamines and nitrosomides:
2. Radiation Carcinogens:
3. Viral Carcinogens:

39. Stages of carcinogenesis, transformation, promotion, progression?

40. Methods of experimental study of tumors: induction, transplantation, explanation. Tumor strains?
41. Signs of benign and malignant tumors?
Characteristics of Malignant and non-malignant tumors

Benign Tumor Malignant tumor

Diploid
Organized
Functional differentiation usually
Low mitotic count, normal mitosis
Structural differentiation retained
Retention of specialization
Nuclear variation in size and shape minimal
Range of ploidy
Non organized
Functional differentiation lost
Low to high mitotic count, abnormal mitosis
Structural differentiation shows wide range of changes
Loss of specialization
Nuclear variation in size and shape often variable

42. Obesity?