Health Information

Neurotransmitters
Acetylcholine
Norepinephrine
Epinephrine
Dopamine
Serotonin
Histamine

Glutamate
Aspartate
Glycine
GABA

Substance P
Vasopressin
Oxytocin etc..

NO
CO
Adenosine

ACETYLCHOLINE
Location;
- Parasympathetic post ganglionic & all the pre- ganglionic neurons of the autonomic nervous system
- Many nuclei & nerve tracts of the CNS - Neuromuscular junction of skeletal muscle
Acetylcholine has a simple structure,
It is the acetyl ester of choline

SYNTHESIS OF ACETYLCHOLINE
Release of Acetylcholine & binding to receptors,
Acetylcholine reuptake,
Aizheimer’s disease –
- senile dementia,
- caused by a decrease of Ach secreting neurons.

Myasthenia gravis –
weakness of skeletal muscles results from a reduction of Ach receptors.
Caused by autoimmune disease
Neostigmine
A drug used in myasthenia gravis.
Inhibits acetylcholine breakdown and increase the amount of available Acetylcholine

What is antigen?
Each toxin or organism contain chemical compound its makeup.
Can initiate acquired immunity.
Most of them are large polysaccharides.
With higher molecular weight - >8000
Has stereochemical character – epitopes – regularly occurring molecular group.

Heptens
Heptens – Molecular weight is low.
Heptens combined with protein and initiate response.

Lymphocyte clones
When antigen contact with lymphocyte only certain lymphocyte activate.
Activated B and T lymphocytes are highly specific for targeted antigen.
Lymphocyte that can produce one B and T specific cells – clone of lymphocytes
Millions of different lymphocytes store in bone marrow capable of producing highly specific B lymphocyte and T lymphocytes.

Origin of Clones
‘Gene segments’ are responsible to produce specific B cells (antibody) and T-cells quality.
These segment can mixed between genes and produce million – billion possible combination .
These combination will produce different type of B cells (antibody) and T-cells.

Activation of a clone
Each B cell has about 100,000 antibody molecules.
Each react only When high specific antigen contact with them.
Then activate long process of producing highly specific antibody.
In T cell, same happen – has surface receptor proteins.

Macrophage helps…..
Macrophage phagocytes most invading organism – partly digest.
Antigenic products are inside cytosol.
Antigen pass to lymphocyte by cell to cell contact.
In additionally, secrete Interleukin-I - promote growth of specific lymphocyte.

Memory cells
Few lymphoblast form by activating B-lymphocyte clone make different B-lymphocyte – memory cells.
Dormant like original clone.
When there is next expose they activate very quickly and overcome antigen.

What is anaemia?
Anaemia is decrease of Hb for that age and sex.
Can be different reasons.

Clinical features
Fatigue, Headache, Faintness, Breathlessness,
Pallor, tachycardia, murmurs, …

Classification
Different types of classifications
Depend on red cell indices
Cause
Depend on MCV
Hypochromic microcytic – low MCV <80fl
Normochromic normocytic – normal MCV
Macrocytic – Large MVC >96fl

Microcytes
Iron deficiency
Thalassaemia
Anaemia of chronic disease
Siderobalstic anaemia

Macrocytes
Two subtypes
Megaloblastic – Vit B12 deficiency
Normoblastic – Liver disease, alcohol, haemolysis.

Normocytes
Acute blood loss
Anaemia of chronic disease
Infection
Collagen diseases
Malignancy
Endocrine disease

Iron deficiency anaemia
Commonest cause of anaemia.
Limited absorption ability.
Increase loss due to haemorrhage.
Iron absorption
Duodenum & jejunum
Affect several factors.

Iron requirement
Iron store in reticuloendothelial cells, hepatocytes, skeletal muscles.
Ferritin is water soluble form – found in plasma.
Haemosiderin is iron/protein complex – found in bone marrow, liver, spleen.
Need
0.5-1mg/day due to loss faeces, urine, sweat.
Menstruating woman (40ml blood loss) 0.7mg/day.
Pregnancy – 1-2mg/day

Causes for iron deficiency anaemia
Blood loss – hookworm, menstrual loss.
Increase demand – pregnancy, growth.
Decreased absorption – postgastrectomy.
Poor intake.

Clinical feature
Common feature for anameas.
Koilonychia –spoon-shaped nails.
Angular stomatitis.

Treatment
Oral iron
IV iron
Treat the cause.

Anaemia of Chronic disease
A microcytic or normocytic.
Due to chronic disease
Tuberculosis
Osteomyelits
SLE, Rheumatoid arthritis,
Malignant disease

Anaemia of Chronic disease
It can be due to
Decrease release of iron from born marrow to developing erythroblasts.
Inadequate erythropoietin response to anaemia.
Decreased red cell survival.

Other Microcytic anamias
Siderobastic anaemia –
Inheritrd or acquired
Ring siderblasts in bone marrow
Lead poisoning
Lead inhibit some enzymes involved in haem synthesis.
Thalassaemia trait.

Normocytic anaemia
Can be seen in
Anaemia of chronic disease.
Some endocrine disorder – hypothyroidism, hypoadrenalism, hypopituitarism.
Aplastic anaemia

Macrocytic anaemia
Megaloblastic anaemia
Macrocytic but no megaloblasts.
Alcohol excess, Liver disease,
Pregnancy, New born.

Megaloblastic anaemia
Megaloblasts in bone marrow.
Delay in nuclear maturation.
Due to
Vit B12 deficiency
Folate deficiency

Vitamin B12 deficiency
Pernicious anaemia – intrinsic factors deficiency.
Malabsorbtion of vit B12 due different causes.
Low dietary intake.

Pernicious anaemia
Intrinsic factor secret from gastric mucosa.
Gastric mucosal atrophy.
Common in elderly.

Aplastic anaemia
Bone marrow failure.
Cause –
Congenital
Chemical, drugs, radiation.

Haemolytic anaemia
Increase RBC destruction.
Red cells are removed in reticuloendothelial system.
Different causes.
Haemolytic anaemia
Inherited haemolytic anaemias
Hereditary spherocytosis
Hereditary elliptocytosis
Haemoglobin abnormalities – Thalassaemia, Sickle cell anaemia
Acquired haemolytic anaemia
Autoimmune haemolytic anaemia

Eating organisms or toxins in contaminated food.
Affect one person or an outbreak in a group of people.
Infants and elderly people - high risk.

caused by:
Staph aureus
E. coli enteritis
Salmonella
Shigella
Campylobacter
Cholera
Botulism
Symptoms
Common poisoning start within 2 - 6 hours of eating the food
Longer or shorter - depending on the toxin or organism

Symptoms include:
Nausea/vomiting
Abdominal cramps/pain
Diarrhoea
Fever
Weakness
Headache

Complications
Dehydration
Prolonged diarrhoea.
Temporary lactose intolerance afterwards.

Hemolytic uremic syndrome (E.coli)

Staph aureus food poisoning
Staphylococcus aureus bacteria.
Contaminates food products served or stored at room temperature - desserts.
Prepared by a person with a skin infection.
Full recovery - 24 to 48 hours - no antibiotics.

E. coli enteritis
Caused by Escherichia coli (E. coli) – enterotoxigenic form.
Toxins or bacterial invasion into the intestine.
Common cause for traveller’s diarrhoea.
Common cause in children.
Recover in 1 - 3 days - no antibiotics for most.

Shigellosis
Acute infection
Organisms - Shigella dysentriae, S.flexneri, S. boydii
Incubation 2 days.
Acute onset – fever, abdominal pain, watery diarrhoea,
Can be blood and mucus diarrhoea.
Can be vomiting, convulsions.
Self limiting – symptomatic treatment.

Campylobacter enteritis
Caused by Campylobacter jejuni.
Contaminated food or water - raw poultry, fresh produce, or milk.
Incubation 2-4 days.
Symptoms generally last one week.
Self limiting – no antibiotics needed for most case.

Salmonellosis
S. typhi, S.paratyphi, S.choleraesuis, S.enteritidis
Thermal death point – 60°c but can survive sometime in dry & freezing condition.
Transmit by contaminated food or water.
Eggs, poultry products.
Colonize in small intestine and peyer’s patches.
Enter to blood.

Clinical syndrome
Food poisoning
Enteric fever – typhoid/paratyphoid fever.
Enterocolitis
Extra-intestinal focal – osteomyelitis.

What is Hypersensitivity.
Basic mechanism of Type I - V hypersensitivities.
Few common example for Type I - V hypersensitivities.
What is Hypersensitivity?
Immune response that damages the body’s own tissues.
Several types – depend on mechanism.
Type I - type V (type VI).

Type I hypersensitivity
IgE mediated.
Called allergy.
Allergic reaction provoked by re-exposure to a specific antigen.
Pollen, mites, drugs, food….
Release of histamine, arachidonate and derivatives from basophils and mast cells.
Develop 15-30 min.
The reaction - local or systemic.
Allergic asthma, Allergic conjunctivitis, Allergic rhinitis, Anaphylaxis.
Allergic tendency
Some people get allergy often.
Called – atopic allergies.
Genetically passed.
High IgE in body.

Type II hypersensitivity
Antigens on the patient’s own cell surfaces.
Ig G & Ig M mediated.
complement activation.
Intrinsic/”self” antigen or extrinsic.
Autoimmune haemolytic anaemia & transfusion reactions.

Type III hypersensitivity
Form immune complex and deposit.
Ig G, Ig M, Ig A mediated.
complement activation.
Examples
Immune complex glomerulonephritis
Rheumatoid arthritis
Serum sickness
Subacute bacterial endocarditis
Type IV hypersensitivity
Delayed type - two to three days to develop.
Cell medicated.
Macrophages activated and release chemicals.
Contact dermatitis, transplant rejection.

Type V & VI hypersensitivity
Type V - Cell surface receptors destroyed (not whole cell like type II)
Graves’ disease
Myasthenia gravis

Type VI – antibody dependent cell mediated cytotoxicity.

Entamoeba histolytica
Cyst can survive outside the body and spread.
Can spread by feco-orally and male homosexual contact.
Asymptomatic cases – can act as carrier.
Amoebiasis
Can invade mucosa of small intestine.
Make intestinal ulcers.
Can enter portal vein and liver.

Clinical features
Incubation – few days to several months.
Gradual onset – mild intermittent diarrhoea, abdominal discomfort, can lead to bloody diarrhoea with mucus.
Headache, nausea, anorexia.
Can be present – severe acute dysentery.
Complications
Toxic dilatation of colon.
Stricture formation.
Amoeboma – fibrotic granulation tissue in caecum, sigmoid colon.
Liver abscess.

Diagnosis
Stool examination – fresh sample or sigmoidoscopy sample.

Treatment - Metronidazole.

Cause by S. typhi
Human is the only known reservoirs.
Incubation is 10-14 days.
Colonize in small intestine and peyer’s patches Lymphatics Blood Reticuloendothelial system.

Clinical features
Headache is one main symptom.
Fever – gradually increase.
Constipation (diarrhoea later)
Splenomegaly.

Complications
Pneumonia
Meningitis
Intestinal perforation, intestinal hemorrhage.

Treatment
Chloramphenicol
Ciprofloxine
Typhoid Carriers
Chronic carriers – at least one year.
Convalescent carriers.

Prevention
Safe drinking water, good hygiene of those who handle food.
Vaccine – short term, not full protection.

Viral hepatitis – hepatitis A and hepatitis B.
Hep A – common type, faecal-oral spread.
Hep B – spread via intravenous route.
Hepatitis A
Picornaviruse group virus.
Can be epidemics.
Excreted in faeces – 14 days before illness up to 7 days after.
No carrier state.

Hepatitis A – Clinical features
Preicteric /prodromal phase – upto 2 weeks.
Vomiting, diarrhoea, anorexia, headache, malaise, mild fever, liver tender (not enlarge).
After 1-2 weeks – icteric/jaundice
Feel batter.
liver enlarge.
Can be extrahepatic complication - arthritis, vasculitis…etc

Can lead to sever hepatitis and die.

Investigations
Liver biochemistry –
Bilirubin in urine.
Urobilinogen increase.
AST increase.
Viral markers – antibody to Hep A virus.

Treatment
No specific treatment.
Usually need not to admitted to hospital.

Prevention
Good hygiene.
Virus is resistance to chlorination, but kill with boiling water for 10 min.
Immunization
Active – people who travel to endemic area.
Passive – Immunoglobulin – person at risk.

Picornaviruse group virus - a RNA virus
Affect spinal code –anterior horn, cranial nerve motor neurones.
Spread faecal-oral – virus excrete in the faeces.
Vaccination reduced the incident world wide.

Clinical features
Incubation 7-14 days.
Mainly children.

Several types of clinical manifestations.
Inapparent infection – common form, 95% cases.
Abortive poliomyelitis – 4-5% cases, fever, sore throat, and myalgia.
Non-paralytic poliomyelitis – features of abortive with meningeal irritation.
Paralytic poliomyelitis – affect 0.1% affected children, 1.3% adults.
Bulbar poliomyelitis – occur in 5-30% case, cranial nerve involvement.
Post-polio syndrome – increase in muscle atrophy of affected limb many year after primary attack.

Paralytic poliomyelitis
Factors predispose to develop to paralytic form
Male sex, exercise early in illness, trauma.
Start with abortive type and subside after 4-5 days.
Then meningeal irritation, muscle pain.
Asymmetric paralysis, no sensory involvement – mainly lower limbs.

Treatment & prevention
Clinical diagnosis.
Symptomatic treatment – respiratory support, rehabilitation.
Prevention
Immunization – Oral or intramuscular.

Haemoglobin splits and globin and heme release.
Heme consists of four pyrrole rings.
Heme ring open and release pyrrole rings.
Pyrrole will under go several reaction and bilirubin form.
Unconjugated bilirubin enter to hepatic cells.
Conjugate
80% - bilirubin glucuronide.
10% - bilirubin sulfate.
10% - other substances.

Form biliverdin.
Further reduced to bilirubin.
First form is unconjugated/free bilirubin.
Release from macrophage to plasma.
Not soluble and bind to protein.

Conjugated bilirubin turn to urobilinogen by bacteria in the intestine.
Excrete via stool.
Urobilinogen can be reabsorbed to blood.
5% excrete via urine.

Urobilinogen turn to urobilin by oxidization when expose to air.
Stercobilinogen turn to stercobilin by oxidization when expose to air.
Jaundice
Excess bilirubin in the extracellular fluid.
Haemolysis
increase unconjugated bilirubin in plasma.
Urobilinogen increase

Intrahepatic cholestasis
acute and chronic liver diseases including cirrhosis
increase in both type bilirubins

Jaundice
Obstructive jaundice
Stones, tumour in the biliary tract, pancreatic head tumour.
Increase conjugated bilirubin.
No/less urobilinogen
Stool became clay colour.
Significant amount of conjugated bilirubin in urine.