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PATH 360 Lecture 5.2

Path 360 Lecture 5.2

by medicaltechtestprep, Sep. 2014

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	Pathology of immune system Diseases	Hypersensitivity diseases Immune deficiency diseases
	Pathology of immune system Diseases HYPERSENSITIVITY _________ IMMUNE DEFICIENCY ___________	diseases diseases
	Pathology of immune system Diseases ________________ diseases _______________ diseases	Hypersensitivity Immune deficiency
	Pathology of immune system Diseases	Hypersensitivity diseases Immune deficiency
	Hypersensitivity diseases What is it generally?	Overreaction to an antigen
	Hypersensitivty diseases Over_____ to an ________	reaction antigen
	Hypersensivity diseases _____reaction to an ________	over antigen
	Hypersensitivity ___________ to an ___________	Overreaction antigen
	Hypersensitivity What is it generally?	An overreaction to an antigen
	Hypersensitivity diseases Causes	Autoimmunity Response to microbes and environmental antigens
	Hypersensitivity diseases Causes Auto____________ Response to _____ and environmental _____	immunity microbes antigens
	Hypersensitivity Cuases ____ immunity ________ to ____ and _________ antigens	Auto response microbes environmental
	Hypersensitivity Causes ________________ _________ to_________ and _______	autoimmunity response to microbes and environmental antignes
	Hypersensitivity Causes	Autoimmunity Response to microbes and environmental antigens
	Hypersensitivty Categorization	Type I,II,III,IV
	Hypersensitivity Categorization Type __________	I,II,III,IV
	Type I hypersensitivity Mechanism	1. Activation of T lymphocyte by environmental antigens 2. IgE antibodies production 3. Mast cells is sensitized and release mediators 4. Allergic responses on: Blood vessels, SM and leukocytes
	__________ hypersensitivity ________________ 1. Activation of T LYMPHOCYTE by environmental ANTIGENS 2. IgE antibodies PRODUCTION 3. MAST cells is sensitized and release mediators 4. ALLERGIC responses on: Blood vessels, SM and leukocytes	Type I mechanism
	Type I hypersensitivity Mechanism 1. ACTIVATION of T ___________ by ENVIRONMENTAL _________ 2. Ig__ ANTIBODIES_____________ 3. ______ cells is SENSITIZED and release MEDIATORS 4. ___________responses on: Blood VESSELS, SM and LEUKOCYTES	lymphocyte antigens E production Mast Allergic
	Type I hypersensitivity Mechanism 1. __________ of _ lymphocyte by __________ antigens 2. Ig_ __________production 3. __________ cells is ___________ and release ______________ 4. _____________ responses on: Blood ____, ___ and leu________	activation T environmental E antibodies Mast sensitized mediators Allergic vessels SM leukocytes
	Type I hypersensitivity Mechanism 1. Activation of ___________ by environmental __________ 2._____ antibodies _____________ 3. ____________ is sensitized and __________ mediators 4. Allergic _________ on: _______ vessels, __ and ____________	T lymphocytes triggers IgE production Mast cells release response vessels SM Leukocytes
	Type I hypersensitivity Mechanism 1. ___________ of ___________by ______________ 2.___________________ 3. ___________ is _________ and ____________ 4. _______________ on: ______________ and ______	1. Activation of T lymphocyte by environmental antigens 2. IgE antibodies production 3. Mast cells is sensitized and release mediators 4. Allergic responses on: Blood vessels, SM and leukocytes
	Type I hypersensitivity Mechanism	1. Activation of T lymphocyte by environmental antigens 2. IgE antibodies production 3. Mast cells is sensitized and release mediators 4. Allergic responses on: Blood vessels, SM and leukocytes
	Type I hypersensitivity Clinical presentation	2 types - Location reactions - Systemic reactions
	Type I hypersensitivity Clinical presentation How many types there are?	2
	Type I hypersensitivity Clinical presentation 2 types Local _____ Systemic _______	reaction
	Type I hypersensitivity Clinical presentation 2 types ____________ reaction ____________ reaction	Local Systemic
	Type I hypersensitivity Clinical presentation 2 types	Local reaction Systemic reaction
	Type I hypersensitivity Clinical presentation: Local reactions Mechanism	Surface exposure to allergens
	Type I hypersensitivity Clinical presentation: ______ reactions Mechanism: surface exposure to allergens	local
	Type I hypersensitivity Clinical presentation: Local reactions Mechanism: ________ exposure to __________	surface allergens
	Type I hypersensitivity Clinical presentation: Local __________ Mechanism: surface __________ to allergens	reactiosn exposure
	Type I hypersensitivity Clinical presentation: Local reactions Mechanism: ______________ to _________	surface exposure allergens
	Type I hypersensitivity Clinical presentation: Local reactions Mechanism	surface exposure to allergens
	Type I hypersensitivity Clinical presentation Two types	Local Systemic reaction
	Type I hypersensitivity Clinical presentation: systemic reaction Disease	Anaphylaxis
	Type I hypersensitivity Clinical presentation: _________ reaction Disease: Anaphylaxis	systemic
	___________ hypersensitivity Clinical presentation: systemic _________ Disease: Anaphylaxis	Type I reaction
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: _____phylaxis	Ana
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Ana_____	phylaxis
	Type I hypersensitivity Clinical presentation: systemic reaction Disease:	Anaphylaxis
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Causes	Parenteral exposure to antigens Ex. Bee stings, drugs
	Type ___ hypersensitivity Clinical presentation: __________ reaction Disease: ___________ Causes: Parenteral exposure to antigens Ex. Bee stings, drugs	I Systemic anaphylaxis
	Type I hypersensitivity Clinical presentation: systemic __________ Disease: ____________ Causes: Parenteral EXPOSURE to antigens Ex. Bee stings, drugs	reactions anaphylaxis
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Causes: PARENTERAL____________ to ANTIGENS Ex. Bee STINGS, drugs	exposure
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Causes: _________ exposure to ___________ Ex. BEE _________, DRUGS	Parenteral antigens stings
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: ____________ Causes: ______________ to antigens Ex. ______ stings, _________	Anaphylaxis Parenteral exposure Bee drugs
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Causes: ___________ to __________ Ex. _____________________	parenteral exposure antigens Bee stings, drugs
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Causes and examples	Parenteral exposure to antigens Ex. Bee stings, drugs
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome	Without intervention: systemic vasodilation and subsequent shock can develop
	Type I hypersensitivity Clinical presentation: _________ reaction Disease: _____________ Possible _____________ Without intervention: systemic vasodilation and subsequent shock can develop	systemic anaphylaxis outcome
	___________ hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis _________________ Without intervention: systemic VASODILATION and subsequent SHOCK can develop	Type I Possible outcome
	Type I hypersensitivity Clinical presentation: systemic _______ Disease: Anaphylaxis Possible outcome Without intervention: _________ vaso_______ and subsequent _______ can develop	reaction systemic dilation shock
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome WITHOUT intervention: systemic ________ and subsequent _______ can DEVELOP	vasodilation shock
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome ____________ intervention: ___________ and subsequent _________ can __________	without systemic vasodilation shock develop
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome Without _________ : systemic ___________ and subsequent _________ can ___________	intervention vasodilation shock develop
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome ________________: ______________ and ________ can ______________	Without intervention Systemic vasodialation shock develop
	Type I hypersensitivity Clinical presentation: systemic reaction Disease: Anaphylaxis Possible outcome	Without intervention: systemic vasodilation and subsequent shock can develop
	Type I hypersensitivity Notes	Atopy
	Define Atopy	Familial predisposition to the allergy
	______ FAMILIAL predisposition to the ALLERGY	Atopy
	Atopy ___________ Predisposition to the ________	familial allergy
	Atopy Familial ___________ to the ____________.	deposition allergy
	Atopy _________ ____________ to the _________.	familial deposition allergy
	Atopy	Familial predisposition to the allergy.
	Type II hypersensitivity Cause	Self-targeting antibodies
	Type ___ hypersensitivity Cause: Self-TARGETING antibodies	II
	Type II hypersensitivity Cause: Self-____________antibodies	targeting
	Type II hypersensitivity Cause: _____-targeting __________	self antibodies
	Type II hypersensitivity Cause: _______________ antibodies	self-targeting
	Type II hypersensitivity Cause	Self-targeting antibodies
	Type II hypersensitivity Cause: self-targeting antibodies What do they target?	Normal molecules 1. on the cell membrane 2. in the cellular matrices 3. outside antigens observed by the cells
	Type ____ hypersensitivity Cause: ____-targeting _______ What do they target? Normal molecules 1. on the cell membrane 2. in the cellular matrices 3. outside antigens observed by the cells	II self antibodies
	Type II hypersensitivity Cause: self-_______antigens What do they target? NORMAL molecules 1. on the cell MEMBRANE 2. in the cellular MATRICES 3. outside antigens observed by the cells	targeting
	Type II hypersensitivity Cause: self-targeting antibodies What do they target? ____________ molecules 1. on the cell ______________ 2. in the cellular _____________ 3. outside antigens OBSERVED by the cells	Normal membrane matrices
	Type II hypersensitivity Cause: self-targeting __________ What do they target? Normal _________ 1. on the CELL _____________ 2. in the CELLULAR _______________ 3. OUTSIDE _______ ___________ by the CELLS	antibodies molecules antigens membrane matrices antigens observed
	Type II hypersensitivity Cause: self-targeting antibodies What do they target? _______________ 1. on the _______ membrane 2. in the __________ matrices 3. ___________ antigens observed by the ________	normal molecules cell cellular outside cell
	Type II hypersensitivity Cause: self-targeting __________ What do they target? __________________ 1. on the _______________ 2. in the _____________ 3. ______________ observed by the ______	antibodies normal molecules cell membrane cellular matrices outside antigens observed cell
	Type II hypersensitivity Cause: ________________ What do they target? _________________ 1. _____ cell membrane 2. __________ cellular matrices 3. outside antigens observed ______ cells	self targeting antibodies normal molecules on the in the by the
	Type II hypersensitivity Cause: self-targeting antibodies What do they target?	Normal molecules 1. on the cell membrane 2. in the cellular matrices 3. outside antigens observed by the cells
	Type II hypersensitivity Consequences	Marked cells are opsonized and phagocytosized or Normal functions are interfered
	Type ___ hypersensitivity ____________ MARKED cells are opsonized and phagocytosized or NORMAL functions are interfered	II consequences
	Type II hypersensitivity Consequences _____________ cells are OPSONIZED and PHAGOCYTOSIZED or ___________ functions are INTERFERED	Marked normal
	Type II hypersensitivity Consequences ___________ cells are op_______ and phag___________ or ____________ FUNCTIONS are ___________	Marked opsonized phagocytosized Normal interfered
	Type II hypersensitivity Consequences Marked _________ are opsonized and _________ or Normal _________ are interfered	cells phagocytized functions
	Type II hypersensitivity Consequences _____________ are __________ and _____________ or __________________ are _________	Marked cells opsonized phagocytized Normal functiosn interfered
	Type II hypersensitivity Consequences	Marked cells are opsonized and phagocytosized or Normal functions are interfered
	Type II hypersensitivity Name one disease	Graves disease
	Type II hypersensitivity Name one disease: Graves _______	disease
	Type II hypersensitivity Name one disease: ___________	Graves diseases
	Type ____ hypersensitivity Graves disease	II
	Graves disease	Antigen: TSH receptor Results: hyperthyroidism
	___________________ Antigen: TSH RECEPTOR Results: HyperTHYRODISM	Graves disease
	Graves disease Antigen: TSH ___________ Results: Hyper_________	receptor thyroidsm
	Graves disease _________: TSH _________ _______: Hyper____________	Antigen receptor Results thyroidsm
	Graves disease Antigen: _____ receptor Results: ____Thyrodism	TSH hyper
	Graves disease Antigen Results	Antigen: TSH receptor Results: hyperthyrodism
	Graves disease	Antigen: TSH receptors Results: hyperthyroidsm
	Notes Autoimmune hemolytic anemia	Antigen: RBC membrane proteins Results: hemolysis anemia
	Notes Pemphigus vulgaris	Antigen: Proteins in intracellular junctions of epidermis Results: skin vesicles
	Notes Goodpasture's syndrome	Antigen: proteins of basement membranes of alveoli and glomeruli Results: lung hemorrhage and nephritis
	Notes Acute rheumatic fever	Antigen: Strep. Cell wall antigen, cross reactivity with myocardial antigen Results: Myocarditiis; arthritis
	Notes Myasthenia Gravis	Antigen: Acetylcholine receptor Results: Muscle weakness and paralysis
	Notes Pernicious anemia	Antigen: intrinsic factor of gastric parietal cells Results: abnormal erythropoiesis; anemia

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