Permanent magnetic materials

PERMANENT MAGNETIC MATERIALS

Q.Permanent magnetic material is/are
a) Niobium-titanium
b)Alnico
c)Barium ferrite (BaF12O19)
d)Somarium Cobalt (SmCo5)
e)Neodymium-ironboron (NdFeB)


ANS  ----BCDE,Niobium-titanium  is a semi-conductor

TRIANGULAR CORD SIGN

              TRIANGULAR CORD SIGN
Q.Triangular cord sign and absent or small gall bladder on USG is predictive of

a.biliary atresia
b.cholangitis
c.choledochal cyst
d.duodenal atresia


ANS---Biliary atresia
Triangular sign----Biliary atresia is characterized by fibrous obliteration of the extrahepatic bile duct with fibrous ductal remnant in the porta hepatis .The hepatic ducts transform into a fibrous ductal remnant that is usually anterior and slightly cranial to the hepatic artery and the portal vein.

 The Triangular sign  refers  to  the presence of an abnormal  triangular or tubular echogenic area in the region of the porta hepatis on a transverse or longitidinal US scan,which is nothing but obliterated ductal remnant .

Several investigators  consider the Triangular  sign as a useful and specific US finding for the differential diagnosis of biliary atresia from neonatal hepatitis

COBRA HEAD APPEARANCE (IVU)

COBRA HEAD APPEARANCE

Q.Cobra head appearance on IVU is noted in

a.hydronephrosis

b.ureterocele

c.ureteric diverticulum

d.duplication of ureter

ANS   ===URETEROCELE

THE CENTRAL DOT SIGN

                                        THE CENTRAL DOT SIGN

Q.The central dot sign on CT scan of liver is pathognomonic of

a.Haemangioma

b.Caroli’s disease

c.FNH

d.HCC

  

PULMONARY EDEMA (RADIOGRAPHIC FEATURES)

Development of pulmonary edema (increased extravascular lung water) is a common problem . There are three principal varieties:

1.cardiac, commonly resulting from myocardial or valvular heart disease;

2. overhydration, usually caused by excess saline effusion or renal failure with retention of salt and water;

3.capillary permeability, which can be caused by a wide variety of pathologic, traumatic, and infective conditions resulting in injury to the pulmonary microvasculature.

The three principal mechanisms of edema formation are

(1) increased hydrostatic pressure gradient across the capillary wall

(2) diminished osmotic pressure gradient across the wall

 (3) increased capillary permeability (damage to the endothelial cell junctions, which permits both fluid and large molecules to leak out of the vessels). Change in plasma oncotic pressure is usually a contributory rather than a primary cause of pulmonary edema.

(4) A fourth, and often neglected factor, is the ability of the lymphatics to remove excess extravascular lung water (EVLW).

The chest film remains the most frequently used clinical method for the diagnosis of pulmonary edema

The three principal radiologic factors that had the greatest statistical significance in determining  type of edema  are the distribution of pulmonary blood flow,distribution of pulmonary edema, and the width of the vascular pedicle.

Distribution of pulmonary blood flow:

A, Normal; occurs principally in capillary permeability edema.

B, Balanced; occurs principally in overhydration or renal failure.

c. Inverted; occurs principally in cardiac failure.

Distribution of pulmonary edema.

There are three principal patterns, each of which corresponds to specific type of edema:

A. Even: principally basal (gravitational) and homogeneous from chest wall to heart but with perihilar component also. Principally occurs in cardiac edema.

B, Central; occurs principally in overhydration or renal failure.

C, Peripheral; markedly patchy,often spares costophrenic angles. Note air bronchograms.This type of distribution occurs almost exclusively in capillary permeability.

Vascular pedicle width(VPW). There are  three possible variations:

 A, Normal; commonest in capillary permeability or acute cardiac failure.

B, Widened; commonest in overhydration/renal failure and chronic cardiac failure.

C, Narrowed;commonest in capillary permeability edema.

 Normal VPW (for an erect 70-kg patient) is defined as 43-53 mm (48 mm ± 1 SD), diminished is less than 43 mm, and increased is more than 53 mm .

Septal Lines, Peribronchial Cuffing, Air Bronchograms, and Pleural Effusions :None of these factors is of much value in differentiating cardiac from  renal/overhydration edema, but they are value in differentiating capillary permeability edema from the other two varieties.

Radiographic features of pulmonary edema (SUMMARY)

                                                      Cardiac                    renal                         injury

1.Heart size            :                   enlarged             enlarged                     normal

2.Vascular pedicle  :                normal /enlarged    enlarged           normal/reduced

3.Pulmonary blood   :              inverted                  balanced             normal/balanced

   Flow distribution

4.Pulmonary blood    :             normal/increased       increased          normal

Volume

5.Septal line               :               not common              not common        absent

6.Peribronchial cuffs:              very common           very common       not common

7.Air bronchogram :                 not common        not common            very common

8.Lung edema ,regional

distribution(horizontal axis):  even                central                              peripheral

9.Pleural effusion   :                  very common        very common        not common

From book Faust( by Johhann Wolfgang von Goethe)

 Nothing can be known---------

I’ve studied now Philosophy

And Jurisprudence, Medicine,—

And even, alas! Theology,—

From end to end, with labor keen;

And here, poor fool! with all my lore

I stand, no wiser than before:

I’m Magister—yea, Doctor—hight,

And straight or cross-wise, wrong or right,

These ten years long, with many woes,

I’ve led my scholars by the nose,—

And see, that nothing can be known!

That knowledge cuts me to the bone.

I’m cleverer, true, than those fops of teachers,

Doctors and Magisters, Scribes and Preachers;

Neither scruples nor doubts come now to smite me,

Nor Hell nor Devil can longer affright me.

For this, all pleasure am I foregoing;

I do not pretend to aught worth knowing,

I do not pretend I could be a teacher

To help or convert a fellow-creature.

Then, too, I’ve neither lands nor gold,

Nor the world’s least pomp or honor hold—

No dog would endure such a curst existence!

Wherefore, from Magic I seek assistance,

That many a secret perchance I reach

Through spirit-power and spirit-speech,

And thus the bitter task forego

Of saying the things I do not know,—

That I may detect the inmost force

Which binds the world, and guides its course;

Its germs, productive powers explore,

And rummage in empty words no more!

Pulmonary Hypertension

Dana Point Classification of Pulmonary Hypertension

DEFINITION:

• A resting mean pulmonary arterial pressure of 20 mmHg or less is considered normal. 
• Pulmonary hypertension is defined as a resting mean pulmonary arterial pressure of 25 mmHg or more at catheterization of the right side of the heart, a hemodynamic feature that is shared by all types of pulmonary hypertension in the Dana Point classification system
• Use of the term pulmonary arterial hypertension is restricted to those with a hemodynamic profile in which high pulmonary pressure is a result of elevated precapillary pulmonary resistance and normal pulmonary venous pressure and is measured as a pulmonary wedge pressure of 15 mmHg or less, a hemodynamic profile that is shared by groups 3, 4, and 5 in the Dana Point classification system, which was updated during the 4th World Symposium on Pulmonary Hypertension held in Dana Point, California, in 2008 
• A diagnosis of pulmonary arterial hypertension is made only in the absence of other causes of precapillary pulmonary hypertension such as that resulting from lung disease (group 3), chronic thromboembolic pulmonary hypertension (group 4), and disease resulting from multifactorial mechanisms (group 5).

Pathophysiology:

 

• The normal adult pulmonary vascular bed is a low-pressure, low-resistance system that is able to accommodate increases in blood flow with minimal elevation in pulmonary arterial pressure.
• In patients with pulmonary hypertension, pulmonary arterial pressure and vascular resistance are chronically elevated, leading to right ventricular dilatation and hypertrophy .
• Normal right ventricles have a thin wall and, when viewed in cross section, a crescent shape that is appropriate for pumping blood across the pulmonary vascular system 
• Pulmonary hypertension results in right ventricular hypertrophy, followed by dilatation and right atrial enlargement . Initially, these changes are compensatory mechanisms that allow the right ventricle to produce a larger stroke volume and maintain cardiac output. 
• In patients with severe pulmonary hypertension, the hypertrophied right ventricle has a spherical shape that has a greater cross-sectional area than that of the left ventricle, resulting in abnormal septal motion that impairs left ventricular function . 
• Eventually, the demand of the right ventricle for oxygen exceeds the available supply, causing chamber dilation that leads to tricuspid regurgitation, a result of tricuspid annular dilatation and incomplete valve closure. These processes eventually result in decreased cardiac output and right-sided heart failure
• The ability of the right ventricle to cope with the progressive increase in pulmonary arterial pressure is the main determinant of patients’ functional capacity and survival .
• Morphologic and functional assessment of the right ventricle plays a central role in both diagnosing pulmonary hypertension and performing serial follow-up examinations. The most useful noninvasive parameters for assessing right ventricular size and function are right ventricular volumes and ejection fraction, which are most accurately measured at cardiac MR imaging.

   Chest Radiography

Chest radiography is usually the initial imaging study performed and may depict features of pulmonary hypertension that are indicative of its underlying cause, such as interstitial lung disease, emphysema, chest wall deformities, and left-sided heart disease.

The classic radiographic findings of pulmonary hypertension are evident only late in the disease process.

findings include:

1.central pulmonary arterial dilatation; pruning of the peripheral arteries;

 2.increased diameter (15 mm in women and 16 mm in men) of the right interlobar artery, measured from its lateral aspect to the interlobar bronchus;

 3.and reduced retrosternal air space on lateral views, a result of right ventricular dilatation

Multidetector CTPA

Vascular Signs.—The classic CTPA findings of pulmonary hypertension may be divided into three categories: vascular, cardiac, and parenchymal.

Vascular signs

1.On transverse images, the main pulmonary artery is evaluated at the level of its bifurcation, orthogonal to its long axis . A pulmonary artery with a diameter of 29 mm or more has a positive predictive value of 97%, sensitivity of 87%, and specificity of 89% for the presence of pulmonary hypertension . However, it is important to emphasize that a diameter of less than 29 mm does not necessarily exclude pulmonary hypertension.

2.The diameters of the segmental pulmonary arteries should also be equal to those of adjacent bronchi. In the presence of a dilated (29 mm or more) main pulmonary artery, a segmental artery–to-bronchus diameter ratio of 1:1 or more in three or four lobes has a specificity of 100% for the presence of pulmonary hypertension

3.At CTPA, a main pulmonary arterial diameter larger than that of the ascending aorta is also a sign of pulmonary hypertension, with a positive predictive value of 96% and specificity of 92%, especially in patients younger than 50 years old.

 Cardiac Signs.—

Findings of adaptation and failure of the right side of the heart that may be seen at ECG-gated CTPA include

1.right ventricular hypertrophy, which is defined as wall thickness of more than 4 mm;

2.straightening or leftward bowing of the interventricular septum;

3. right ventricular dilatation (as a right ventricle–to–left ventricle diameter ratio of more than 1:1 at the midventricular level on axial images);

4.decreased right ventricular ejection fraction;

5.dilatation of the inferior vena cava and hepatic veins;

6. pericardial effusion

Parenchymal Signs

1.Centrilobular ground-glass nodules are a feature of pulmonary hypertension and are especially common in patients with idiopathic pulmonary arterial hypertension

Cardiac MR Imaging

Cardiac MR imaging is used to assess ventricular volume, morphologic characteristics, mass, function, and changes in pulmonary circulation

It is the modality of choice for studying the right ventricle because no geometric assumptions are required, and its three-dimensional, anatomic,morphologic measurements are unaffected by body habitus, lung disease, and chest wall deformity

REFERENCE

Radiographics   JAN-FEB 12-13

INSULAR RIBBON SIGN

Q.Insular ribbon sign is a finding of

a.Posteror cerebral artery infarction

b.anterior cerebral artery infarction

c.Middle cerebral artery infarction

d.anterior cerebellar artery

RADIATION ISSUES :AN OVERVIEW

RADIATION  ISSUES :AN OVERVIEW

1.Deterministic and stochastic effects

The damaging effects of radiation can be divided into two categories: deterministic effects and stochastic effects.

Detreministic effects-------

• Deterministic effects occur at high dose levels, such as those given in radiotherapy treatments and are due to radiation-induced cell death.
• Deterministic effects are characterized by having a threshold dose below which the effect is not observed. The severity of the effect increases with dose and dose rate.Cataract formation and skin damage are examples of deterministic effects. Normally, in diagnostic procedures, doses are well below the threshold where deterministic effects are observed .

Stochastic effects-----

• The stochastic effects are of a random statistical nature and the probability of occurrence (but not the severity of the effect) is related to dose. In this effects, the probability of an effect occurring increases with dose up to a maximum, above which the curve flattens off .Cancers and genetic effects  are such effects.
• The timing of the appearance of radiation-induced cancers varies, with a mean incidence for leukaemia at about 7 years postirradiation, about 5 years for thyroid and bone cancers and 20 or more years for most other cancers.
•  In case of damage  to the germ cells, genetic effects may occur in future offspring. To date, no hereditary effects have been demonstrated convincingly in humans; however, based on animal experiments, it is concluded that hereditary effects are a possibility. 

2.Fetal irradiation

• Cell killing and cancer induction may occur as a result of in utero radiation and it is recognized that the fetus is highly radiosensitive during prenatal development.
• There are radiation-related risks throughout pregnancy, associated with the stage of pregnancy at which irradiation occurs and the fetal absorbed dose.
• Risks are most significant during organogenesis and the early fetal period, less in the second trimester and least in the third.
• Irradiation of a fetus can result in a reduction in IQ (if irradiation takes place 8–25 weeks postconception when the central nervous system is developing), an increased risk of cancer in later life, an increased incidence of congenital abnormality, or a genetic risk to the next generation.
•  However, a recent ICRP report on pregnancy and medical irradiation concludes that, for most well-conducted diagnostic procedures, there is no measurable increase in risk over the background incidence of such effects.
• So.exposure of the fetus to diagnostic levels of radiation should not be a reason to terminate a pregnancy, but efforts should be made to minimize the irradiation of known pregnant or potentially pregnant women.

3.PRINCIPLES OF RADIATION PROTECTION

• The aim of radiation protection practice is to restrict radiation dose so that, with the exception of radiotherapy treatments, doses to staff, patients and the public remain below the level at which deterministic effects occur and the probability of stochastic effects occurring is limited to an acceptably low level.
• To achieve this aim, the ICRP recommends the application of three principles: justification, optimization and limitation.
• Justification implies that no practice resulting in exposure to ionizing radiation should be adopted unless it results in sufficient net benefit to exposed individuals or society to offset the detriment. The use of radiation in healthcare is a justified practice
• Optimization requires that the individual dose, the number of people exposed and the likelihood of inadvertent exposure should be kept as low as reasonably achievable (ALARA), economic and social factors being taken into account. In UK legislation this is translated into as low as reasonably practicable (ALARP).
• Limitation: The exposure of individuals should be subject to dose limits designed to ensure that no individual is exposed to an unacceptable radiation risk.

4.SUMMARY OF ANNUAL DOSE LIMITS

	Effective whole body dose (mSv)	Individual organs or tissues (skin, hands, forearms, feet, ankles) (mSv)	Lens of eye limits (mSv)
Employees aged 18 years and over	20	500	150
Trainees aged under 18 years	6	150	45
Any other persons	1	50	15

Pregnant staff 

The dose to the fetus during the declared term of pregnancy (i.e. after the employer has been informed in writing) should be less than 1 mSv. For those receiving exposure to diagnostic X-rays this is equivalent to about 2 mSv to the surface of the abdomen.

5.PATIENT DOSES IN DIAGNOSTIC IMAGING  

   A. ECTIVE DOSES FOR COMMON RADIOLOGICAL EXAMINATIONS EXPRESSED IN TERMS OF THE EQUIVALENT NUMBER OF CHEST X-RAYS AND LENGTH OF EXPOSURE TO BACKGROUND RADIATION THAT WOULD GIVE THE SAME DOSE

Examination	Typical effective dose (mSv)	Equivalent number of chest X-rays	Equivalent length of background exposure
Limbs and joints (except hip)	< 0.01	< 0.5	< 1.5 d
Chest PA	0.02	1	3 d
Skull	0.06	3.0	9 d
Thoracic spine	0.7	35	4 months
Lumbar spine	1	50	5 months
Hip	0.4	20	2 months
Pelvis	0.7	35	4 months
Abdomen	0.7	35	4 months
IVU (intravenous urogram)	2.4	120	14 months
Barium swallow	1.5	75	8 months
Barium meal	2.6	130	15 months
Barium follow-through	3	15	16 months
Barium enema	7.2	360	3.2 years
CT head	2.0	100	10 months
CT chest	8.8	400	3.6 years
CT abdomen or pelvis	10	500	4.5 years
Lung ventilation 133Xe	0.3	15	7 weeks
Lung perfusion 99mTc	1	50	6 months
Kidney 99mTc	1	50	6 months
Thyroid 99mTc	1	50	6 months
Bone 99mTc	4	200	1.8 years
Dynamic cardiac 99mTc	6	300	2.7 years
PET head 18FDG	5	250	2.3 years

 B.FETAL DOSES FROM A SELECTION OF COMMON DIAGNOSTIC PROCEDURES

Procedure	Mean fetal dose (mGy)	Maximum fetal dose (mGy)
AP abdomen	1.4	4.2
Barium enema	6.8	24
PA chest	< 0.01	< 0.01
Pelvis	1.1	4
CT abdomen	8.0	49
Bone 99mTc	3.3	4.6
Dynamic cardiac 99mTc	3.4	3.7
GFR (EDTA) 51Cr	<0.01	<0.01

REFERENCE:

Adam: Grainger & Allison's Diagnostic Radiology, 5th ed.

Copyright © 2008 Churchill Livingstone, An Imprint of Elsevier