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Manjooran Test 3 Reading

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Bell's palsy

TEXT A

A patient with Bell 's palsy on the right side of his face, with the muscles on this side
appearing to be paralyzed.
Bell's palsy involves a weakness or paralysis on one side of the face. Symptoms often appear
first thing one morning. A person wakes up and finds that one side of their face does not
move.
The person may find that they suddenly cannot control their facial muscles, usually on one
side. The affected side of the face tends to droop. The weakness may also affect saliva and
tear production, and the sense of taste.
Many people are afraid they are having a stroke, , but if the weakness or paralysis only
affects the face, it is more likely to be Bell 's palsy.
Approximately 1 in 5,000 people develop Bell's palsy each year. It is classed as a relatively
rare condition.
In very rare cases, Bell's palsy can affect both sides of the face

TEXTB

The f acial nerve contro ls most of t he muscles in t he face an d parts of th e ear. The facial
nerve goes through a narrow gap of bone from the brain to the face.
If the facial nerve is inflamed, it will press aga inst the cheekbone or may pinch in the
narrow gap. This can result in damage t o the protective covering of the nerve.
If the protective covering of the nerve becom es damaged, th e signals t hat t ravel from the
brain to the muscles in the face may not be t ra nsmitted properly, leading to w eakened or
paralyzed facial muscles. This is Bell's palsy.
The exact reason why this happens is unclear.
It may result when a virus, usually the herpes virus, inflames the nerve. This is the same
virus that causes cold sores and genital herpes.
Other viruses that have been linked to Bell 's palsy include :
Chickenpox
and shingles virus, coldsores and genital herpes virus, Epstein-Barr virus, or EBV,
responsible for mononucleosis, cytomegalovirus, mumps virus
Influenza B, hand-foot-and-mouth disease (coxsackievirus)
Bell's palsy risk factors
Women who are in the last trimester of their pregnancy or who have just given birth may
be at risk from Bell's palsy.
Some risk factors have been established.
Links have been found between migraine and facial and limb weakness. A study carried
out in 2015 found that people with migraine may have a higher risk of bell's palsy.
The condition more commonly affects:
people aged 15 to 60 years, those with diabetes or upper respiratory diseases,

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women during pregnancy, especially in the third trimester, women who gave birth less
than 1 week ago.
Bell's palsy affects men and women equally.

TEXTC
Treatment
Most people will recover from Bell 's palsy in 1-2 months, especially those who still have
some degree of movement in their facial muscles.
Treatment with a hormone called prednisolone can speed up recovery. Astudy found that
prednisolone, if administered within 72 hours of onset, can significantly reduce symptom
severity and incidence after 12 months.
Prednisolone
This steroid reduces inflammation. This helps accelerate the recovery of the affected nerve.
Prednisolone prevents the release of substances in the body that cause inflammation, such
as prostagland ins and leukotrienes.
Patients take it by mouth, usually two tablets a day for 10 days.
Possib le side effects include:
abd ominal pain, bloatin g, acne, difficulty sleeping, dry skin, Head ache, dizziness (spinn ing
sensation), increase d appetite, increased sweating
·Indigestion
· mood changes
·nausea
· Oral Thrush
·slow wound healing
·thinning skin
·tiredness
These side effects normally get better after a couple of days.
An allergic reaction to prednisolone, such as difficulty breathing, should immediately be
reported to a healthcare professional.
Any allergic reaction to prednisolone should be reported to the doctor immediately.
Allergy symptoms may include :
Hives
breathing difficulties
swelling of the face
lips
tongue
throat
If the patient feels dizzy or drowsy they should refrain from driving or operating heavy
machinery. As this symptom may not appear straight away, it is advisable to wait a day
before driving or operating machinery.
Doctors usually reduce the dose gradually towards the end of the course of steroid
medication. This helps prevent withdrawal symptoms, such as vomiting or tiredness.
Eye lubrication

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If the patient is not blinking properly the eye will be exposed and tears will evaporate. Some
patients will experience a reduction in tear production. Both may increase the risk of
damage or infection in the eye.
The doctor may prescribe artificial tears in the form of eye drops and also an ointment. The
eye drops are usually taken during the waking hours, while the ointment is applied before
going to sleep.
Patients who cannot close their eye properly during sleep will need to use surgical tape to
keep it shut. Patients who experience worsening eye symptoms should seek medical help
immediately. If you cannot get hold of your doctor, go the emergency department of your
nearest hospital.
Antivirals
In some cases, an antiviral, such as acyclovir may be taken alongside prednisolone;
however, evidence that they can help is weak.
Care at home
Facial exercises: As the facial nerve begins to recover, tightening and relaxing facial muscles
can help strengthen them.
Dental care : If there is little or no feeling in the mouth it is easy for food to build up leading
to decay or gum disease. Brushing and flossing can help prevent this.
Problems with eating: If there are difficulties with swallowing, the individual should chew
food well and eat slowly. Choosing soft foods, such as yogurt can also help.
OTC pain relief: To ease an y discom fort. Some pai n rel ief medications may be purchased
online, includ ing ibu profen and Advi l.

TEXTD

Symptoms
The facial nerves control blinking, opening and closing of the eyes, smiling, salivation,
lacrimation (production of tears), and frowning. They also connect with the muscles of the
stapes, a bone in the ear involved in hearing.
When the facial nerve malfunctions, as in Bell 's palsy, the following symptoms can occur:
sudden paralysis/weakness in one side of the face
difficulty closing one of the eyelids
irritation in the eye because it does not blink and becomes too dry
changes in the amount of tears the eye produces
dropping in parts of the face, such as one side of the mouth
drooling from one side of the mouth
difficulty with facial expressions
sense of taste may become altered
an affected ear may cause sensitivity to sound
pain in front or behind the ear on the affected side
headache

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Bell's palsy

Questions 1-7

For each question, 1-7, decide wh ich text (A, B, Cor D) the information comes from. You may use
any letter more than once.

In wh ich text can you find information about

1. Tightening and facial muscle relaxation is done during recovery period

2. Excretory functions like salivation & tear production is affected in Bell's palsy

3. Sense of taste may become altered

4. Risk and damage to eye is associated with bell's palsy

5. Most of the people misunderstand bell's palsy as stroke

6. The real etiology for bell's palsy is idiopathic

7. Pathogen esis of bell's pa lsy.

Questions 8-14
Answer each of the questions, 8-1 4, with a word or short phrase from one of the texts. Each
answer may include words, numbers or both .

8. Two over the count medications wwhich can be used at home to relieve pain?

9. At what t ime eye drops are generally administere d?

10. Which causative agent is responsible for mononucleosis?

11. What is the main reason for irritation in the eye?

12. Which part of the nerve is affected in bell's palsy?

13. Which age group of people are commonly affected?

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Questions 15-20
Complete each of the sentences, 15-20, with a word or short phrase from one of the texts.
Each answer may include words, numbers or both

14. Taking foods like------------------------------- can help in making swallowing easier.

15. -------------------------- can be used if patient cannot close their eye while sleeping.

16. We should be cautious regarding hypersensitivity reaction to ------------------------------- .

17. In exceptional cases, bell's palsy affect------------------------------ of the face.

18. Bell's palsy can cause-------------------------- to sound

19. ---------------------------------speed up rehabilitation of affected nerve.

20. People with---------------------------- are vulnerable to get bell's palsy.

Part B

In this part of the test, there are six short extracts relating to the work of health professionals. For
questions 1-6, choose answer (A, B or C) which you think fits best according to the text.

Treatment of congenital fibrinogen deficiency

Afibrinogenemia is a rare bleeding disorder with an estimated prevalence of 1:1,000,000. It is


an autosomal recessive disease resulting from mutations in any of the 3 genes that encode
the 3 polypeptide chains of fibrinogen and are located on the long arm of chromosome 4.
Spontaneous bleeding, bleeding after minor trauma and excessive bleeding during
interventional procedures are the principal manifestations. We review the management of
afibrinogenemia. Replacement therapy is the mainstay of treatment of bleeding episodes in
these patients and plasma-derived fibrinogen concentrate is the agent of choice.
Cryoprecipitate and fresh frozen plasma are alternative treatments that should be used only
when fibrinogen concentrate is not available. Secondary prophylactic treatment may be
considered after life-threatening bleeding whereas primary prophylactic treatment is not
currently recommended. We also discuss alternative treatment options and the management
of surgery, pregnancy and thrombosis in these patients. The development of new tests to
identify higher risk patients and of safer replacement therapy will improve the management
of afibrinogenemia in the future.

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1. Fibrogenemia's treatment is

a) Replacement therapy

b) Prophylactic treatments

c) Alternative treatments.

Fibrochond rogenesis

Fibrochondrogenesis is a severe skeletal dysplasia characterized by a flat midface, short long


bones, short ribs with broad metaphyses, and vertebral bodies that show distinctive
hypoplastic posterior ends and rounded anterior ends, giving the vertebral bodies a pinched
appearance on lateral radiographic views. The chest is small, causing perinatal respiratory
problems which usually, but not always, result in lethality. Affected individuals who survive
the neonatal period have high myopia, mild to moderate hearing loss, and severe skeletal
dysplasia (summary by Tompson et al., 2012 ). For a discussion of genetic heterogeneity of
fibrochondrogenesis

2. Fibrochondryogenesis is characterized by

a) Long ribs an d broa d meta physes

b) Perinat ed respiratory problems

c) High to moderate hearing loss.

Fibromuscular Dysplasia

Renal artery stenosis, the most common cause of secondary hypertension, is predom inantly
caused by the atherosclerotic renovascular disease. Fibromuscular dysplasia (FMD) is a rare
systemic vascular disease, affecting younger women and accounting for 10% to 20% of the
cases of renal art ery st enosis. FMD is an idiopat hic, non-inf lammat ory, non-at herosclerot ic
disease commonly involving renal and carotid arteries; however, it can affect any arterial bed.
FMD classically presents as renovascular hypertension but can also manifest as stroke in
young adults. Early diagnosis and treatment are important for long-term prognosis. Etiology
of FMD is unclear despite extensive research. Environmental and genetic factors have been
associated with FMD. Biggazi et al. reported bilateral FMD in identical twins, raising the
possibility of inheritance. In a retrospective analysis of 104 patients with renal FMD, Pannier-
Moreau et al. reported an 11% prevalence of familial cases where at least one sibling showed
angiographic evidence of renal FMD

3. Fibromuscular Dysplasia affect:

a) Younger Women

b) Older Women

c) Young adults

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Fibrochondrogenesis

Adult fibrosarcoma, defined by the World Health Organization as a 'malignant neoplasm


composed of fibroblasts with variable collagen production and, in classical cases, a
"herringbone" architecture ', is a very rare soft tissue sarcoma. Once considered the most
common adult sarcoma, the incidence of adult fibrosarcoma has declined dramatically over
the past several decades. This is due to (i) evolution in the classification of soft tissue tumours
(ii) recognition of clinically, morphologically and genetically distinctive subtypes of
fibrosarcoma and (iii) increased understanding of the many other mesenchymal and non-
mesenchymal tumours that may mimic fibrosarcoma. This review article will summarize the
current state of our knowledge about strictly defined adult fibrosarcoma and discuss
important entities in its differential diagnosis, including various fibrosarcoma variants,
monophasic synovial sarcoma and other potential mesenchymal and non-mesenchymal
mimics.

4. Various fibrosacroma varieties:

a) W ill mimic non-m esenchymal

b) Rese mbles non-mesen chymal and other potential mesesnchyma

c) None of the above.

Fibrosing alveolitis

Fibrosing alveolitis is a disease of unknown cause mainly involving the gas-exchanging


portions of the lungs. It may occur in isolation and be called cryptogenic or idiopathic, in which
case the clinical manifestations are mainly respiratory, or it may be associated with other
disorders, such as rheumatoid arthritis. The histopathologic abnormalities of the pulmonary
tissue are identical in either instance. Other names used for the disease have included usual
interstitial pneumonia, desquamative interstitial pneumonia and the Hamman-Rich
syndrome; these terms may describe different stages of the same pathologic process. Many
authors in North America and those in the United Kingdom favour the term fibrosing alveolitis
when describing chronic interstitial pneumonias. There may be accompanying nonspecific
Immunologic abnormalities, which may denote that fibrosing alveolitis is part of the wide
spectrum of diseases known as connective tissue disorders. Recently immune complexes have
been found in the lung parenchyma; they probably result in the granulocyte destruction and
reticuloendothelial proliferation seen in the acute phase of the disease.

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5. Fibrosignalveoletis's cause is:

a) Unknown

b) Infection

c) Lung disease

Fibrous Dysplasia

Fibrous dysplasia (FD) is an uncommon mosaic disorder falling along a broad clinical spectrum.
It arises from post-zygotic mutations in GNAS, resulting in constitutive activation of the cAMP
pathway-associated G-protein, Gsa, and proliferation of undifferentiated skeletal progenitor
cells. FD may occur in isolation, or in association with skin pigmentation and hyperfunctioning
endocrinopathies, termed McCune-Albright syndrome (MAS). Disease may involve any part
or combination of the skeleton, ranging from an isolated, asymptomatic monostotic lesion,
to severe polyostotic disease resulting in fractures, deformity, functional impairment, and
progressive scoliosis. FD may be diagnosed clinically in patients with polyostotic disease
and /or extraskeleta l features of MAS; however biopsy is t ypically required to diagnose
mon ostotic disease. M an agement is focused on t reating endocrino pathies, preventing
fractures, optimizing f un ction, an d treating pa in. All patients should be eva lu ated an d tre at ed
for extraskeletal features of MAS at the time of diagnosis. In particular control of growth
hormone excess is important to prevent cra niofacial FD expansion, and control of FGF23-
mediated hypophosphatemia is importa nt to prevent fract ure, deformity, and bone pain. A
mainstay of FD treatment is surgical, and pract itioners should be aw are th at tech ni qu es and
procedures used in other skeletal disorders, such as bone graftin g an d prophyl actic optic
nerve decompression, are frequently ineffective in FD. There are currently no medical
therapies capable of altering the disease course in FD. Bisphosphonates may be effective in
treating FD-related bone pain, but are unlikely to impact bone quality or lesion expansion.
There is a critical need to develop novel therapies capable of altering the disease activity of
FD lesions. Ongoing efforts include developing drugs to target the mutant Gsa, and devising
strategies for targeting mutant skeletal progenitor cells.

6. Fibrous Dysplasia is a ___ disorder:

a) Unknown mosaic

b) Functional impairment

c) Genetic

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Viral Infection- Yellow Fever
Yellow fever is a viral infection spread by a particular species of mosquito. It's most common
in the areas of Africa and South America, affecting both travellers to and residents of those
areas. In mild cases, it causes fever, headaches, nausea and vomiting. However, it can become
more serious, causing heart, liver and kidney problems along with bleeding (haemorrhaging).
Up to 50 percent of people with the more severe form of yellow fever die of the disease.

There's no specific treatment for yellow fever, but getting a yellow fever vaccine before
travelling to an area in which the virus is known to exist can protect you from the disease.
During the first three to six days after contracting yellow fever- the incubation period -
there won't be any signs or symptoms of the disease. After this, the virus enters an acute
phase and, in some cases, a toxic phase follows which can be life-threatening.

Once the yellow fever virus enters the acute phase, you may experience signs and symptoms
including: fever, headaches, muscle aches - particularly in your back and knees - nausea,
vomiting or both, loss of appetite, dizziness, red eyes, face or tongue. These signs and
symptoms usually improve and disappear within several days.

Although signs and symptoms may disappear for a day or two following the acute phase, some
people w ith acute yellow fever th en enter a toxic phase. During the toxic phase, acute signs
and symptoms return and more severe an d life-th re atening ones also appea r. These ca n
inclu de: ye llowing of th e skin an d the w hites of t he eyes Uau ndice), abdominal pain and
vomiting- sometimes of blood -decreased urination, bleeding from your nose, mouth and
eyes, heart dysfunction (arrhythmia), liver and kidney failure, and brain dysfunction, including
delirium, seizures and coma.The toxic ph ase of yellow fever can be fatal.

Make an appointment to see your doctor fou r to six weeks before travelling to an area in
which yellow fever is known to occur. If you don't have that much t ime to prepare, ca ll your
doctor anyway. Your doctor will help you determine whether you need vaccinations and can
provide general guidance on protecting your health while abroad. Seek emergency medical
care if you 've recently travelled to a region where yellow fever is known to occur and you
develop severe signs or symptoms of the disease. Even if you develop mild symptoms, call
your doctor.Yellow fever is caused by a virus that is spread by the Aedes aegypti mosquito.
These mosquitoes thrive in and near human habitations where they can breed in even the
cleanest water. Most cases of yellow fever occur in sub-Saharan Africa and tropical South
America.

Humans and monkeys are most commonly infected with the yellow fever virus; mosquitoes
transmit the virus back and forth between monkeys, humans or both. When a mosquito bites
a human or monkey infected with yellow fever, the virus enters the mosquito's bloodstream
and circulates before settling in the salivary glands. When the infected mosquito bites another
monkey or human, the virus then enters the host's bloodstream, where it may cause the
illness to develop.

You may be at risk of the disease if you travel to an area where mosquitoes continue to carry
the yellow fever virus. These areas include sub-Saharan Africa and tropical South America.

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Even if there aren 't current reports of infected humans in these areas, it doesn't necessarily
mean you 're risk-free. It's possible that local populations have been vaccinated and are
protected from the disease, or that cases of yellow fever just haven 't been detected and
officially reported. If you 're planning on travelling to these areas, you can protect yourself by
getting a yellow fever vaccine at least 10 to 14 days before travelling. Anyone can be infected
with the yellow fever virus, but older adults are at greater risk of becoming seriously ill.

Diagnosing yellow fever based on signs and symptoms can be difficult because, early in its
course, the infection can be easily confused with malaria, typhoid, dengue fever and other
viral hemorrhagic fevers. To diagnose your condition, your doctor will likely:

lliAsk questions about your medical and travel history

Ill Collect a blood sample for testing

If you have yellow fever, your blood may reveal the virus itself. If not, blood tests known as
enzyme-linked immune sorbent assay (ELISA) and polymerase chain reaction (PCR) can also
detect antigens and antibodies specific to the virus. Results from these tests may take several
days.

No antiviral medications have proved helpful in treating yellow fever and, as a result,
treatment consists prima rily of supportive care in a hospital. Th is includes provid ing fluids an d
oxygen, maintai ning ade quate bl ood pressure, replaci ng blood loss, provid ing dialysis for
kidn ey f ailure, and tre ating an y other infections t hat develop. Some people receive
transfusions of plasma to replace blood proteins that improve clotting. If you have yellow
fever, you may also be kept away from mosquitoes, to avoid transmitting the disease to
others.

Questions

Viral Infection- Yellow Fever

7. Yellow fever is common in

A. Africa

B. South America

C. Both

D. Not given

8. Which of the following is not a sign of yellow fever?

A. Back pain

B. Vomiting

C. Nausea

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D. Dry tongue

9. Signs/symptoms of toxic phase

A. Loss of appetite

B. Yellowness of eyes

C. Brain dysfunction

D. Band C

10. Seizures may occur during

A. Acute phase

B. Toxic phase

C. Sometimes in both the phases

D. Not given

11. Yellow fever, wh ich is a viral disease, is spread by

A. Ae des agypti mosq uito

B. Aed es aegypti mosquito

C. Female mosquito

D. Contamination

12. Mosquitoes transmit the virus from

A. Humans to monkeys

B. Monkeys to humans

C. Human to human

D. None

13. Being vaccinated ............... days before travelling to areas where the disease is common

is recommended.

A. 10 days

B. 12 days

C. 14 days

D. 10-14 days

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14. Typhoid is

A. Similar to malaria

B. Just similar to yellow fever

C. One of common hemorrhagic fevers

D. Not given

Aortic Dissection or Dissecting Aneurysm

An aortic dissection is a serious condition in which a tear develops in the inner layer of the
aorta, the large blood vessel branching off the heart. Blood surges through this tear into the

middle layer of the aorta, causing the inner and middle layers to separate (dissect). If the
blood-filled channel ruptures through the outside aortic wall, aortic dissection can be fatal.

Aortic dissection, also called dissecting aneurysm, is relatively uncommon. Anyone can
develop the con dition, but it most fre qu ently occurs in men between 60 and 70 yea rs of age.
Symptoms of aortic dissection may mimic th ose of other dise ases, often leadi ng to delays in
diagnosis. However, wh en an ao rtic disse ction is detected ea rly an d treated promptly, your
chance of su rvival greatly improves.

Aortic dissection symptoms may be simil ar to those of other heart problems, such as a heart
attack. Typical signs and symptoms include: sudd en severe chest or upper back pain (oft en
described as a tearing, ripping or she ari ng sensation , t hat rad iates to th e neck or dow n the
back), loss of consciousness (fainting), shortness of breath, swe ati ng, wea ker pulse in on e arm
compared to the other etc.

If you have signs or symptoms such as severe chest pain, fainting, sudden onset of shortness
of breath or symptoms of a stroke then seeking medical assistance is imperative. While
experiencing such symptoms doesn't always mean that you have a serious problem, it's best
to get checked out quickly because early detection and treatment may help to save your life.

An aortic dissection occurs in a weakened area of the aortic wall. Chronic high blood pressure
may stress the aortic tissue, making it more susceptible to tearing. You can also be born with
a condition associated with a weakened and enlarged aorta, such as Marfan syndrome or
bicuspid aortic valve. Rarely, aortic dissections may be caused by traumatic injury to the chest
area, such as during motor vehicle accidents.

Aortic dissections are divided into two groups, depending on which part of the aorta

is affected :

Type A: This is the more common and dangerous type of aortic dissection. It involves a tear
in the part of the aorta just where it exits the heart or a tear extending from the upper to
lower parts of the aorta, which may extend into the abdomen.

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Type 8: This type involves a tear in the lower aorta only, which may also extend into the
abdomen.

Risk factors for aortic dissection include:

Ill Uncontrolled high blood pressure (hypertension), found in at least two-thirds of all cases

Ill Hardening of the arteries (atherosclerosis)

Ill Weakened and bulging artery (pre-existing aortic aneurysm)

Ill An aortic valve defect (bicuspid aortic valve)

Ill A narrowing of the aorta you're born with (aortic coarctation)

People with certain genetic diseases are more likely to have an aortic dissection than other
people.

These genetic diseases include: Turner's syndrome, high blood pressure, heart problems, and
a number of other health conditions may be a result of this disorder.

M arfan syndrome:

This is a conditio n in which connective t issu e, which su pports various structures in the bod y,
is w eak. Pe opl e with this disorder often have a fa mily history of aneurysms of t he aorta and
other blood vessels. These weak blood vessels are prone to tears (dissection) and rupt ure
easily.

Ehlers-Danlos syndrome:

This group of connective tissue disord ers is cha racterized by skin th at bruises or t ears easily,
loose joints and fragile blood vessels.

Loeys-Dietz syndrome:

This is a connective tissue disorder marked by twisted arteries, especially in the neck. People
who have Loeys-Dietz syndrome are thought to be at risk of developing aortic dissections and
aneurysms.

An aortic dissection can lead to death, due to severe internal bleeding, including into the lining
around the heart (pericardia! sac), organ damage (such as kidney failure or life-threatening
damage to the intestines), strokes (possibly including paralysis), and aortic valve damage,
such as causing the aortic valve to leak (aortic regurgitation).

Detecting an aortic dissection can be tricky because the symptoms are similar to those of a
variety of health problems. Doctors often suspect an aortic dissection if the following signs
and symptoms are present: sudden tearing or ripping chest pain, widening of the aorta on a
chest X-ray, blood pressure difference between the right and left arms.

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15. In aortic dissection a tear develops in

A. Outer layer of aorta

B. Inner layer of aorta

C. Middle aorta

D. A blood vessel branching off the heart

16. Dissecting aneurysm is common among

A. Men

B. Women

C. Both

D. Children

17. Sympt oms of aortic disse ction include

A. Ch est pa in and swelling

B. Wea k pulse in both arms

C. Loss of consciousness

D. All of the above

18. Aortic dissection can also be caused due to

A. High BP

B. Weak aortic wall

C. Inborn symptoms

D. Traumatic injury to chest during accidents

19. The most dangerous type of aortic dissection is

A. Type A

B. Type B

C. Aortic aneurism

D. Aortic coarctation

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20. A condition in which connective tissue is weak is called

A. Turner's syndrome

B. Loeys-Dietz syndrome

C. Ehlers-Danlos syndrome

D. Marfan's syndrome

21. People with Loeys-Dietz syndrome are likely to develop

A. Aneurysms

B. Ruptured blood vessels

C. Twisted arteries in the neck

D. Aortic complications

22. Aortic dissection is

A. Extremely fatal at all times

B. Sometimes fatal

C. Not very severe

D. Sometimes severe

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ANSWERS
Part A

l.C
2.A

3.0

4.C

S.A

G.B
7.B

8.1buprofen and Advil

9.waking hours

10.EBV OR EPSTEIN BARR VIRUS

1l.lt doesn't blink

12.protective covering of t he facia I nerve

13.15-16 years

14.yougurt

15.surgical tape

16.prednisolone

17.both side

18.sensit ivity

19.prednisolone

20.m igra ine

PARTB

l.A
2.B

3.A

4.A

S.A

G.A

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PART C

7.C
8.D

9. B ANDC

10. B
11. B

12. A /B

13. D

14. D

15 . B
16.A

17.C
18. D

19.A

20.D

2l.A

22.A

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