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Path. > Week 9 Part 1 > Flashcards

Week 9 Part 1 Flashcards

1
Q

type 1 (anaphylactic type, allergy)

A

hypersensitivity reaction there is release ofvasoactive amines and other mediators derived from the mast cells or basophiles and affecting vascular permeability and smooth muscles in various organs***

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2
Q

(allergen)

A

-one of the most known allergens is pollen.
-pollen into body (allergen) CD4 and T cells of the TH2 type secretion of cytokines IL4 and IL5 from lymphocytes (functional cells of the immune system- CD4 etc) IgE
production, recruitment of eosinophil which contain antihistamines in their granules.
(eosinophilia)
-second encounter with the same allergen, there is already IgE on the cell surfaces. The
antibodies and antigens bind to form a complex which results in degranulation of mast
cells, rupture of vessels and release of vasoactive amines (histamine) causes type 1 HSR (caused by histamine)

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3
Q

REVIEW of allergenic mechanism

A

-the first exposure to the antigen (allergen is extrinsic) there is comparing of the specificimmune response
-leads to production of igE which are located on the surface of mast cells
-second encounter degranulation of mast cells: opening of granules and release of
vasoactive amines (HISTAMINE)
-histamine leads to type one HSR

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4
Q

TWO TYPES OF TYPE 1 HSR:

A
  1. Systemic anaphylaxis

2. local reactions

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5
Q

Types of hypersensitivity reactions (HSR)

A 
type 1 (anaphylactic type, allergy)
type 2 (antibody dependent type) 
type 3 (immune complex mediated type) 
type 4 (cell mediated type) HSR
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6
Q

Systemic

anaphylaxis

A

-develops when there is parenteral administration- drug gets into the blood through the veins.
 Can be intravenous
 Not though the mouth or respiratory tract
-can spread through the blood.

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7
Q

MANIFESTATIONS of Systemic

anaphylaxis

A
  • itching
  • hives
  • bronchospasms.
  • laryngeal edema
  • abdominal cramps, diarrhea, vomiting.
  • vascular shock (anaphylactic shock)*
  • patients are allergic to Novocain (aesthesia) so if a person has allergies to this they can not get it.
  • parenteral administration of drugs can lead to bad outcomes.
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8
Q

-hives

A

(URTICARIA- rash that develops after nettle contact)
Occurs after a “bite” (rubs on you) from a nettle, which causes a
rash.
Nettle is an (1) important source of vitamins and microelements(soup) (2) women use nettle to wash the hair= strengthens hair follicles.
Hives with a little bit of projection above the skin

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9
Q

-bronchospasms.

A 
Histamine= increased permeability and vasodilation also (1) 
bronchospasm and(2)  increased mucous production.  
  (1) Narrowing of bronchi 
  (2) mucous into bronchial tree which results in DYSPNEA. Similar to bronchiole asthma but it is not. This is temporary
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10
Q

-laryngeal edema *

A

most dangerous)
 serous problem
 dramatic swelling of mucosa of pharynx and larynx.
 When you inhale, air goes through trachea to the vocal cords
(larynx) which undergoes swelling and can lead to strangulationbecause of full obstruction of trachea.
 Inability to breathe
 Occurs almost immediately
 There is swelling dyspnea patient turns blue patient dies
due to strangulation.
 What to do: find a knife, sterilize it with a flame, puncture above the sternal notch above the trachea.

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11
Q

-abdominal cramps, diarrhea, vomiting.

A

These areas are sensntivie to allergens

This isn’t a big problem but after allergies people need to go to thebathroom

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12
Q

-vascular shock (anaphylactic shock)*

A

Sudden vasodilation everywhere through the body, of all BVs due
to HISTAMINE
If there is vasodilation in the abdomen, the blood falls down from
the brain due to gravity and the patient will lose consciousness and may even die.

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13
Q

local

reactions

A
  • occurs where there is application of an allergen

- this does not spread depending on the area of application

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14
Q

MANIFESTATIONS of local reactions

A
  • urticaria
  • hay fever
  • atopic bronchial asthma
  • diarrhea
  • contact allergic dermatitis
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15
Q

-hay fever

A

This is if it was contacted with the eyes/nose (allergic rhinitis and allergic congunctivitis)
No hay and no fever.
This active substance is histamine increased permeability of
BVs red eyes.

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16
Q

-atopic bronchial asthma

A

Known as bronchial asthma
 In the majority of cases it has this mechanism of development- a
local reaction of type 1 HSR (allergy)
 There is another type of bronchial asthma (intrinsic)- not
associated with allergy but has the same manifestations.
 Bronchial asthma= 1. bronchial spasm, 2. increased production of mucous partial of complete obstruction of bronchial tree
problems with breathing/ death.

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17
Q

-diarrhea

A

If you eat a food that you are allergic to, it goes into the GI tractdiarrhea

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18
Q

-contact allergic dermatitis

A 
Not utricaria (not hives) 
Can develop in some cases.  
Ex. When the person is allergic to ink after they got a tattoo.
19
Q

ATOPY

A

Familial predisposition to local reaction in allergen

If someone in your family (blood family) has allergies, you areprone to develop the allergies as well.

20
Q

ATOPIC-

A

an adjective. Means characterized by type 1 HSR. This isits mechanism of disease.

21
Q

-type 2 (antibody dependent type)

A

HSR is mediated by antibodies (AB) directedagainst target antigens (AG) on the surface of cells or other tissue components.

22
Q

-there are three subtypes of type 2

A

complement dependent reaction
antibody dependant cytoxicity
antibody mediated cellular dysfunction

23
Q

complement dependent

reaction

A

-classic example of immune reactions with activation of complements.
-Complement activation is a biochemical cascade characterized by
activation of components of C1Q.
-C3 is the most important
-leads to activation of component 9.
-this is an important factor for immune reactions (without complements,the immune reaction is not complete)

24
Q

-leads to activation of complements through two directions

A

(1) classic activation of complement

(2) alternative pathway

25
Q

(1) classic activation of complement

A

-results in activation of all complements membrane attack complex-results in mechanical and biochemical destruction of the target cell
(RBC)= direct lysis (classic pathway)

26
Q

(2) alternative pathway

A

-the same situation: formation of AG AB complex
-leads to activation of alternative pathway with activation of C3B which
is an important attractor of phagocytic cells- they move towards the areaof target tissue with AB and complement and digest them.
-this is called opsonization (alternative pathway)

27
Q

-example of glomeruli: (complement dependant reactions)

A

They often under go autoimmune pathologies
 The AGs on the basal membrane confer the wrong auto immuneresponse auto Abs against self cells.
 AB attach by AB fragments to AG activation of complement attraction of phagocytic cells release enzymes  digestion of tissue development of disease.

28
Q

-activation of complement by formed

A

AG-AB complex

29
Q

EXAMPLES of complement dependent reactions:

A
  • hemotransfusion reactions(blood transfusion)
  • erythroblastosis fetalis
  • autoimmune hemolytic anemia
  • certain drug reactions
30
Q

-hemotransfusion reactions (blood transfusion)

A

There are four blood groups, which have different AGs
If you need to donate blood to someone you need to make surethey have the same AGs so you don’t create a reaction
(complement dependent)
All the RBCs will be destroyed

31
Q

-erythroblastosis fetalis

A

Understand that there are 4 groups of blood, but later is was
found there is an addition AG on RBCs in some people
It was found primarily in monkeys= RH(+) in 85% of people in this world.
Rh (-) in 15%. These people do not have the AG on the RBCs.
This is important during pregnancy. Assume that the father is +
and mother is -. The fetus will be + within the – mother. The
blood of the mother communicated with fetus through the
placenta. The blood cells of the fetus can not go to the mother

32
Q

-autoimmune hemolytic anemia

A

Characterized by the wrong reaction of the immune system against the RBC when there is production of Abs against theRBCs.
Results in destruction of RBCs
There are many of these anemias.

33
Q

-certain drug reactions

A

When we take medications, we never know how they react since the immune system of everyone is different.
Production of Abs against the combination of drugs
It occurs very often.
He saw a case with neutropenia (decreased neutrophils in
circulation) because the medication in conjunction with proteinsantineutrophils
No neutrophils infection

34
Q

HAPTONS-

A

together with proteins they work with auto antigens
 example= pemphigus vulgaris
Pemphix greek word= blister, bubble

35
Q

desmosomal proteins-

A

keep proteins together (located between epidermis and dermis)

36
Q

antibody

Dependent cell mediated cytoxicity

A

-there is not activation of complement
-no phagocytosis
-it has its own mechanism of formation: in the circulation there are blood cells which have Receptors for FC portion of Ab. When thre is
binding of Ab to AG the FC protion is still open to surrounding
-if the body contains cells with receptors to the FC portion, the
immunoglobulin can bind lysis of target cell without phagocytosis

37
Q

CELLS THAT CAN DO 2

A
  • non T/ non B lymphocytes known as natural killer cells (NKC)-monocytes/ macrophages
  • neutrophils
  • eosinophils
  • only against IgG and iGE
  • usually only IgG (the FC receptor will be for IgG only)
38
Q

THIS HAPPENS WITH:

A
  • parasites
  • virus infected cells
  • tumor cells
  • it is important because it clears our bodies from all these cells
  • it only happens when the body forms ABS against these cells.
  • it takes 10-14** days until the AB is produced and then after the cells can be killed with this mechanism so this occurs later in the process of disease of later in the development of cancer.
39
Q

antibody mediated
cellular
dysfunction

A

-this is not associated with complements of phagocytosis.

40
Q

-myasthenia gravis

A

-an autoimmune disease that affects the musculature.
-normally: there is spread of the conduction from nerves to the muscle atthe motor end plate. There is ACH that is released from vesicles into the
presynaptic space. The ACH has special receptors on the muscle.when
ACH binds to receptors on muscle contraction
-in this case: Abs are made for the receptors of ACH (so the Ach
receptors are occupied)
-anti ACH receptor auto antibody is the name of the AB that is produced. -these antibodies are everywhere and they have a tendency to be
attached to the ACH receptors.

41
Q

other examples that work through the same mechanism:

A
  • hashiomoto’s thyroiditis
  • grave’s disease
  • pernicious anemia
42
Q

-hashiomoto’s thyroiditis

A

-most common cause of hypofunction of thyroid gland in the USA*
HYPOTHYROIDISM
-normally the endocrine works together and they are under the control othe pituitary gland.
-if there is need for thyroid hormones stimulation of hypothalamus
Thyroid releasing hormone anterior pituitary thyroid stimulating
hormone(TSH) TSH binds to the thyroid gland and gives out T3 and
T4.

43
Q

-grave’s disease

A

-hyperfunction of the thyroid gland
-autoimmune disease, females are more common (20-25 years old)
-production of Abs against the receptors for TSH but in this case the Absstimulate the receptor (they do not simply block it, they permanently
stimulate them) (AB replaces TSH)
-dramatic increase of metabolic rate.

44
Q

-pernicious anemia

A
  • same mechanism of development as graves
  • one of the Abs produced are auto Abs knowing as binding ABS who bind to receptors for intrinsic factor
  • vit B12 can not go to the blood circulation
  • this is an autoimmune disease as well**

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