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There is a new government bill about writing and spreading viruses. If the bill goes through, it is going to be a criminal act to make and spread viruses in Finland and one could get two years in prison or a fine, if one spread or write viruses. If a person make a virus it would be same thing in court than a person were planning to bum something. It is criminal to make viruses in England, Italy, Netherlands, Switzerland and Russia.
It is not punished to make or spread viruses in Finland, according today's penal code. If viruses make harm to somebody that could be punished. Nobody has been punished for that in Finland, even though some F inns has made viruses, for example Finnish Spryer. That virus formatted about 600 hard disks and did lots of damage. They say that it was made in Espoo, but they never got the persons that made that virus.
Virus business in Finland is pretty big. Businesses that have specialized in viruses have about 100 million in sales together. It costs money to stop working and clean up the viruses. Computer viruses put in danger general safety, says Pihlajamaki from Ministry of Justice. It is dangerous if viruses get to programs that control trains or airplanes.
Computer viruses can also be used as a weapon. It is sad that America used computer viruses to slay and to make Iraq's computers non-functional.
6. How computer viruses have spread out around the world
Computer viruses are a problem all over the world. The following picture tells us how many times people have accessed Data Fellows, a company that makes anti-virus program F-Prot, more than 1,672,846 per month. It means that people are interesting in virus information. One reason is that people have to deal with viruses. Viruses in not only a problem in Finland and USA, it is a problem around the world.
Today's most common virus is the macro virus. Cap virus is one of the macro viruses. Last month there were 3100 Cap macro virus accesses during the last 30 days in Data Fellows. Next common virus was Join the Crew with 1171 accesses and third common was Pen pal Greetings with 895 accesses.
7. Computer viruses and network security
Computer viruses are one network security problem. A few people when asked if computer viruses can cause network security problems answered as follows.
"The only information that is leaked is the thing you should be worried about, your password! The trojan sends an E-mail to the hackers fake name and then he has your account at his hands," wrote CJ from American Online.
"Rarely, a Word macro virus may accidentally pick up some user information and carry it along; we know of one case where a macro virus "snatched" an innocent user macro that contained a password, and spread it far outside the company where that happened. In the future, however, it is entirely possible that more network-aware viruses will cause significant network security problems," wrote David Chess from IBM.
Marko Helenius wrote from Virus Research Unit, that there has been some cases when hackers have used trojan horses to gain information. There is one example in one finnish corporation where some money were transferred illegally a year ago. There has been a trojan in the University of Tampere too where the trojan pretend to be a host transfer program. The trojan saved users login name and password to hard disk.
8. Conclusions
There are lots of viruses in the world and new viruses are coming up every day. There are new anti-virus programs and techniques developed too. It is good to be aware of viruses and other malware and it is cheaper to protect you environment from them rather then being sorry.
There might be a virus in your computer if it starts acting differently. There is no reason to panic if the computer virus is found.
It is good to be a little suspicious of malware when you surf in the Internet and download files. Some files that look interesting might hide a malware.
A computer virus is a program that reproduces itself and its mission is to spread out. Most viruses are harmless and some viruses might cause random damage to data files.
A trojan horse is not a virus because it doesn't reproduce. The trojan horses are usually masked so that they look interesting. There are trojan horses that steal passwords and formats hard disks. Marco viruses spread from applications which use macros. Macro viruses spreads fast because people share so much data, email documents and use the Internet to get documents. Macros are also very easy to write.
Some people want to experiment how to write viruses and test their programming talent. At the same time they do not understand about the consequences for other people or they simply do not care.
Viruses mission is to hop from program to other and this can happen via floppy disks, Internet FTP sites, newsgroups and via email attachments. Viruses are mostly written for PC-computers and DOS environments.
Viruses are not any more something that just programmers and computer specialist have to deal with. Today everyday users have to deal with viruses.
Congenital Heart Disease
Definition:-
- Anomalies of heart and large vessels development due to embriogenesis disturbances during 2-8th weeks of pregnancy
Epidemiology:-
- Frequency - 1%
- 50-70 % die before 1 year of age (if without surgery)
- Only ½ of cases are diagnosed in maternity house; 93% - before 1st year
- More than 40 defects are described; 8 are most common (80%)
Most common defects:-
- Ventricular septal defect (VSD)
- Atrial septal defect (ASD)
- Patent ductus arteriosus (PDA)
- Coarctation of aorta (CA)
- Stenosis of aorta (SA)
- Transposition of magistral vessels (TMV)
- Fallot’s tetralogy (FT)
Etiology – 1:-
- Viral infections (rubella, URIs, mumps, chickenpox)
- Radioactive rays
- Drugs (thalidomide)
- Toxicosis of pregnancy
- Starving
- Polyhypovitaminosis
Etiology – 2:-
- Some diseases of pregnancy (diabetes, heart diseases)
- Chromosomal diseases (Down’s syndrome, Marfan’s syndrome, Turner’s syndrome…)
- Mother’s age over 35 years
- Maternal alcohol consumption
- Family history of a cardiac or noncardiac defect
Classification – I:-
- With left-to-right shunting (↑ pulmonary circulation)
- With right-to-left shunting (↓ pulmonary circulation)
- Without shunting
With left-to-right shunting:-
- Ventricular septal defect
- Atrial septal defect
- Patent ductus arteriosus
With right-to-left shunting:-
- Transposition of magistral vessels
- Fallot’s tetralogy
- Left heart hypoplasia
Without shunting:-
- Coarctation of aorta
- Stenosis of aorta
- Stenosis of pulmonary artery
Classification – II:-
- With increase of pulmonary circulation
- With decrease of pulmonary circulation With decrease of greater systemic circulation
- Without hemodynamic disturbances
- ___________
- With or without cyanosis
Echocardiography:-
- 3-dimensional (3D) echocardiographic images with a Doppler system with superimposing a color-coded direction and velocity of blood flow on the real-time images
Ventricular septal defect:-
- Most common: 17-30 %
- Size: 0.1 cm – 3 cm
- Localization: in membranous or muscular part
- Delayed diagnosis: first months pulmonary pressure is higher → no cardiac murmur
Ventricular septal defect:-
- Small VSD: no significant hemodynamic derangement; loud murmur; can close spontaneously (in muscle segment)
- Large VSD: progressively leads to higher pulmonary resistance → irreversible pulmonary vascular changes, so-called Eisenmenger syndrome (reversal of shunt to right-to-left shunt)
Clinics:-
- Mild defect: recurrent upper respiratory infections, effort intolerance and fatigue
- Severe defect:
- Development deficit, failure to thrive
- CHF
- Pulmonary hypertension
Clinics in early infancy:-
- Dyspnea
- Feeding difficulties
- Poor growth
- Profuse perspiration
- Recurrent pulmonary infections
- Cardiac failure
Physical exam:-
- Rough pansystolic murmur in 3-4th intercostal space on the left border of sternum
- Accent of S2 over pulmonary artery (pulmonary hypertension)
- Left and right ventricular enlargement (palpable parasternal lift, laterally displaced apical impulse, widened heart borders)
ECG:-
- Small VSD → Normal
- Moderate VSD → signs of LV volume overload (deep Q and tall R waves with tall T waves in leads V5 and V6), LA overload (broad P wave), atrial fibrillation
- Severe VSD → right ventricular hypertrophy, with further progression - biventricular hypertrophy
Chest X-ray:-
- Small VSD → Normal
- Moderate VSD → Increased cardiac silhouette, increased pulmonary vascular markings
- Severe VSD → Markedly prominent main PA and adjacent vessels, RV hypertrophy
Medical management:-
- Increased calories of feedings
- Diuretics (furosemide 1-3 mg/kg/d)
- Captopril (0.1-0.3 mg/kg every 8 h) to reduce systemic and pulmonary afterload
- Digoxin (5-10 mcg/kg/d) - if diuresis and afterload reduction do not relieve symptoms adequately.
Surgical Care:-
- Transcatheter closure
- Surgical closure
- Indications for surgical repair:
- Uncontrolled CHF
- Large, asymptomatic defects associated with elevated PA pressure
- Pulmonary to systemic flow greater than 2:1.
- Prolapse of an aortic valve
Complications:-
- Eisenmenger complex
- Secondary aortic insufficiency
- Aortic regurgitation
- RV outflow tract obstruction
- Subaortic obstruction
- Infective endocarditis (antibiotic prophylaxis with dental or surgical procedures)
Prognosis:-
- 25 % - spontaneous closure (mostly during the first 2 years of life, can be in adults)
- 7% of infants with large defects and congestive heart failure - also spontaneous closure
- Among small defects, 80% of muscular VSDs closed and 35% of membranous
- 10 % - death during 1st year of life
- Mean life expectancy – 40 years
Atrial septal defect:-
- Frequency: 8-15 %
- Size: small – to complete absence
- Open oval window → no clinics (30% of adults)
- Diagnosis at 1st year – only 40% of cases
Clinics:-
- Rarely symptomatic
- Decreased exercise tolerance
- Large shunt → fatigue, dyspnea and arrhythmias
Physical exam:-
- Moderate systolic murmur in 2nd intercostal space on the left border of sternum
- Accent of S2 over pulmonary artery (pulmonary hypertension)
- Signs of cardiac enlargement
ECG:-
- Right ventricular hypertrophy (lengthened PR interval and incomplete right bundle branch block)
- Atrial enlargement (P wave)
Chest x-ray:-
- Prominent right atrium
- Prominent main pulmonary artery
- Increased heart size and pulmonary vascularity
Complications:-
- Sinus node dysfunction
- Pulmonary venous obstruction
- Atrial fibrillation
- Pulmonary hypertension
- Pericardial effusion or post-pericardiotomy syndrome
Prognosis:-
- Poor if CHF at early age
- Mean life expectancy – 40 years
- Best time for surgery – 1st two decades of life
- No Px for septic endocarditis
Patent ductus arteriosus:-
- Frequency: 10-25 %
- Prematures: 50-80%
- Normal finding at 1st week of life
- Ductus between descending aorta and pulmonary artery bifurcation
Clinics:-
- Repeated respiratory infections
- Later – liver enlargement, cyanosis
- Growth retardation
- Septic endocarditis
- CHF
Physical exam:-
- Loud systolic or systolic-diastolic murmur in the 2nd intercostal space left from sternum
- 1st sound accent over pulmonary artery
- Murmur diminishes at deep breath-in
- Murmur disappears with pulmonary hypertension → appears again with shift reverse
Chest X-ray:-
- LV enlargement; later + RV enlargement
- Prominent pulmonary vessels
Management:-
- Can be closed with indometacin prescription (PG E2 & I2 synthesis inhibitor) – 0.1 mg/kg q8h IV first 8-14 days of life
- Surgery best after 6 months but before severe pulmonary hypertension
Prognosis:-
- Many defects will spontaneously close before 6 mo of age
- Without surgery mortality is 20%
- Mean life expectancy is 35 years
Coarctation of aorta:-
- 5-8% of all congenital heart defects
- May occur as isolated defect or in association bicuspid aortic valve, ventricular septal defect and others
Clinics:-
- Infants – CHF (acute afterload increase after ductus arteriosus closure)
- Older children – hypertension (enough time for collaterals development)
- Left ventricle overwork → increased wall stress and compensatory ventricular hypertrophy
Physical exam:-
- Blood pressure discrepancies between upper and lower extremities
- Reduced or absent lower extremity pulses
- Differential cyanosis (pink upper extremities with cyanotic lower extremities) - rare
- Murmur: nonspecific, under the left scapula
Chest X-ray:-
- Early onset of CoA: cardiomegaly, pulmonary edema, and other signs of CHF.
- Late onset of CoA: cardiomegaly, arch indentation in the area of the coarctation, and rib notching
ECG:-
- Early onset of symptoms: RV rather than LV hypertrophy and evidence of ischemia.
- Late onset of symptoms: LV hypertrophy and signs of LV ischemia or strain.
Other tests:-
- Preductal and postductal pulse oximetry readings
- Cardiac catheterization (evaluation and possible balloon aortoplasty)
Management:-
- Prostaglandin E1 (0.05-0.15 mcg/kg/min) IV to open the ductus arteriosus
- Treatment of hypertension (beta-blockers and vasodilators)
- Treatment of CHF and shock in infants
Surgery:-
- End-to-end anastomosis
- Patch aortoplasty
- Left subclavian flap aortoplasty (left subclavian artery is brought back toward the left carotid artery to enlarge an area of transverse arch hypoplasia)
Complications:-
- Hypertension
- Intracranial hemorrhage and aneurysms
- Aortic rupture or dissection
- CHF
- Recurrent coarctation after surgery
- Aortic aneurythm
- Paralysis (spinal cord ischemia)
- Cardiomyopathy
Prognosis:-
- Mean life expectancy is 35 years
- Without surgery 1-st year mortality is 25%
- Requires bacterial endocarditis prophylaxis
Transposition of magistral vessels:-
- Aorta comes from RV and pulmonary artery comes from LV → 2 separated circulations
- No disturbance of fetal circulation
- Postnatal life is only possible with blood shunts (VSD, ASD, PDA)
Clinics:-
- Early total cyanosis from birth, not responsive to oxygen
- Tachycardia, tachypnoe, decreased BP
- Developmental deficit
- CHF by 1st-2nd month of life
Physical exam:-
- Murmurs – due to other defects (VSD, ASD, PDA)
- Cardiac borders widening
Chest X-ray and ECG:-
- Signs of RV (or both) hypertrophy
Management:-
- Urgent surgery!
Prognosis:-
- 95% die during 1st year of life without surgery
- Mean life expectancy is 3 months
Fallot’s tetralogy:-
- Most common among cyanotic heart defects
- Right-to-left shunt
Defects of TOF:-
- Ventricular septal defect
- Dextraposition of the aorta
- Obstruction of the right ventricular outflow tract (PA stenosis)
- Right ventricular hypertrophy
- Pentade: + Atrial septal defect
- Triade: no VSD, shunt through Open oval fenestra
Clinics:-
- 4 phases:
- “Relative stable well-being”
- “Gray attacks”
- “Blue attacks”
- “Stabilization of the condition”
“Relative stable well-being”:-
- First 4-6 weeks of life
- PDA & Physiologic polycytemia → mild clinics and mild murmur (if any)
“Gray attacks”:-
- First 2-9 months of life
- Hypoxic attacks after physical strains (feeding, anxiety) – 20-25 times per day
- No cyanosis
- No complaints between attacks
- Failure to thrive
“Gray attacks” - Hypoxic attacks:-
- Sudden dyspnoe
- Grayish skin color
- Crying
- Short-period loss of consciousness
- Short-period seizures
“Blue attacks”:-
- 9 months – 3-5 years of life or all life long
- Systemic cyanosis first at attacks, then permanent
- Drumstick fingers
- Polycytemia
- Polyhlobulinemia
- Paresis and palsies (brain hemodynamics disturbances)
“Blue attacks” - Hypoxic attacks:-
- Involuntary position (knees at chest, older – squatting down): aortic pressure is increased → better shunt to pulmonary artery
- Cyanosis and dyspnea
“Stabilization of the condition”:-
- After 3-5 years:
- Permanent cyanosis, but without attacks
- Tachypnea at rest
- Murmus is less
- ECG, X-ray, Echo - worse
Physical exam:-
- Murmur of VSD
- Decreased 2nd sound over pulmonary artery
ECG:-
- Right ventricular hypertrophy
- Left ventricular overload and some left ventricular enlargement
- Right atrial enlargement may also be present
Chest X-ray:-
- Aneurysmally dilated central pulmonary arteries with otherwise normal peripheral pulmonary vascularity.
- Cardiomegaly results from dilation of the right ventricle, particularly its outflow tract (infundibulum)
- Appearance of “boot”
Management:-
- Attacks – position, oxygen, sedatives
- Surgery!
Prognosis:-
- Without surgery – 75% mortality before 2 years of age
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