Glossary
Starting with A for "ACE inhibitor" and continuing through to Y for "Yolk Sac Tumour", we give you succinct explanations for scientific and medical terms in clear and simple words.
- HaemagglutinsName for substances which cause the agglomeration of blood cells (haemagglutination), e.g. the surface antigens of certain viruses, such as the measles, mumps, German measles and influenza viruses.
- HaemoglobinAbbreviated to Hb
Haemoglobin is the so-called red blood dye and is a vertebrate protein which contains iron and which transports oxygen. It occurs predominantly in red blood cells (erythrocytes).
- Haemophilus influenzaealso known as Influenza Bacteria
Bacterium, that used to be thought to be the cause of influenza. It is now regarded as the cause of secondary diseases after respiratory viral infections, e.g. when influenza caused by influenza viruses is already present. Haemophilus influenzae type b in babies and small children is the primary cause of inflammation of the cerebral membrane (meningitis) and of the larynx, more rarely of pneumonia, sepsis, inflammation of the paranasal sinuses or otitis media.
Prevention
Protective vaccination against Haemophilus influenzae type b for babies and small children. - HaemorrhoidsKnot-like widening of the blood vessels round the anus. They may arise during chronic constipation with intense pressure by defecation, or with low roughage nutrition or protracted misuse of laxatives for an extended period. Haemorrhoids may also develop during pregnancy, from sedentary work, from lack of movement or from disturbances in blood flow through the liver (e.g. Liver Cirrhosis).
4 Stages are distinguished:
Stage 1: Light protrusion which is not externally visible or palpable;
Stage 2: Haemorrhoids which protrude during pressing and which draw back spontaneously;
Stage 3; Haemorrhoids which protrude during pressing and which must then be pushed back with the finger;
Stage 4; Haemorrhoid knots which cannot be pushed back.
Symptoms: The main symptoms of haemorrhoids are intestinal bleeding (pale blood) and itching round the anus. From stage 3 there can also be secretion of slime (mucus). There can also be a dull feeling of pressure and burning and pain in the rectum. There may also be prolapse of the anus and inflammation, with eczema and ulceration.
Complications: Problems may occur from intense bleeding, possibly with resulting anaemia. Prolapsed haemorrhoids can also be pinched and faecal incontinence may develop.
Diagnosis: The disease can be diagnosed on the basis of a rectal examination. Other sources of bleeding must sometimes be excluded by performing an enteroscopy (inspection with a mirror) or an X-ray after a contrast enema. Haemorrhoids must be distinguished form tumours, inflammation, thrombosis and injuries in the anal region.
Therapy: Conservative therapy consists of stool regulation (soft defecation), anal hygiene, use of anti-inflammatory ointments or suppositories and sometimes in loss of weight. Haemorrhoids may also be cauterised (obliterated by chemical treatment) or removed by operation in various ways. - HandicapGeneral term for a restriction in the ability to sense, think, speak, learn and/or behave. The World Health Organisation makes a distinction between impairment, disability and handicap. A handicap either requires special individual effort to be made good, assistance from others or physical aids. A general distinction is made between physical handicap (e.g. paraplegia), mental handicap (e.g. extreme difficulty in learning) and psychiatric handicap (e.g. from chronic psychiatric disease).
- Hardening of the arteriesColloquial expression for arteriosclerosis
- HDLAbbreviation for high density lipoproteins
Lipoproteins of high density which are formed in the liver and intestinal mucosa. HDL consists 50 % of proteins and 50 % of cholesterol and phospholipids. HDL transports cholesterol from cells into the liver. A high blood concentration of HDL is believed to reduce the risk of arteriosclerosis.
- HeartMuscular hollow organ which has the task of keeping the blood stream in motion in the blood vessels, which it does by alternating contraction (systole) and relaxation (diastole) of the atria and chambers (ventricles) (cf. circulation of the blood). The heart is enclosed in the pericardium on the diaphragm and between the lungs. A partition, the septum, divides the heart into left and right halves. Each half is then split into an upper and weaker section, known as the atrium, and a stronger and lower section known as the ventricle. The left ventricle is stronger than the right.
The heart wall consists of three layers; internal wall (endocardium), intermediate layer (myocardium) and external wall (pericardium).
The caval veins (vena cava superior and vena cava inferior) carry low oxygen blood from the body into the right atrium. The pulmonary veins (venae pulmonales) carry oxygen rich blood from the lungs into the left atrium. The trunk of the pulmonary arteries (truncus pulmonalis) leaves the right side of the right ventricle and transports low oxygen blood into the lungs. The large artery, the aorta, transports oxygen rich blood from the left ventricle to the rest of the body.
The heart has four valves, which are attached to the skeleton of the heart. The leaflet valves can seal the passage between the atria and ventricles. The semilunar valves lie at the start of the truncus pulmonalis and the aorta and hinder the reflux of blood into the ventricles during diastole.
- Heart catheterisationMethod to investigate the cardiovascular system using preformed catheters of small diameter which are visible in X-rays
Performance
For the left heart catheter, an artery is pierced (punctuated) or surgically opened. For the right heart catheter a vein is pierced. Probing of all central sections of the heart and vessels is then possible.
Uses
Many sorts of investigations can be carried out with heart catheterisation. These include measurement of pressure, probing the heart cavities and sections of the vessels which are near to the heart (controlled by X-rays), registration of pressure-time curves at rest and under various conditions of stress, to evaluate cardiac function. Calculation of various parameters related to blood flow, inclusion resistance to circulation, surfaces of valve opening, heart work, work per beat, power per beat. Therapeutic uses include coronary angioplasty (see PTCA), coronary thrombolysis (dissolution with drugs of a blood clot in the coronary arteries) after acute myocardial infarction or when a heart pace maker is being inserted. - Heart cyclealso known as heart period
Duration of a total action of the heart, consisting of systole (development of tension and contraction of the heart muscle) and diastole (relaxation of the heart muscle after a systole). - Heart echoColloquial expression for echocardiography.
- Heart failurealso known as myocardial insufficiency or heart muscle weakness.
Inadequate function of the heart, which is no longer capable of pumping blood in the required manner.
Classification
On the basis of the affected section of the heart, as left, right or bilateral heart failure;
on the basis of the stability of the equilibrium, which is influenced by therapy and the body's mechanisms, as compensated or decompensated heart failure; on the basis of the clinical course as acute or chronic heart failure; on the basis of the severity as failure at rest or on exercise. The New York heart Association (NYHA) has classified heart failure into four grades, depending on the severity of the symptoms: Grade I: Asymptomatic at rest and during exercise; Grade II: Restricted functional capacity at intermediate physical stress, Grade III: Clear restriction to functional capacity even at low levels of physical stress, but no symptoms at rest, Grade IV: symptoms even at rest.
Causes
Myocardial Infarction, cardiomyopathy, in-born or acquired heart defect, high blood pressure (hypertension), cardiac arrythmias, inflammation of heart muscle
Symptoms
The function of the heart is restricted and no longer in equilibrium, so that there are signs of congestion in both the systemic and pulmonary circulation (pulmonary oedema, water collects in tissues, particularly the legs), reduction in perfusion of the peripheral circulation, increase in heart size, increased heart rate, cyanosis (blue-red colouration of the skin and mucous membranes from low blood oxygen)
Diagnosis
Symptoms and physical examination, echocardiography (ultrasound study of the heart), electrocardiography, chest X-ray
Therapy
ACE inhibitors, Beta-receptor blockers, diuretic drugs, cardiac glycosides, drugs to increase the strength of the heart, organic nitrates, other - Heart muscle weaknesssee heart failure
- Heart periodsee heart cycle
- Heart sonographysee echocardiography
- hematocritpercentage of red blood cells in the blood
- hematologicalpertaining to the blood and blood-forming tissues
- hematopoiesisthe formation of blood or blood components in the body; also called hemopoiesis
- hemodialysisthe process of removing blood from an artery, purifying it by dialysis, adding vital substances and returning it to a vein
- hemoglobin concentrationa measure of the amount of hemoglobin in the blood
- hemoglobin cyclinga phenomenon that occurs in dialysis patients receiving ESA therapy in which hemoglobin levels fluctuate in a cyclic pattern
- hemoglobin levelThe hemoglobin level indicates how much red blood pigment is contained in the red blood cells.
Normal/reference values
The level measured in otherwise healthy men should be between 14 and 18 g/dl.
The level measured in otherwise healthy women should be between 12 and 16 g/dl.
The normal value is subject to considerable individual variation because the body adjusts both the amount of hemoglobin (red blood pigment that binds oxygen) and the number of erythrocytes (red blood cells) to its needs. Hemoglobin measurement is a simple routine analysis with rapid turnaround of results. Unexplained low hemoglobin levels always require medical clarification. - hemolysisthe breakdown of red blood cells
- hemolytic anaemiaanemia caused by excessive destruction of red blood cells
- HeparLiver.
- HeparinHeparin is a substance which inhibits blood coagulation and occurs in the lungs, liver , spleen and other tissues. It inhibits the action of certain coagulation factors, the aggregation of blood platelets and the contraction of blood clots.
Clinical uses
Heparin is used for the prevention and treatment of thromboses and emboli and to prevent undesired blood clotting, for instance in blood dialysis for kidney failure.
Side-effects
Drop in the number of platelets caused by heparin, allergies, bleeding, increase in the enzymes which are mostly formed in the liver (transaminases), hair loss, osteoporosis. - Hepatic VeinsThe liver veins take up the blood which has been purified in the liver and empty into the vena cava. There the blood returns to the main circulation.
- Hepatitis Aalso known as epidemic hepatitis
Acute inflammation of the liver (hepatitis) caused by hepatitis A viruses (abbreviated as HAV)
Frequency: Hepatitis A is the most frequent infectious form of acute hepatitis throughout the world. It is a typical travellers disease (Mediterranean, Africa, South America, the East, ex-Soviet Union).
Infection: Transmission of the virus usually occurs through consumption of drinking water or food which has been contaminated with faeces, contact with excretions (nursing) or through sexual contact. The interval between infection and outbreak of the disease is 15-45 days, mostly 25-30 days.
Symptoms: There are often no symptoms during the disease. Symptoms may develop 2-8 weeks after infection and mostly resemble flu, with slightly raised temperature, general feeling of being unwell or washed out, sense of fullness, pain in the upper abdomen and diarrhoea. Jaundice (Icterus) is fairly rare. The clinical course of the disease is occasionally delayed or may exhibit two peaks (after up to 6 months). A sudden massive attack is rare (0.1%) and chronic disease does not occur. The disease clears up after about 4 weeks without long term effects. While the virus is being excreted, there is a danger of being infected from the faeces. This decreases rapidly when the symptoms become evident. There is immunity after the disease.
Diagnosis: Clinical chemistry: Detection of acute antibodies in the blood for at least 3 months, detection of other specific antibodies in the blood for the rest of the patients life, indicating immunity.
Therapy: There is no specific drug treatment.
Prophylaxis: General hygienic measures, active immunisation by inoculation (see Hepatitis A Vaccine). Passive immunisation (administration of antibodies) affords protection for about 3 months. When travelling in countries with poor hygiene, drinking water should be disinfected and no unpeeled fruit, ice or sea food should be consumed. Condoms should be used during sexual intercourse. - Hepatitis A VaccineVaccine for active immunisation (Protective Inoculation) against hepatitis A virus (cf. Hepatitis A) from killed hepatitis A viruses, cultured in human cells and bound to aluminium hydroxide. There is usually protection for 5 years after two inoculations (control of the blood concentrations is necessary). Inoculation is recommended for individuals at risk and for travellers in areas in which the disease is frequent (also in combination with hepatitis B vaccine). Cf. Hepatitis Viruses, Acute hepatitis.
- Hepatitis BAcute inflammation of the liver (hepatitis) caused by hepatitis B viruses (abbreviated as HBV)
Frequency: More than 2.5 thousand million individuals throughout the world are infected with HBV.
Infection: The most frequent transmission routes are transmission from mother to child during birth and sexual transmission (ca. 50% of the infections which are highly transmissible), shared needles by infected drug addicts and blood or blood products. The latter route has become rare since the introduction of standard controls for blood donors. Special groups at risk or risk factors are drug addicts, recipients of blood products, close contact with infected individuals and frequent changes in the sexual partner.
Symptoms: The interval between infection and outbreak of the disease is 1-6 months. In 30-50% of patients, symptoms then develop, such as pains in the joints, rash, general feeling of being unwell, feeling of fullness, upper abdominal pain and kidney problems (rare). Sudden illness with acute liver failure is rare (ca. 1%). In ca. 5-10% of cases, chronic hepatitis may develop. The risk of this is clearly greater with drug addicts who inject themselves (ca. 20-25%).
Diagnosis: Clinical chemistry: Detection of antibodies and virus genes in the blood.
Therapy: There is no specific drug therapy. Avoidance of factors which damage the liver.
Prophylaxis: General use of disinfectants, screening of blood from blood donors, if possible avoidance of treatment with blood products, use of condoms. Vaccination: active (see Hepatitis B Vaccine) or passive immunisation (specific antibodies). The two routes may be combined if acute infection is suspected; cf. Protective Vaccination. - Hepatitis B VaccineVaccine isolated by genetic engineering and which is used for the active immunisation of groups at high risk of hepatitis B virus (see Hepatitis B), particularly for protective inoculation of dialysis patients, patients who frequently receive blood or blood products, individuals with frequently changing sex partners, drug addicts and medical personnel.
The basic immunisation consists of two or three inoculations and a booster after 6 to 12 months. A further booster should be administered after ca. 5 years (control of the blood concentration is necessary). As it takes a relatively long time before the protection is fully effective, passive immunisation (antibodies to hepatitis B virus) is recommended to individuals who are suddenly exposed to a high rate of infection. Protective immunity is present in more than 95% of inoculated individuals one year later. Combination vaccines against hepatitis A and B are also available. Cf. Hepatitis Viruses, Hepatitis, acute. - Hepatitis CAcute inflammation of the liver (hepatitis) caused by hepatitis C viruses (abbreviated as HCV)
Frequency: The World Health Organization estimates that more than 170 million individuals throughout the world are chronically infected with HCV. Hepatitis C is the most frequent form (ca. 90%) of liver inflammation as a result of blood transfusions.
Infection: Transmission usually occurs from (untested) blood or blood products and the shared use of needles when injecting drugs. Transmission from mother to child or through sexual contact is rare. The most important risk groups are drug addicts and recipients of blood products. Infection from transplanted organs is possible.
Symptoms: The interval between infection and outbreak of the disease is 2-26 weeks. Symptoms only develop in 30% of cases. These include exhaustion, a feeling of being washed out, symptoms like flu and (rarely) jaundice (Icterus). Sudden and massive illness is rare (ca. 1%). In 50-80% of cases, the clinical course is chronic. In 5-10% of cases, cirrhosis of the liver develops and in 1-5% of cases carcinoma of the liver.
Diagnosis: Clinical chemistry: Detection of antibodies and viral RNA in the blood.
Therapy: Drugs.
Prophylaxis: General use of disinfectants, blood from blood donors screened, avoidance if possible of the use of blood products, use of condoms. Inoculation is not possible. - Hepatitis DAcute inflammation of the liver (hepatitis) caused by hepatitis D viruses (abbreviated as HDV)
Occurrence: The virus occurs throughout the world, but particularly in the Mediterranean, in the Balkans, in the Middle East and in parts of Africa and North America. There are only isolated cases in Central and Northern Europe, in groups at high risk.
Infection: Transmission occurs through direct blood contact, infected blood products, unprotected sexual intercourse and from mother to child during birth. The most important groups at risk and risk factors are drug addicts, recipients of blood products, medical personnel, close contact with infected individuals and frequent changes in the sexual partner.
Symptoms: The interval between infection and outbreak of the disease is 40-160 days. Illness only occurs if there is simultaneous infection with HBV (see Hepatitis B) or if the patient is already chronically infected with HBV. Although the latter case is rare, the clinical onset is often sudden; the course is almost always chronic and usually severe.
Diagnosis: Clinical chemistry: Detection of antibodies or viral RNA in the blood.
Therapy: There is no standard treatment.
Prophylaxis: Protective inoculation against hepatitis B (see Hepatitis B Vaccine).
Otherwise general use of disinfectants, screening of blood donors blood, avoidance if possible of the use of blood products, use of condoms. - Hepatitis EAcute inflammation of the liver (hepatitis) caused by hepatitis E viruses (abbreviated as HEV).
Occurrence: The virus is endemic in India, North Africa, Central and South America and probably also in the Balkans.
Infection: Transmission occurs as a result of consumption of food or drinking water which is contaminated with faeces, or from contact with excretions (nursing) or through sexual contact.
Symptoms: The time between infection and outbreak of the disease lies between 2 weeks and 2 months. The symptoms are frequently only mild and resemble flu, with a slight increase in temperature, general feeling of being unwell or washed out, feeling of fullness, pain in the upper abdomen and diarrhoea. The clinical course may be acute and severe in up to 25% of patients who are pregnant, but in only 5-10% of other patients. This may then lead to acute liver failure, which is usually fatal. There is the possibility of infection when virus is secreted in the faeces.
Diagnosis: Clinical chemistry: Detection of antibodies and virus RNA in the blood.
Prophylaxis: General hygienic measures. When travelling in countries with poor hygiene, drinking water should be disinfected and no unpeeled fruit, ice or sea food should be eaten. There is no protective inoculation or passive immunisation. - Hepatitis GAcute inflammation of the liver (hepatitis) caused by hepatitis G viruses (abbreviated as HGV).
This is a form of acute liver inflammation which was discovered in 1995. It is presumed to occur frequently throughout the world, has many similarities with hepatitis C and is often accompanied by simultaneous or additional infection with hepatitis B virus (cf. Hepatitis B) and hepatitis C virus. - Hepatitis VirusesPathogens of a generalised and infectious disease in man which occurs at least partially in the liver
(Acute Hepatitis, Chronic Hepatitis).
Classification:
1. Hepatitis A Virus (Abbr. HAV):
Pathogen of hepatitis A. This is a cube-shaped virus of diameter 27 nm, which can be detected in man and in some great apes.
2. Hepatitis B Virus (Abbr. HBV):
Pathogen of hepatitis B. This is a cube-shaped virus of diameter 42-45 nm.
3. Hepatitis C Virus (Abbr. HCV):
Pathogen of hepatitis C. This is a virus of diameter 50-60 nm and with a great potential for genetic change. There are at least 6 genetically different types (1-6) and 3 subtypes (a-c), with highly variable geographical distribution.
4. Hepatitis D Virus (Abbr. HDV):
Pathogen of hepatitis D. This is a naked minivirus or viroid, which only consists of genetic information.
5. Hepatitis E Virus (Abbr. HEV):
Pathogen of hepatitis E. This virus has been assigned to its own genus; it only occurs in man.
6. Hepatitis G Virus (Abbr. HGV):
Pathogen of hepatitis G. This virus is similar to HCV. It only rarely causes inflammation of the liver. Several studies have suggested that there are further hepatitis viruses. - Hepatitis, acuteAcute general inflammation of the liver. A general reaction of the liver to noxious factors of many different types. The term is also frequently used for liver inflammation which is specifically caused by hepatitis viruses.
Symptoms: Symptoms only occur rarely, in particularly in children (exception: Hepatitis A, Hepatitis E). In cases when symptoms occur, these develop gradually over 2 to 9 days and are generalised, including a feeling of being severely ill, nausea, loss of appetite, often markedly raised temperature, sometimes pain in the joints and rash for a short time. The heart rate may be decreased. After this comes the phase in which the liver is attacked (ca. 6-10 weeks). In about a third of all cases this involves jaundice (Icterus), itch, discolouration of the faeces, darkening of the urine and sometimes enlargement of the liver and spleen.
Complications: Obstruction of the bile flow within the liver may develop (cholestasis syndrome). The most severe, massive and acute clinical forms, particularly hepatitis D and hepatitis E, may be fatal, when there is no possibility of liver transplantation. Transition to chronic liver inflammation (Chronic Hepatitis), the development of liver cirrhosis and even liver cell cancer (Liver Cell Carcinoma) are possible if the viruses remain in the liver.
Diagnosis: Clinical chemistry: Detection of raised liver enzymes. If there is jaundice, bilirubin and urobilirubin are raised. Increase in blood iron. The count of white blood cells is often reduced (cf. Probes of Liver Function). Detection of the disease in the blood with specific antibodies.
Therapy: Aside from general measures such as avoiding alcohol and drugs (particularly those which are poisonous to the liver) and bed rest in the acute phase, there is no specific therapy for acute hepatitis.
Forms:
1. Acute liver inflammation from hepatitis viruses, also known as infectious hepatitis:
a) Hepatitis A
b) Hepatitis B
c) Hepatitis C
d) Hepatitis D
e) Hepatitis E
f) Hepatitis G
g) so-called hepatitis of unknown origin. Name for acute liver inflammation, which is presumed to be due to a viruses which are as yet unknown, as hepatitis viruses A to G and other viruses which are typical of the liver are not detectable.
2. Acute liver inflammation in the context of other infectious diseases which affect the whole organisms:
a) from viruses, particularly herpes viruses, Coxsackie viruses, arboviruses and arenaviruses (e.g. Lassa fever)
b) from bacteria , particularly brucellosis, leptospirosis and typhus
c) from parasites, such as malaria and amoebae
3. Toxic acute hepatitis from drugs or alcohol
4. Acute liver inflammation in the context of other liver diseases (e.g. tumours, such as primary liver cell carcinoma or metabolic diseases). - Hepatitis, autoimmunesee Chronic Hepatitis.
- Hepatitis, chronicGeneral inflammation of the liver which lasts for longer than 6 months. This is a general reaction of the liver to harmful factors of many different sorts. There are two different forms, with apparently about the same chance of being cured:
1. Chronic persistent hepatitis (prolonged) hepatitis (Abbreviation: CPH)
2. Chronic aggressive (destructive) hepatitis (Abbreviation CAH)
Symptoms: Chronic hepatitis either exhibits no symptoms or symptoms which are not typical of the disease (e.g. exhaustion, loss of energy). In the inflammatory phase, the clinical picture is the same as for acute liver inflammation (Acute Hepatitis). The symptoms of liver cirrhosis may develop after this.
Complications: Chronic liver inflammation may develop into liver cirrhosis. There is also a danger that cancer of the liver (Liver Carcinoma) may develop
Diagnosis: Clinical chemistry: Increased liver values (cf. Probes of Liver Function), determination of antibodies, ultrasound investigation of the liver, computer tomography (CT), nuclear spin tomography, extraction of a tissue sample from the liver (Liver Biopsy), ventroscopy.
Similar diseases: Certain forms of liver cirrhosis and some metabolic diseases of the liver have a similar clinical course to chronic hepatitis.
Therapy: General measures such as avoiding alcohol and certain drugs, particularly those which are poisonous for the liver, bed rest, drugs (alpha-Interferon, Glucocorticoids), liver transplantation.
Forms:
1. Chronic liver inflammation from infection with hepatitis viruses
a) Hepatitis B:
Most frequent form of chronic liver inflammation (frequency throughout the world, ca. 5%). About 20% of individuals with acute infection develop chronic liver inflammation, which mostly develops into liver cirrhosis if not treated.
b) Hepatitis B and Hepatitis D: chronic liver infection, mostly as a consequence of additional infection with hepatitis D virus. The prospects of cure are poor, even with treatment.
c) Hepatitis C
Frequent chronic inflammation of the liver. Clinical course mostly not so severe. Occasionally occurs together with autoimmune diseases. Long term successful treatment is only achieved in 25% of patients. Treatment is less successful when the patient is old, if the disease has been present for a protracted period, or if the blood virus count is high.
2. Autoimmune chronic liver inflammation
This autoimmune disorder occurs particularly in young women. There is a hereditary predisposition and other organs, such as the thyroid and joints, are often affected. Treated with drugs.
3. Toxic chronic liver inflammation
This form of liver inflammation is caused by drugs, toxins or alcohol. There is no specific treatment for the disease, but the patient should avoid contact with the substances which cause the disease. - Hepatitis, neonatalUnusually protracted neonatal jaundice is characteristic of this condition (see Icterus neonatorum, Icterus). The chances of a cure are good.
Cause: Neonatal jaundice can be caused by viral infections, feeding by infusion, increased production of metabolic products which stain yellow (posthaemolytic cholestasis) or a hereditary genetic error.
Diagnosis: X-ray detection of substances from the bile. Investigation of tissue samples from the liver
Similar diseases: Hepatitis B transmitted during birth and hereditary obstruction of the bile ducts are similar to neonatal jaundice.
Therapy: Treatment is carried out according to the symptoms. - Hepatitis, Protective VaccinationProtective vaccination against liver inflammation caused by viruses (cf. Acute Hepatitis, Hepatitis A Vaccine, Hepatitis B Vaccine). Vaccines to hepatitis are now mostly produced by genetic engineering. They contain either inactivated proteins from hepatitis A viruses, which stimulate the body to develop immunity without falling ill, or they consist of antigen from the surface of hepatitis B viruses. The vaccination against hepatitis A consists of two injections which are administered within 6 to 12 months, depending on the preparation. Protection lasts for about 10 years. Vaccination against hepatitis B can consist of three injections. The second injection is one month after the first and the third injection after 6 to 12 months. Hepatitis B vaccination only protects from infection for 3 to 5 years. There is now a combined vaccine for hepatitis A and B. This must be administered three times (second injection after one month, third after 6 to 12 months).
- HepatocytesMedical term for liver cells. Numerous important chemical processes occur in liver cells (see Liver Functions).
- HepatomaMedical expression for liver tumours*.
- HepatovirusType of virus which infects the liver, including hepatitis A virus. This virus occurs in man and in monkeys and may be concentrated in mussels. The hepatitis A virus can cause illness in man. It is transferred by smear (or dirt) infection in faeces and excretions. The course of the infection may be unnoticed or may be accompanied by symptoms such as liver inflammation and jaundice. In rare cases, the disease may develop suddenly and massively (cf. Hepatitis Viruses).
- Hereditary diseasessee genetic diseases
- Hereditary traitsee gene
- Hereditary traitHereditary factor (gene) as cause of certain diseases. Genetically-linked absence of an enzyme can cause characteristic metabolic abnormalities.
- Heroin AddictionThis is a physical and mental dependence on heroin, which is either taken as snuff or (most usually) injected into the circulation, and which leads to feelings of elation and giddiness, but which also depresses the central nervous system. Discontinuing the drug in patients with heroin dependency leads to a severe withdrawal syndrome, with giddiness, diarrhoea, vomiting, sweating attacks, increase in blood pressure, insomnia and pain. The withdrawal syndrome reaches its peak ca. 36 to 72 hours after the last injection and can last 5 to 8 days. Protracted heroin dependency usually leads to severe social consequences, as acquisition, possession and dealing with the narcotic are criminal offences. There is also an increased risk of diseases which are transmitted by blood if used syringes are employed, so-called needle sharing. These include HIV disease (AIDS), hepatitis B and hepatitis C.
Therapy: The goal is, in principal, freedom from the drug. With this aim in mind, there is usually withdrawal under in-patient conditions, followed by long term and intensive psychological and social care (dishabituation). Under certain conditions, drug replacement therapy with methadone is performed as an alternative treatment. - HexosesMonosaccharides with six carbon atoms. There are eight aldoses (e.g. glucose, mannose, galactose) and six ketoses (e.g. fructose), with different chemical structures.
- High blood pressuresee hypertension
- high density lipoprotein (HDL) cholesterola form of cholesterol that circulates in the blood; HDL is commonly called good cholesterol because high blood levels lower the risk of heart disease; the normal level of HDL cholesterol in adults is >45 mg/dl for men and >55 mg/dl for women
- High pressuresee hypertension
- histidineone of the 20 amino acids that are used as building blocks for proteins; must be obtained from the diet
- HistiocytomaSmall benign tumour on the lower extremities which is often brownish or yellowish. The tumour can occasionally become a malignant tumour (dermatofibroma).
- HIVAbbreviation of the English term, human immunodeficiency virus. A virus from the group of the retroviruses. A distinction is made between HIV-1 and HIV-2. The latter occurs mostly in East Africa. The virus infects cells of the immune system such as T-helper cells and others, which normally provide defence against infective agents and which annihilate body cells with abnormal changes and leads to the destruction of these cells. HIV remains permanently in the macrophages.
- HIV Dementiaalso known as HIV encephalopathy
- HIV Diagnosissee HIV Disease
- HIV DiseaseInfection of the immune system with the human immunodeficiency virus (HIV), which weakens the immune system, leading in this way to various opportunistic infections and to tumour disease.
Occurrence: Throughout the world, with regional concentration in sub-Saharan Africa, Latin America and in parts of Asia: The World Health Organisation (WHO) estimates that ca. 40 million individuals throughout the world are infected with HIV. The first cases were described in the USA in 1981 and were in homosexual men, addicts of injected drugs and patients with abnormal blood coagulation. It is assumed that the first cases occurred in the late 1970s, but were not classified as coming from a single disease. In 1983 the human immunodeficiency virus was identified as the cause of this disease. In Europe and in North America today most HIV patients are homosexual men and addicts of injected drugs. In contrast, in Central and East Africa, Asia and in the ex-Soviet Union, a considerable proportion of the whole population is already infected.
Transmission routes: The most frequent route for transmission is unprotected sexual intercourse, followed by sharing of syringes and needles when injecting drugs. Transmission between mother and child is possible during pregnancy or birth. The virus can also be transmitted in blood or blood products (cf. blood replacement), although this has become rare since the introduction of routine examinations of blood products. The risk of transmission and infection depends on the type and duration of the contact with infectious substances. If the administration of the virus is massive (as in the transfusion of infected blood), the danger of infection is greater than when small quantities of blood are transferred. Infected individuals with a heavy virus load (cf. virus load) are also more infectious than individuals with a low virus load. Infection is also favoured by additional factors, such as poor nutrition, vitamin A deficiency or simultaneous infection of the urinary or genital organs.
Clinical course: If the disease is left untreated it develops in the following phases:
Seroconversion disease: 6-16 weeks after infection transient symptoms develop, including fever, feeling of being washed out, swelling of the lymph nodes, sometimes rash and other non-specific symptoms.
Asymptomatic phase: For an average of 8 to 12 years there are normally no symptoms from HIV. In this phase, the virus reproduces (replicates) and infects more immune cells.
Initial immune deficiency: also known as AIDS-related complex. Diseases develop which are caused by the immune deficiency, but which are not the so-called AIDS defining diseases. Examples are infections of the area of the mouth and throat with the fungus Candida albicans, viral infection of the tongue (oral hairy leukoplakia), shingles (Herpes zoster).
AIDS: Marked immune deficiency with occurrence of the so-called AIDS-defining diseases: e.g. Pneumocystis carinii pneumonia, Toxoplasma infection of the brain, severe cytomegaly infection, Kaposi syndrome, tumours of the lymphatic system (lymphoma) i.a.
Diagnosis: Before the investigation, a thorough consultation should be carried out, to clarify whether there was risk of an infection, why an investigation should be performed and what is the correct procedure with possible results. This consultation can be carried out in specialised units.
In routine diagnosis, tests are carried out to detect the presence of antibodies. These antibodies can be detected in 99% of infected individuals 12-16 weeks after infection. As however these tests can lead to the false detection of antibodies, every positive test which indicates the disease must be confirmed by a second test with another method. This is usually detection of virus-RNA by Western blotting or polymerase chain reaction. During the course of the infection, the virus load, the number of T-helper cells and the CD4/CD8 ratio are measured at fairly large intervals.
Therapy: A distinction is made between the treatment of the HIV disease itself with antiviral therapy and the treatment of the opportunistic infections. Antiviral combination therapy composed of different drugs with different mechanisms of action can reduce or suppress the replication of the virus for an extended period. Side effects may develop during this treatment, some of which are serious. The virus may also develop resistance. It is recommended at the moment to start with the antiviral therapy if the count of T-helper cells is rapidly decreasing, if the count of T-helper cells is under 350 per µl and if there is rapid virus replication or a virus load of above 10,000 copies per ml or an HIV-dependent disease. Since 1996 the antiviral therapy has lead to a reduction in the death rate. It is however not yet possible to cure HIV disease.
Prevention: Avoid contact with blood, blood products, sperm or vaginal secretions. Use of condoms during sexual intercourse, avoid shared use of needles and syringes, avoidance of needle prick injuries by medical personnel, testing of blood and organ donors, prevention of transmission from mother to child by antiviral therapy and caesarean section before the start of the contractions. Protective inoculation is being developed (see HIV Inoculation). - HIV Encephalopathyalso known as HIV dementia
A condition of the brain which occurs in advanced HIV disease. Progressive abnormalities in movement and in the mental state are observed.
Occurrence: Marked in ca. 15% of all AIDS patients. The less extreme form is much more common.
Symptoms: Disturbances in concentration and in memory, reduction in drive (because of decrease in motivating energy), slowing of motions.
Diagnosis: Once HIV infection has been proved, these symptoms can be ascribed to HIV encephalopathy, if all other causes of abnormal brain function have been excluded (such as depression or infection).
Therapy: Antiviral combination therapy, also for protection
Prognosis: HIV encephalopathy reduce survival time in HIV disease - HIV InoculationThe development of an inoculation against the HI virus has not yet been competed. As the virus changes very rapidly, it is difficult to develop an inoculation which gives full protection. The first tests on HIV-infected patients have been successfully performed.
- homeostasisthe maintenance of relatively stable internal physiological conditions (such as body temperature or blood pH) under fluctuating environmental conditions
- Hormone replacement therapyalso known as hormone substitution, oestrogen replacement therapy or oestrogen substitution
Treatment of menopausal problems in women with oestrogens, to make good the loss of natural function of the ovaries. Oestrogens prevent osteoporosis and are used when there are signs of atrophy in the genital region or urinary tract and (controversially) for cardiovascular disease. gestagens can be used in addition to the oestrogens, to avoid benign proliferation of the mucous membrane of the womb, which is caused by oestrogens. There are cases in which hormone replacement therapy should not be carried out, for instance after thrombosis and with some forms of womb or breast cancer.
Drug Treatment
The dosage and manner of use depend on the requirements. The hormones may be taken orally, through the skin or as vaginal capsules, more rarely as an intramuscular injection or as an implant under the skin. For the prevention of osteoporosis, the initial dose is low and this is then slowly increased.
Side-Effects
Oestrogens: Tension in the chest, oedema, increase in weight, abdominal problems (sense of fullness) and others; Gestagens: Signs of intolerance such as acne may occur. When combined treatment is used and side-effects occur, the initial doses are first checked and then either the oestrogen dose is reduced or the gestagen is changed. - Hormone substitutionsee hormone replacement therapy
- HormonesHormones are organic compounds which act as signalling substances between cells and which are often produced in organs which release them directly into blood. As a result of the circulation of the blood, hormones reach the organs they act on, in either the free or bound forms. They are active at extremely low concentrations and influence metabolism in a characteristic manner. The specific actions of hormones are mediated by hormone receptors (see hormone receptors). The complex interactions between hormones, hormone-dependent metabolic products and the nervous system are regulated by feedback control systems. Hormones may be inactivated by metabolic breakdown.
Biochemical classification
1. Steroid hormones; 2. The peptide or proteohormones of the hypothalamus and the pituitary, insulin, glucagon (from the pancreas), parathromone (from the parathyroids), calcitonin (from the C-cells of the thyroid) and the hormones involved in digestion are all formed as prohormones, which are inactive precursors; 3. Hormones derived from aminoacids, e.g. thyroid hormones, adrenaline and noradrenaline, histamine and acetylcholine; 4. Hormones formed from unsaturated fatty acids, such as the prostaglandins.
- Human insulinHuman insulin; Hormone which consists of two polypeptide chains with in all 51 aminoacids (A-chain: 21, B-chain: 30 aminoacids) which are connected to each other by chemical bonds (disulphide bridges). Human insulin differs from bovine insulin by three aminoacids and from porcine insulin by one aminoacid. Bovine and porcine insulin may be used for the therapy of insulin-dependent type 2 diabetes or type 1 diabetes, although bovine insulin in particular is not as well tolerated as human insulin, because of the structural differences. The use of human insulin allows the almost total avoidance of undesired drug effects, such as local allergies.
Production
1. Purely chemical; disadvantage: high costs. 2. Biosynthetic (gene engineering), by inserting the genetic material (DNA) which is responsible for the production of insulin in man into microorganisms (Escherichia coli, Bacillus subtilis or yeast cells). In this way the microorganisms are converted into producers of human insulin or its precursors. 3. Conversion of porcine insulin into semi-synthetic human insulin (abbreviation SHI), with approximately the same activity as porcine insulin. - HungerGeneral feeling which leads to eating. The available levels of glucose in the organism, unrelated to blood sugar concentrations, are most often seen as the trigger, which probably acts through glucoreceptors (cf. receptors) in the middle brain, small intestine, liver and stomach. Cf. appetite.
- Hunger osteopathysee osteopathy, alimentary
- Hunger osteopathysee osteopathy, alimentary
- HypercalcaemiaIncrease in the blood concentration of calcium to more than 2.7 mmol/l, resulting from increased intestinal absorption of calcium, decreased calcium elimination through the kidneys or increased release of calcium from bone tissue.
- Hypercalcaemia syndromeComplex of symptoms which can result from raised blood concentration of calcium (hypercalcaemia): increased urine volume, increased thirst and fluid intake, nausea, vomiting, constipation, muscular weakness, signs of paralysis, lack of strength, cardiac arrythmia, psychological changes which may even include psychosis and calcium deposition in organs (eye, joint cartilage or kidneys).
Complications
Hypercalcaemic crisis with kidney failure, sleepiness, coma and cardiac arrest.
Therapy
If the calcium concentrations are above 3 mmol/l give fluid, diuretics, perhaps bisphosphonates or glucocorticoids.
- HypercholesterolaemiaIncreased blood concentration of cholesterol. Hypercholesterolaemia is a risk factor for the development of arteriosclerosis.
Forms
Primary hypercholesterolaemia, which occurs frequently in a family; secondary form as a result of diabetes mellitus (type 2 diabetes mellitus, type 1 diabetes), excessive thyroid function, liver disease - hypercoagulabilitytendency of the blood to coagulate or form clots more rapidly than is normal
- hyperfiltrationa glomerular filtration rate (GFR) that is above the normal range
- HyperglycaemiaIncreased concentration of glucose in blood (more than 120 mg/dl or 6.7 mmol/l). Occurs for example in type 2 diabetes, type 1 diabetes, recent heart attack, excessive function of the adrenal cortex, shock, carbon monoxide poisoning and disturbances in the central nervous system.
- Hyperinsulinism1. Increased blood concentration of the hormone insulin as a result of increased insulin production, with the consequence of hypoglycaemia (decreased blood sugar concentration. Hyperinsulinism occurs during cellular proliferation in the islets of Langerhans in the pancreas, the site of insulin production, and in patients with insulinoma, a tumour which produces insulin. 2. Insulin resistance with the consequence of hyperglycaemia (increased blood sugar) in patients with type 2 diabetes.
- Hyperkalaemia syndromeSyndrome from an increased blood concentration of potassium (hyperkalaemia).
Causes
Excessive acidification of the body (acidosis, e.g. in diabetic coma), blood transfusion, kidney failure, severe multiple injury, burns (due to potassium release from the destroyed tissue) and others.
Symptoms
1. Lack of energy, weakness, confusion; 2. Low heart rate (bradycardia), sometimes cardiac arrest, cardiac arrythmia, changes in the electrocardiogram; 3. Subjective abnormalities in the senses (parasthesia), e.g. itching, burning feeling on the skin, metallic taste in the mouth, signs of muscular paralysis.
Therapy
Ion exchanger (oral, slow onset of action), alkalinisation (treatment with compensating substances, such as isotonic sodium carbonate solution administered intravenously), glucose-insulin infusion, sometimes dialysis.
- HyperlipidaemiaIncrease in serum lipids (blood fat); collective term for hypercholesterolaemia and hypertriglyceridaemia; see hyperlipopoteinaemias
- HyperlipoproteinaemiasDisturbances in fat metabolism with increased blood concentrations of certain lipoproteins and sometimes changes in the proportions of some lipoproteins. Cf. fat metabolism, hypercholesterolaemia, hypertriglyceridaemia.
Forms
1. Primary hyperlipoproteinaemia: hereditary conditions which are classified into five types, depending on the fundamental defect or on the constellation of the raised lipoproteins. 2. Secondary Hyperlipoproteinaemias; Occurrence, e.g. in diabetes mellitus (type 2 diabetes mellitus, type 1 diabetes), overweight, inflammation of the pancreas, excessively low thyroid function, after alcohol consumption, fatty meals or from drugs (e.g. hormonal contraceptives).
Therapy
Treatment of the underlying disease, loss of weight, diet, sometimes lipid sinkers or plasmapheresis (technical procedure to remove lipoproteins from blood plasma). - Hyperosmolar comaComa resulting from a functional disturbance in brain cells resulting from a high level of extracellular fluid. Hyperosmolar coma arises from a very marked decrease in body water (dehydration or drying out), blood poisoning from substances which are subject to urinary excretion and extremely high blood sugar concentrations. This coma is typical of type 2 diabetes. Cf. diabetic coma.
- Hyperparathyroidism, primaryExcessive function of the parathyroid glands, with increased formation of parathormone. Generally caused by a benign tumour which comes from glandular tissue (adenoma), but also from cancer of the parathyroid glands.
Symptoms
Primary hyperparathyroidism can make itself evident as kidney stone disease, stomach or duodenal ulcer, inflammation of the pancreas, osteodystrophia fibrosa generalisata, gout and chalk deposits in various organs (lungs, stomach, conjunctiva and cornea). There are also symptoms from the increase in blood calcium.
Diagnosis
Raised blood and urinary calcium, raised blood phosphate, raised alkaline phosphatase and parathormone, osteodensitometry, perhaps bone biopsy.
Treatment
Surgically, by removal of the adenoma or partial removal of the parathyroid glands. After the operation, calcium salts or vitamin D can be administered to prevent muscular spasm caused by calcium deficiency. - Hyperparathyroidism, secondaryIncrease in the size of all four adrenal glands, with increased formation of parathormone. Secondary hyperparathyroidism may be evoked by a decrease in blood calcium concentrations (hypocalcaemia), for example, due to impairment of calcium absorption in the intestine from vitamin D deficiency, pregnancy, breast feeding or low calcium nutrition. Other causes of secondary hyperparathyroidism include raised blood phosphate levels (for example, when kidney function is greatly impaired) or maternal hyperparathyroidism in new born babies.
Symptoms
Normal or raised blood calcium
Treatment
Treatment of the underlying disease - hypersensitivityan exaggerated response of the immune system to a substance; allergy
- Hypertensionalso known as arterial hypertension or high blood pressure
Continuous increase in blood pressure, with systolic (upper) values above 140 mm Hg and diastolic (lower) values above 90 mm Hg. Depending on the origin of the disease, a distinction is made between cardiac output hypertension and resistance hypertension. Cardiac output hypertension is characterised by a raised cardiac output per minute, which predominantly leads to an increase in systolic blood pressure, for example during excessive thyroid function (hyperthreosis). In resistance hypertension there is an increase in the tension of peripheral resistance vessels, which leads predominantly to an increase in diastolic blood pressure, for example in so-called essential hypertension. As a result of changes in vessels caused by hypertension, cardiac output hypertension transforms after some time to resistance hypertension.
I. Classification according to diastolic blood pressure. Definition of the World Health organisation (WHO).
Blood Pressure(mm Hg)
85-89 mm Hg: so-called borderline hypertension
90-104 mm Hg: mild hypertension
105-114 mm Hg: intermediate hypertension
from 115 mm Hg: severe hypertension
II. Classification according to organ damage
WHO Grade I: No clinically detectable damage to heart, kidneys or brain, normal eyeground, WHO Grade II: Damage to heart, kidneys or brain, changes in the eyeground, WHO Grade III: damage to several organs, severe changes in the eyeground.
Symptoms
Non-specific and very variable symptoms, including giddiness, headache, visual problems and others. The clinical course is also frequently asymptomatic or without symptoms until these occur as the result of organ damage, particularly early development of arteriosclerosis with coronary heart disease, disturbances in cerebral perfusion, sclerotic kidneys cause by arteriosclerosis, accompanied by long-term inadequate renal function (chronic renal failure) and peripheral occlusive arterial diseases.In so-called malignant hypertension, the diastolic blood pressure remains above 120 mm Hg, leading to the development of extremely severe changes in the eyeground and rapidly deteriorating kidney function, which, if untreated, often leads to death within 1-2 years.
Diagnosis
The criteria for the diagnosis of hypertension are raised values for blood pressure after measurements which are repeated twice and made at at least two times points. It frequently happens that the first measurement in the medical practice is too high. Out-patient long-term measurements of blood pressure (24 hours) under daily conditions give more reliable results.
Therapy
In primary hypertension (hypertension of unknown cause), the symptoms are treated with antihypertensive drugs and with non-specific measures, particularly salt reduction, weight reduction, reduction of stress factors and the practice of endurance sports, such as cycling, swimming and jogging. The aim is the extensive normalisation of blood pressure. In secondary hypertension, the treatment of the primary disease is of the greatest importance. Cf. indirect measurement of blood pressure, direct measurement of blood pressure - HypertensionIncrease in tension or pressure; e.g. increase in arterial blood pressure (cf. hypertension).
- Hypertension, PortalAlso portal vein hypertension.
Portal hypertension means increased blood pressure in the liver circulation. The illness usually originates from mechanical obstruction to flow in the portal vein circulation (cf. Portal Vein), which means the blood vessels which collect the blood from the whole abdominal cavity and transport it into the liver. In most cases (70-80%), the obstruction to flow is within the liver, for example, in liver cirrhosis. Obstructions to flow before the liver (e.g. portal vein thrombosis) are much rarer (15-25%). Obstruction after the liver occurs in only 1% of cases.
Circulatory shunts may develop as a result of portal hypertension and these can lead to the formation of oesophageal varices, caput medusae or to haemorrhoids.
The condition may become evident from bleeding of oesophageal varices (see Ascites). In some cases, the liver condition may lead to brain damage or to involvement of the spleen (hypersplenism).
Therapy: The treatment depends on the illness which caused the condition. In some cases it is helpful to reduce the portal vein hypertension with drugs or to prepare a shunt between the abdominal cavity and the vascular system. - Hypertensive crisisalso known as hypertonic crisis, blood pressure crisis or high pressure crisis
Sudden and massive increase in systolic blood pressure, usually accompanied by an increase in diastolic pressure. The initial values may be normal or increased and with or without signs of end organ damage (heart, brain or kidneys). The hypertensive crisis must be distinguished from the diagnosis of malignant hypertension.
Causes
High blood pressure, sudden discontinuation of antihypertensive drugs (drugs to reduce blood pressure), disease of the nervous system (e.g. paraplegia, cerebral bleeding, infection)
Symptoms
Headache, confusion, visual problems, somnolence, coma, spasm, angina pectoris, breathing difficulties, cardiac arrythmia, strongly reduced or total lack of urine production.
Therapy
1. In hypertensive crisis with end organ damage, the patient must be immediately treated with drugs to reduce blood pressure. 2. In hypertensive crisis without end organ damage, the patient should first be observed, environmental irritation reduced, possibly followed by drug treatment.
Complications
Acute left heart failure with pulmonary oedema, myocardial infarction if there is coronary heart disease, cerebral oedema, cerebral bleeding, bleeding after an operation
- hypertensive encephalopathya set of symptoms, including headache, convulsions and coma, caused by diffuse cerebral edema or swelling following an abrupt elevation of blood pressure in a patient with long-standing hypertension
- Hypertensive retinopathyalso known as retinopathia angiospastica and retinopathia hypertensiva
Changes in the retina of the eye during high blood pressure (hypertension with WHO Stages II/III and malignant hypertension , often with renal participation).
Symptoms
All vessels narrowed. Lines of bleeding in the retina. Accumulation of fat from the vessels, distension of the nerve fibres , seen as white and blurred spots (so-called cotton wool foci), accumulation of water in the retina (caused by poor perfusion), deterioration in vision, which can largely be rectified if the hypertension is corrected. - HyperthyreosisExcessive function of the thyroid, with increased production and release of thyroid hormones. Hyperthyreosis leads to pathological increases in metabolism in the whole organism.
Symptoms
Goitre, eye symptoms (particularly protruding eyeballs), increased heart rate, high blood pressure (hypertension), restlessness with slight trembling, moodiness, warm and moist skin, sweating attacks, preference for cold environments, diarrhoea, loss of weight in spite of intense hunger, hair loss, muscular weakness, in patients with heart failure this may deteriorate. Protracted hyperthyreosis can lead to damage of the heart muscles and to osteoporosis, often with simultaneous abnormal function of other glands and metabolic abnormalities, such as increased insulin requirement in individuals with diabetes mellitus. Typical symptoms are mostly exhibited by younger individuals; older patients frequently exhibit only one or a few of the different symptoms (senile hyperthyreosis).
Diagnosis
Increase in the overall concentrations of the thyroid hormones thyroxine (T4) and/or triiodothyronine (T3) in serum. In about 5 % of patients only triiodothyronine increases, although the symptoms are the same (so-called T3 hyperthyreosis). The blood concentration is lowered of TSH, the hormone which stimulates the thyroid, which is an expression of the inhibition of TSH release in the frontal lobe of the pituitary. Clarification of the underlying disease with ultrasound diagnosis and scintigraphy, sometimes cell diagnosis (by taking a biopsy of the thyroid).
Therapy
Depending on the cause, operative or drug treatment with the so-called thyreostatic drugs, which inhibit the production and release of hormones from the thyroid. An operation preceded by thyreostatic treatment may be indicated, or therapy with radioactive iodine. - HypertriglyceridaemiaHypertriglyceridaemia means an increased concentration of triglycerides in blood serum. 1. Primary Hypertriglyceridaemia (familial hypertriglyceridaemia) with a deficiency in the enzyme lipoprotein lipase, which hydrolyses triglycerides. 2. Secondary Hypertriglyceridaemia, i.e. as a consequence of e.g. diabetes mellitus, overweight, alcohol abuse, pancreatitis, chronic renal failure or glycogen storage disease. Cf. hyperlipoproteinaemia.
- hypertrophyabnormal enlargement of an organ or tissue; refers to an increase in cell size rather than cell numbers
- hypervolemiaabnormal increase in the volume of circulating fluid (plasma) in the body
- hypoalbuminemiaan abnormally low concentration of the protein albumin in the blood
- HypocalcaemiaLowered serum calcium concentration (less than 2.0 mmol/l or 8.0 mg/dl).
Causes
Lowered production of parathormone, vitamin D deficiency, rickets, disturbed intestinal uptake of food, permanent reduction in kidney function (chronic renal failure), inflammation of the pancreas (acute pancreatitis) and others.
Symptoms
Increased neuromuscular excitability with attacks of muscular spasm. - HypocholesterolaemiaLowered blood concentration of cholesterol. Cf. hypolipoproteinaemias.
Forms
1. Primary (familial) hypocholesterolaemia; 2. Secondary hypocholesterolaemia as a result of excessive thyroid function (hyperthyreosis), digestive abnormalities (malabsorption syndrome), type 2 diabetes, treatment with certain drugs or as a result of nutrition. - hypochromicrefers to red blood cells that are deficient in hemoglobin
- HypoglycaemiaReduction of the blood concentration of glucose below the normal value for the age (30 mg/dl for neonates, 50 mg/dl for children and adults).
Causes
In patients with type 2 diabetes or type 1 diabetes, hypoglycaemia can develop some time after a meal as a result of overdosage with insulin. Additional causes include drug treatment with sulphonylureas, increased glucose metabolism (e.g. with an insulin-producing tumour), decreased glucose production (e.g. with disturbances in liver function), alcohol poisoning and deficiencies in hormones which counteract insulin (e.g. glucagons).
Symptoms
1. Expressions of hormonal counterregulation (rebound) include cold sweat, trembling, hunger, skin pallor and others; 2. Neurological deficits, such as problems in coordination, double vision, uncertainty in walking, sometimes listlessness, disturbances in consciousness up to hypoglycaemic shock, sometimes psychotic state with agitation and attacks of rage.
Diagnosis and treatment
Detection of the low blood sugar concentration (e.g. rapid test with test strip). Immediate intravenous treatment with glucose usually leads to disappearance of the hypoglycaemic symptoms. - Hypoglycaemic comasee hypoglycaemic shock
- Hypoglycaemic shockalso known as hypoglycaemic coma
Sudden loss of consciousness caused by a decrease in blood sugar concentration due to hunger or insulin. Symptoms include spasmophilia (tendency to develop cramp), internal muscular reflexes, moist pale skin and a tendency to sweating. In contrast to diabetic coma, which comes from increased concentrations of blood sugar, there is no marked dehydration as a result of loss of fluid. Cf. hypoglycaemia.
Therapy
Rapid improvement by treatment with glucose. - hypoglycemiaan abnormal decrease of sugar in the blood
- HypogonadismLack or reduced release of hormone from the sexual glands (testicles or ovaries), combined with disturbed development or regression of sexual characteristics.
Forms
1. Primary hypogonadism is the result of the lack or inadequate development of the reproductive glands, as the result of an in-born error. 2. Secondary hypogonadism is the result of a disturbance in the centres in the brain which steer the activity of the reproductive glands (hypothalamus, pituitary).
Symptoms
The symptoms depend on the degree of hormonal deficiency. If the hypogonadism develops in children, there is typically no puberty. If there is also a deficiency in growth hormone, growth may be low (microsomia). When hypogonadism only develops in adulthood, there may be regression of sexual characteristics, which may be reversible, and disturbances in the ability to reproduce, decrease in libido (sexual desire) and in potency and general signs of a lack of sex hormone, such as sterility and disturbances in the menstrual cycle. Hypogonadism is one of the most frequent glandular causes of osteoporosis. - Hypolipoproteinaemiaalso known as hypolipidaemia
Diseases with low blood concentrations of lipoproteins. Hypolipoproteinaemia can occur as a primary innate disease or as a secondary disease which leads to lowered concentrations of various lipoproteins and to hypocholesterolaemia or deficiencies in triglycerides in the blood. Secondary hypolipoproteinaemia can occur as a result of hunger, thyroid hyperfunction (hyperthyreosis) or liver diseases. Cf. lipid metabolism. - hypoplasiaa condition of arrested development in which an organ or part remains below the normal size or in an immature state
- hypoproliferativerefers to anemia characterised by inadequate production of erythrocytes (red blood cells)
- HypothalamusThe hypothalamus lies under the thalamus, which is an important coordination centre for external stimulation and reactions. Like the thalamus it is part of the midbrain (diencephalon). The hypothalamus includes the posterior lobe of the pituitary. The higher centres which control the vegetative nervous system lie in the hypothalamus. These control the regulatory processes in the organism such as thermal regulation, waking and sleeping rhythm, regulation of blood pressure and breathing, food uptake (hunger and satiety centre), fat metabolism, water balance, sexual function and sweat secretion. Hormonally active substances are formed in the hypothalamus, such as the hormone ADH and releasing hormones, which then cause release of hormones from the anterior lobe of the pituitary.
- hypoxiainadequate oxygen supply to the tissues of the body
Glossary entries: Roche and Walter de Gruyter, Berlin