brief presentation about angioedema. its definition, causes, clinical manifestations, treatment and prevention.

1. Angioedema

2. Introduction
• Name: Maha
• Age: 21 years
• Symptoms: very tight throat , noisy breathing,
difficulty swallowing , horsey voice, swollen
eyes and lips, anxiety.
• The complaint arose after eating a Magnum
almond ice cream.

3. Objectives:
 The definition of angioedema
 Types of angioedema
 The causes of angioedema
 The Pathophysiology of
angioedema
 The risk factors of angioedema
 The signs and symptoms of
angioedema
 The diagnosis and the differential
diagnosis of angioedema
 The treatment of angioedema
 The prognosis of angioedema

4. Definition Of Angioedema
• Angioedema or Quincke's
edema is the rapid
swelling (edema) of
the dermis, subcutaneous
tissue, mucosa and
submucosal tissues. It is
very similar to urticaria,
but urticaria, commonly
known as hives, occurs in
the upper dermis.

5. Types Of Angioedema
1. Acute or allergic
angioedema – the
swelling is caused by
an allergic reaction,
such as a reaction to
peanuts.
2. idiopathic
angioedema – there is
no known cause for
the symptoms of
swelling .
• 3. drug-induced
angioedema – the
swelling is a side effect
of certain medications.
• 4. hereditary
angioedema – the
swelling is caused by
‘faulty’ genes that are
inherited from a
person’s parents.

6. Types Of Angioedema
• Or Angioedema is classified as either
hereditary or acquired.
1. Acquired angioedema can be immunologic,
nonimmunologic, or idiopathic. It is usually
caused by allergy and occurs together with
other allergic symptoms and urticaria. It can
also occur as a side effect to certain
medications, particularly ACE inhibitors.

7. • Hereditary angioedema (HAE): exists in three forms,
all of which are caused by a genetic mutation inherited
in an autosomal dominant form. They are
distinguished by the underlying genetic abnormality.
Types I
•mutations in
the SERPING1gene
•Lead to diminished
levels of
the C1inhibitor protein
Types II
•mutations in
the SERPING1gene
•Lead to dysfunctional
forms of C1-
inhibitor protein
Types III
•mutations in
the F12 gene,
•which encodes the
coagulation
protein factor XII

8. All forms of HAE lead to abnormal activation
of the , and all forms can
cause swelling elsewhere in the body, such as
the .

9. Causes of Angioedema
• Animal dander
• Exposure to water, sunlight,
cold or heat
• Foods (such as berries,
shellfish, fish, nuts, eggs,
and milk)
• Insect bites

10. • Medicines (drug allergy),
such as antibiotics
(penicillin), nonsteroidal
anti-inflammatory drugs
(NSAIDs), and blood
pressure medicines.
• Pollen
• infections or with other
illnesses
(including autoimmune, and
leukemia and lymphoma).
• Family history ( HAE )

11. Pathophysiology
• Angioedema is swelling due to increased vascular
permeability and extravasation of intravascular
fluid. Known mediators of increased vascular
permeability include the following:
1. Mast cell–derived mediators (e.g. histamine).
2. Bradykinin, a peptide containing nine amino acid
residues produced from α2-globulin by the enzyme
kallikrein. Bradykinin is a potent vasodilator, and
complement-derived mediators.

12. Allergic angioedema: (just like
anaphylaxis):

13. Hereditary angioedema:
• Hereditary angioedema (HAE) is due to mutations
within the C1-INH gene and is transmitted as an
autosomal dominant trait.
• C1INH is important in regulating the classical
complement system and contact cascade .
• Respectively,Insufficient C1INH function leads to
dysregulation of each of these pathways.
• However, contact pathway dysregulation is largely
responsible for the symptoms of HAE via excess
generation of bradykinin

14. Bradykinin is ultimately formed when high
molecular weight kininogen is cleaved by
kallikrein. C1INH specifically inhibits
bradykinin formation via inactivation of
kallikrein,, factor XIIa, and factor XIIf.
In individuals with C1INH deficiency,
production of bradykinin results via
unregulated activation of kallikrein.
Bradykinin binds to the bradykinin-2
receptor, causing vasodilatation,
increased vascular permeability, and
smooth muscle contraction, all of which
lead to symptoms of HAE.

16. Risk factors
• Age: 30-60 years old
• Other conditions:
1. Asthma
2. Eczema
3. Hives
• Gender: female
• Drinking alcohol
• Taking NSAIDs drugs
• Emotional stress
• Hyperthyroidism
• Menstruation

17. The signs and symptoms of
angioedema
Acute Angioedema:
 Large, thick, firm welts
 Swelling of the skin
 Pain or warmth in the
affected areas
 Difficulty breathing or
swallowing, in severe
cases

18. Hereditary Angioedema:
• Sudden and severe
swelling of the face,
arms, legs, hands, feet,
genitalia, digestive tract
and airway
• Abdominal cramping as a
result of digestive tract
swelling
• Difficulty breathing due
to swelling that obstructs
your airway

19. Diagnosis and investigations
The doctor will examine the welts and areas of
swelling if they are still present and take a
careful medical history to identify possible
causes, If the cause isn't apparent from the
medical history or symptoms ,the doctor may
recommend an allergy skin test.

20. Prick , patch (percutaneous) test.
 This is the type of skin test
that's usually performed
first. Tiny drops of purified
allergen extracts are
pricked or scratched into
the skin's surface. This test
is usually performed to
identify allergies to pollen,
animal dander, foods,
insect venom and
penicillin.

21. Intradermal test.
• Purified allergen extracts
are injected into the skin
of the arm. Doctors may
perform this test if they
strongly suspect allergy
to an irritant even though
your prick test is negative
— especially to an irritant
to which a future reaction
could be life-threatening,
such as insect venom or
penicillin.

23. blood test
• Mast cell levels may be
elevated if the attack was
due to an acute allergic
reaction.
• When the doctor
suspects hereditary
angioedema, he or she
may order blood tests to
check for depletion of
complement factors 2
and 4, that may indicate
deficiency of C1-inhibitor

24. Differential diagnosis
• Food Allergies
• Hymenoptera Stings
• Hypersensitivity
Reactions, Delayed
• Latex Allergy
• The most common
Differential diagnosis
is urticaria, but urticaria,
commonly known as
hives, occurs in the upper
dermis.
• Un like Angioedema
which occurs in ?
• the dermis, subcutaneous
tissue, mucosa and
submucosal tissues

25. Treatment
• Antihistamines e.g.
Ranitidine (Zantac)
• Anti-inflammatory medicines
(corticosteroids)
• Epinephrine shots (people with
a history of severe
symptoms can carry these with
them)
• Inhaler medicines that help
open up the airways
• Antihistamines and oral
corticosteroid medications —
although useful in treating hives and
acute angioedema — are often
ineffective in treating hereditary
angioedema.
• Medications used to treat
hereditary angioedema on a long-
term basis include certain
androgens (male hormones), such
as danazol, that help regulate levels
of blood proteins.

26. prevention
• Avoid known triggers. These may include
certain foods or medications, or situations
such as temperature extremes, that have
triggered past allergic attacks.
• Keep a diary. If you suspect foods are causing
the problem, keep a food diary. Be aware that
some foods may contain ingredients that are
listed by less common names on the label.

27. prognosis
 Angioedema that does not affect the
breathing may be uncomfortable, but is usually
harmless and goes away in a few days.
 So, Angioedema had a very good prognosis.

28. Conclusion
 Angioedema is a rapid
swelling of
the dermis, subcutaneous
tissue, mucosa and
submucosal tissues.
 Angioedema is classified as
either hereditary or
acquired.
• It caused by many things
such as Animal dander and
Food.
• The main sign is Swelling
of the skin.
• It can be diagnosed by
many tests.
• And it can be easily
treated.
• The prevention is mainly
by avoid the allergens.
• Finally ,The prognosis is
good .

29. References
• http://www.ncbi.nlm.nih.gov/pubmedhealth/
• http://www.mayoclinic.com
• http://emedicine.medscape.com