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Pathophysiology Exam Questions
Pathophysiology Exam Questions
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
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
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?
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
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.
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
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
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. Dolor/pain
2. Tumor/Swelling
3. Rubor/reddening: caused by vasoldilation
4. Calor/warmth
5. Loss of function
1. Vascular
2. Cellular
3. chemical
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
29. Alteration during inflammation. Physical and chemical changes in the inflammation?
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
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?
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:
Temperature measurements:
Advantages of fever:
42. Obesity?