Hypovolemic shock

Definition:

Hypovolemic shock is a particular form of shock in which the heart is unable to supply enough blood to the body. It is caused by blood loss or inadequate blood volume.

Causes, incidence, and risk factors:
Loss of approximately one-fifth or more of the normal blood volume produces hypovolemic shock. The loss can be from any cause, including external bleeding (from cuts or injury), gastrointestinal tract bleeding, other internal bleeding, or from diminished blood volume resulting from excessive loss of other body fluids (such as can occur with diarrhea, vomiting, burns, and so on). In general, larger and more rapid blood volume losses result in more severe shock symptoms.
In another form of shock called cardiogenic shock, there is adequate blood volume, but the heart is unable to pump the blood effectively.

The Heart

The human heart has four chambers: two thin-walled atria on top, which receive blood, and two thick-walled ventricles underneath, which pump blood. Veins carry blood into the atria and arteries carry blood away from the ventricles. Between the atria and the ventricles are atrioventricular valves, which prevent back-flow of blood from the ventricles to the atria. The left valve has two flaps and is called the bicuspid (or mitral) valve, while the right valve has 3 flaps and is called the tricuspid valve. The valves are held in place by valve tendons (“heart strings”) attached to papillary muscles, which contract at the same time as the ventricles, holding the vales closed. There are also two semi-lunar valves in the arteries (the only examples of valves in arteries) called the pulmonary and aortic valves.
The left and right halves of the heart are separated by the inter-ventricular septum. The walls of the right ventricle are 3 times thinner than on the left and it produces less force and pressure in the blood. This is partly because the blood has less far to go (the lungs are right next to the heart), but also because a lower pressure in the pulmonary circulation means that less fluid passes from the capillaries to the alveoli.







The heart is made of cardiac muscle, composed of cells called myocytes. When myocytes receive an electrical impulse they contract together, causing a heartbeat. Since myocytes are constantly active, they have a great requirement for oxygen, so are fed by numerous capillaries from two coronary arteries. These arise from the aorta as it leaves the heart. Blood returns via the coronary sinus, which drains directly into the right atrium.
The Cardiac Cycle
When the cardiac muscle contracts the volume in the chamber decrease, so the pressure in the chamber increases, so the blood is forced out. Cardiac muscle contracts about 75 times per minute, pumping around 75 cm³ of blood from each ventricle each beat (the stroke volume). It does this continuously for up to 100 years. There is a complicated sequence of events at each heartbeat called the cardiac cycle.
Cardiac muscle is myogenic, which means that it can contract on its own, without needing nerve impulses. Contractions are initiated within the heart by the sino-atrial node (SAN, or pacemaker) in the right atrium. This extraordinary tissue acts as a clock, and contracts spontaneously and rhythmically about once a second, even when surgically removed from the heart.

The cardiac cycle has three stages:
1. Atrial Systole (pronounced sis-toe-lay). The SAN contracts and transmits electrical impulses throughout the atria, which both contract, pumping blood into the ventricles. The ventricles are electrically insulated from the atria, so they do not contract at this time.
2. Ventricular Systole. The electrical impulse passes to the ventricles via the atrioventricular node (AVN), the bundle of His and the Purkinje fibres. These are specialised fibres that do not contract but pass the electrical impulse to the base of the ventricles, with a short but important delay of about 0.1s. The ventricles therefore contract shortly after the atria, from the bottom up, squeezing blood upwards into the arteries. The blood can't go into the atria because of the atrioventricular valves, which are forced shut with a loud "lub".
3. Diastole. The atria and the ventricles relax, while the atria fill with blood. The semilunar valves in the arteries close as the arterial blood pushes against them, making a "dup" sound.
The events of the three stages are shown in the diagram on the next page. The pressure changes show most clearly what is happening in each chamber. Blood flows because of pressure differences, and it always flows from a high pressure to a low pressure, if it can. So during atrial systole the atria contract, making the atrium pressure higher than the ventricle pressure, so blood flows from the atrium to the ventricle. The artery pressure is higher still, but blood can’t flow from the artery back into the heart due to the semi-lunar valves. The valves are largely passive: they open when blood flows through them the right way and close when blood tries to flow through them the wrong way.




The PCG (or phonocardiogram) is a recording of the sounds the heart makes. The cardiac muscle itself is silent and the sounds are made by the valves closing. The first sound (lub) is the atrioventricular valves closing and the second (dub) is the semi-lunar valves closing.
The ECG (or electrocardiogram) is a recording of the electrical activity of the heart. There are characteristic waves of electrical activity marking each phase of the cardiac cycle. Changes in these ECG waves can be used to help diagnose problems with the heart.


Exercise and Heart Rate
The rate at which the heart beats and the volume of blood pumped at each beat (the stroke volume) can both be controlled. The product of these two is called the cardiac output – the amount of blood flowing in a given time:

heart rate (beats/min) stroke volume
(cm3/ beat) cardiac output
(cm3/min)
at rest 75 75 5 600


As the table shows, the cardiac output can increase dramatically when the body exercises. There are several benefits from this:
· to get oxygen to the muscles faster
· to get glucose to the muscles faster
· to get carbon dioxide away from the muscles faster
· to get lactate away from the muscles faster
· to get heat away from the muscles faster
But what makes the heart beat faster? Again, this is an involuntary process and is controlled a region of the medulla called the cardiovascular centre, which plays a similar role to the respiratory centre. The cardiovascular centre receives inputs from various receptors around the body and sends output through two nerves to the sino-atrial node in the heart.







How does the cardiovascular centre control the heart?
The cardiovascular centre can control both the heart rate and the stroke volume. Since the heart is myogenic, it does not need nerve impulses to initiate each contraction. But the nerves from the cardiovascular centre can change the heart rate. There are two separate nerves from the cardiovascular centre to the sino-atrial node: the sympathetic nerve (accelerator nerve) to speed up the heart rate and the parasympathetic nerve (vagus nerve) to slow it down.
The cardiovascular centre can also change the stroke volume by controlling blood pressure. It can increase the stroke volume by sending nerve impulses to the arterioles to cause vasoconstriction, which increases blood pressure so more blood fills the heart at diastole. Alternatively it can decrease the stroke volume by causing vasodilation and reducing the blood pressure.



How does the cardiovascular centre respond to exercise?
When the muscles are active they respire more quickly and cause several changes to the blood, such as decreased oxygen concentration, increased carbon dioxide concentration, decreased pH (since the carbon dioxide dissolves to form carbonic acid) and increased temperature. All of these changes are detected by various receptor cells around the body, but the pH changes are the most sensitive and therefore the most important. The main chemoreceptors (receptor cells that can detect chemical changes) are found in:
· The walls of the aorta (the aortic body), monitoring the blood as it leaves the heart
· The walls of the carotid arteries (the carotid bodies), monitoring the blood to the head and brain
· The medulla, monitoring the tissue fluid in the brain
The chemoreceptors send nerve impulses to the cardiovascular centre indicating that more respiration is taking place, and the cardiovascular centre responds by increasing the heart rate.

A similar job is performed by temperature receptors and stretch receptors in the muscles, which also detect increased muscle activity.
Exercise affects the rest of the circulation as well as increasing cardiac output. When there is an increase in exercise, the muscles respire faster, and therefore need a greater oxygen supply. This can be achieved by increasing the amount of blood flowing through the capillaries at the muscles. A large increase in blood flowing to one part of the body must be met by a reduction in the amount of blood supplying other parts of the body, such as the digestive system. Some organs need a stable blood supply (to supply enough oxygen and glucose for respiration), to work efficiently what ever the body is doing. The three main organs that require a constant blood supply are:
· The heart needs a constant blood supply otherwise the heart muscle would starve of oxygen and glucose, making it unable to pump more blood, and might cause a heart attack.
· The brain needs a constant blood supply otherwise the brain would reduce ability to react to danger and might result in unconsciousness/death.
· The kidneys need a constant blood supply otherwise there would be a build-up of toxins in the blood.

Exercise and Breathing
Both the rate and depth (volume) of breathing can be varied. The product of these two is called the ventilation rate – the volume air ventilating the lungs each minute:

Breathing rate
(breaths/min) Tidal volume
(cm3/ breath) Ventilation rate (cm3/min)
at rest 12 500 6 000


When the body exercises the ventilation rate and depth increases so that
· Oxygen can diffuse from the air to the blood faster
· Carbon dioxide can diffuse from the blood to the air faster

How does respiratory centre respond to exercise?
The process is the same as for heart rate, with the chemoreceptors in the aortic and carotid bodies detecting an increase in respiration.

Again, the stretch receptors in the muscles give a more rapid indication of muscular activity, allowing an anticipatory increase in breathing rate even before the carbon dioxide concentration the blood has changed.

Microcirculation Structure and Function

The microcirculation is comprised of arterioles, capillaries, venules, and terminal lymphatic vessels.

Arterioles
· Small precapillary resistance vessels (10-50 ) composed of an endothelium surrounded by one or more layers of smooth muscle cells.
· Richly innervated by sympathetic adrenergic fibers and highly responsive to sympathetic vasoconstriction via both a 1 and a 2 postjunctional receptors.
· Represent a major site for regulating systemic vascular resistance.
· Rhythmical contraction and relaxation of arterioles sometimes occurs (i.e., spontaneous vasomotion).
· Primary function within an organ is flow regulation, thereby determining oxygen delivery and the washout of metabolic by-products.
· Regulate, in part, capillary hydrostatic pressure and therefore influence capillary fluid exchange.

Capillaries
· Small exchange vessels (6-10 ) composed of highly attenuated (very thin) endothelial cells surrounded by basement membrane – no smooth muscle.
· Three structural classifications:
Continuous (found in muscle, skin, lung, central nervous system) – basement membrane is continuous and intercellular clefts are tight (i.e., have tight junctions); these capillaries have the lowest permeability.

Fenestrated (found in exocrine glands, renal glomeruli, intestinal mucosa) – perforations (fenestrae) in endothelium result in relatively high permeability.

Discontinuous (found in liver, spleen, bone marrow) – large intercellular gaps and gaps in basement membrane result in extremely high permeability.

· Large surface area and relatively high permeability (especially at intercellular clefts) to fluid and macromolecules make capillaries the primary site of exchange for fluid, electrolytes, gases, and macromolecules.
· In some organs, precapillary sphincters (a circular band of smooth muscle at entrance to capillary) can regulate the number of perfused capillaries.
Venules
· Small exchange vessels (10-50 ) composed of endothelial cells surrounded by basement membrane (smallest postcapillary venules) and smooth muscle (larger venules).
· Fluid and macromolecular exchange occur most prominently at venular junctions.
· Sympathetic innervation of larger venules can alter venular tone which plays a role in regulating capillary hydrostatic pressure.
Terminal Lymphatics
· Composed of endothelium with intercellular gaps surrounded by highly permeable basement membrane and are similar in size to venules – terminal lymphatics end as blind sacs.
· Larger lymphatics also have smooth muscle cells.
· Spontaneous and stretch-activated vasomotion is present which serves to "pump" lymph.
· Sympathetic nerves can modulate vasomotion and cause contraction.
· One-way valves direct lymph away from the tissue and eventually back into the systemic circulation via the thoracic duct and subclavian veins (2-4 liters/day returned).


Vessel Sizes

Vessel Diameter in Microns
Arterioles 20-50
Capillaries 5-10
Sinusoids 30-40
Venules 30-40

Microcirculation Structure and Function

The microcirculation is comprised of arterioles, capillaries, venules, and terminal lymphatic vessels.

Arterioles
· Small precapillary resistance vessels (10-50 ) composed of an endothelium surrounded by one or more layers of smooth muscle cells.
· Richly innervated by sympathetic adrenergic fibers and highly responsive to sympathetic vasoconstriction via both a 1 and a 2 postjunctional receptors.
· Represent a major site for regulating systemic vascular resistance.
· Rhythmical contraction and relaxation of arterioles sometimes occurs (i.e., spontaneous vasomotion).
· Primary function within an organ is flow regulation, thereby determining oxygen delivery and the washout of metabolic by-products.
· Regulate, in part, capillary hydrostatic pressure and therefore influence capillary fluid exchange.









Capillaries
· Small exchange vessels (6-10 ) composed of highly attenuated (very thin) endothelial cells surrounded by basement membrane – no smooth muscle.
· Three structural classifications:
Continuous (found in muscle, skin, lung, central nervous system) – basement membrane is continuous and intercellular clefts are tight (i.e., have tight junctions); these capillaries have the lowest permeability.

Fenestrated (found in exocrine glands, renal glomeruli, intestinal mucosa) – perforations (fenestrae) in endothelium result in relatively high permeability.

Discontinuous (found in liver, spleen, bone marrow) – large intercellular gaps and gaps in basement membrane result in extremely high permeability.

· Large surface area and relatively high permeability (especially at intercellular clefts) to fluid and macromolecules make capillaries the primary site of exchange for fluid, electrolytes, gases, and macromolecules.
· In some organs, precapillary sphincters (a circular band of smooth muscle at entrance to capillary) can regulate the number of perfused capillaries.
Venules
· Small exchange vessels (10-50 ) composed of endothelial cells surrounded by basement membrane (smallest postcapillary venules) and smooth muscle (larger venules).
· Fluid and macromolecular exchange occur most prominently at venular junctions.
· Sympathetic innervation of larger venules can alter venular tone which plays a role in regulating capillary hydrostatic pressure.
Terminal Lymphatics
· Composed of endothelium with intercellular gaps surrounded by highly permeable basement membrane and are similar in size to venules – terminal lymphatics end as blind sacs.
· Larger lymphatics also have smooth muscle cells.
· Spontaneous and stretch-activated vasomotion is present which serves to "pump" lymph.
· Sympathetic nerves can modulate vasomotion and cause contraction.
· One-way valves direct lymph away from the tissue and eventually back into the systemic circulation via the thoracic duct and subclavian veins (2-4 liters/day returned).


Vessel Sizes

Vessel Diameter in Microns
Arterioles 20-50
Capillaries 5-10
Sinusoids 30-40
Venules 30-40

Constipation

is a common gastrointestinal problem. People who experience constipation have infrequent bowel movements, pass hard stools or strain during bowel movements.

What's considered normal frequency for bowel movements varies widely. In general, however, you're probably experiencing constipation if you pass fewer than three stools a week, and your stools are hard and dry.

Fortunately, most cases of constipation are temporary. Simple lifestyle changes, such as getting more exercise and eating a high-fiber diet, can go a long way toward alleviating constipation. Constipation may also be treated with over-the-counter laxatives.

Not having a bowel movement every day doesn't necessarily mean you're constipated. You likely have constipation, however, if you experience two of the following signs or symptoms:

1.Pass fewer than three stools a week
2.Experience hard stools
3.Strain excessively during bowel movements
4.Experience a sense of rectal blockage
5.Have a feeling of incomplete evacuation after having a bowel movement
6.Need to use manual maneuvers to have a bowel movement, such as finger evacuation or manipulation of your lower abdomen.

Diarrhea

is the frequent passing of loose or watery stools. Acute diarrhea, which is a common cause of death in developing countries, appears rapidly and may last from five to ten days. Chronic diarrhea lasts much longer and is the second cause of childhood death in the developing world. Diarrhea is sometimes accompanied by abdominal cramps or fever. It may be caused by infection, allergy, or could be a sign of a serious disorder, such as IBD (inflammatory bowel disease), or Crohn's disease.
What are the five types of diarrhea?

Secretory diarrhea

Either the gut is secreting more fluids than usual, or it cannot absorb fluids properly. In such cases structural damage is minimal. This is most commonly caused by a cholera toxin - a protein secreted by the bacterium Vibrio cholera.

Osmotic diarrhea

Too much water is drawn into the bowels. This may be the result of celiac disease, pancreatic disease, or laxatives. Too much magnesium, vitamin C, undigested lactose, or undigested fructose can also trigger osmotic diarrhea.

Motility-related diarrhea

Food moves too quickly through the intestines (hypermotility). If the food moves too quickly there is not enough time to absorb sufficient nutrients and water. Patients who had a vagotomy (removal or severing of the vagus nerve) as well as those with diabetic neuropathy are susceptible to this type of diarrhea.

Inflammatory diarrhea

The lining of the gut becomes inflamed. This is usually caused by bacterial infections, viral infections, parasitic infections, or autoimmune problems such as IBS (inflammatory bowel disease). Tuberculosis, colon cancer and enteritis can also cause inflammatory diarrhea.

Dysentery

The presence of blood in the stools is usually a sign of dysentery, rather than diarrhea. Dysentery is caused by a release of excess water caused by an antidiuretic hormone from the posterior pituitary gland. Dysentery is one of the symptoms of Shigella, Entamoeba histolytica, and Salmonella.
When it occurs in people age 60 and older, there's a good possibility bloody diarrhea indicates ischemic colitis, according to the Mayo Clinic, USA.
What are the symptoms of diarrhea?

Some sufferers may pass slightly watery stools and have brief episodes of stomachache, while others may pass very watery stools and have more severe stomach cramping. The most common symptoms include:
Abdominal cramps
Abdominal pain
An urge to go to the toilet, sometimes this may be sudden
Vomiting
Nausea
Temperature (fever)
Headache
Loss of appetite
Fatigue
Loose, watery stools
Bloating
Blood in stool
Anybody who has had diarrhea for more than one week should see their doctor. The UK National Health Service advises parents to take their child to the doctor if:
The child is aged 3 months to 1 year and the diarrhea has lasted over two days
The child is over 1 year of age and the diarrhea has lasted more than five days
You should also see your doctor if you experience or witness any of the following:
You have symptoms of dehydration - excessive thirst, very dry mouth, very little or no urination
Your abdominal pain is severe
You have severe rectal pain
There is blood in the stools, the stools are black
Your temperature is over 39C (102 F)
A baby has not wet the diaper (UK: nappy) in over three hours
A child/baby is very sleepy, irritable, or unresponsive
A child/baby has a sunken abdomen
A child/baby has sunken eyes and/or cheeks
The child's/baby's skin does not flatten after being pinched
What causes diarrhea?

Causes of acute diarrhea (short term diarrhea)

This is usually caused by an infection, and is also a symptom of a bowel infection when the stomach and the intestines become inflamed (gastroenteritis). This may be caused by:
A virus - most commonly a norovirus or a rotavirus. It could also be caused by a hepatitis virus, or the herpes simplex virus. Viral diarrhea spreads easily.

A bacteria - if food or water is contaminated bacteria and parasites can be transmitted into the body. Parasites may include Giardia lamblia and cryptosporidium. Examples of bacteria are campylobacter, salmonella, shigella and Escherichia coli (E. coli). Traveler's diarrhea is usually caused by bacteria or parasites. Researchers at Boston University School of Medicine identified the structure of bacteria responsible for traveler's diarrhea.

An antibiotic - antibiotics can disturb the natural balance of bacteria in our intestines, which can lead to infection, commonly with a bacterium called Clostridium difficile.
The following may also be causes of acute diarrhea:
Anxiety
Consuming too much alcohol
Consuming too much coffee
Some other medications, apart from antibiotics
Causes of chronic diarrhea (persistent, longer term diarrhea)
Bacteria
A virus
Laxatives
Some dietary habits - long term regular alcohol, coffee consumption may cause persistent diarrhea. Regular eating of candy (sweets) can too. Many sugar-free chewing gums containing a sweetener called sorbitol can cause chronic diarrhea, The British Medical Journal reported.
The following long-term conditions can cause chronic diarrhea
Celiac disease
Crohn's disease
Diabetes
Irritable bowel syndrome (IBS)
Lactose intolerance
Pancreatitis
Ulcerative colitis
How is diarrhea diagnosed?

Most cases of acute diarrhea will resolve themselves within a week or so. If the diarrhea lasts longer, or if there is blood in the stools and there are other symptoms, such as dehydration, the GP (general practitioner, primary care physician) will take a stool sample to check for infection.

A sigmoidoscopy may also be performed. This involves introducing a thin fiber-optic tube through the rectum to look into the intestine. The device has a viewing lens.

The doctor will also ask the patient whether he/she is taking any medications, has traveled recently, and possibly some questions about what foods were consumed over the last couple of weeks. The GP may also examine the abdomen to determine where the pain is.
What is the treatment for diarrhea?

In the vast majority of cases the diarrhea will disappear within a week or so. Before it does, the following steps may help ease symptoms:
Drink plenty of fluids - diarrhea often carries a risk of dehydration, especially if it includes vomiting. It is important to make sure babies and children are getting plenty of fluids.

Diarrhea may affect the balance of salts and electrolytes in the body. Special dehydration drinks can be bought in a pharmacy to restore their balance. A pharmacist can advise on which drinks to consume.

Eat as soon as you feel up to it - doctors used to tell people not to eat until the symptoms went away. They now recommend patients start with foods such as pasta, bread, rice or potatoes - foods high in carbohydrates, as soon as possible. Add a bit of salt to the food to replace salt loss. Avoid foods that are high in fat.

Medications - such medicines as loperamide may slow down bowel movements and may also increase the gut's water absorption. Do not give anti-diarrhea medications to children without checking first with a doctor. Do not take anti-diarrhea medications if there is blood in the stools or if you have a fever.

Breastfeeding or bottle-feeding babies - doctors recommend that feeding continue as normal if the baby has diarrhea. If necessary, add rehydration drinks that are bought from a pharmacy.

Painkillers - for fever or headache doctors recommend Tylenol (paracetamol) or ibuprofen. If you have kidney, liver or long-term stomach problems do not take ibuprofen. Do not give aspirin if your child is under 16 years of age.

Probiotics - these are supposed to treat diarrhea, among other things. However, a study published in the British Medical Journal indicated that some of them don't work, while others do.
Doctors may prescribe specific medications, depending on the results of the stool test.

Rigor mortis

is a recognizable sign of human death that is caused by a chemical change in the muscles, causing the limbs of the corpse to become stiff ("rigor") and impossible to move or manipulate. Typically rigor sets in several hours after clinical death and subsides spontaneously in about two days, though the time of its onset and duration depends on ambient temperature.
The biochemical cause of rigor mortis is hydrolysis of ATP in the muscle tissue, the chemical energy source required for movement. Myosin molecules devoid of ATP become permanently adherent to actin filaments and muscles become rigid.

Myasthenia gravis

is a neuromuscular disorder characterized by variable weakness of voluntary muscles, which often improves with rest and worsens with activity. The condition is caused by an abnormal immune response.

Causes
In myasthenia gravis, weakness occurs when the nerve impulse to initiate or sustain movement does not adequately reach the muscle cells. This is caused when immune cells target and attack the body's own cells (an autoimmune response). This immune response produces antibodies that attach to affected areas, preventing muscle cells from receiving chemical messages (neurotransmitters) from the nerve cell.
The cause of autoimmune disorders such as myasthenia gravis is unknown. In some cases, myasthenia gravis may be associated with tumors of the thymus (an organ of the immune system). Patients with myasthenia gravis have a higher risk of having other autoimmune disorders like thyrotoxicosis, rheumatoid arthritis, and systemic lupus erythematosus.
Myasthenia gravis affects about 3 of every 10,000 people and can affect people at any age. It is most common in young women and older men.

Muscle weakness, including:
Swallowing difficulty, frequent gagging, or choking
Paralysis
Muscles that function best after rest
Drooping head
Difficulty climbing stairs
Difficulty lifting objects
Need to use hands to rise from sitting positions
Difficulty talking
Difficulty chewing
Vision problems:
Double vision
Difficulty maintaining steady gaze
Eyelid drooping
Additional symptoms that may be associated with this disease:
Hoarseness or changing voice
Fatigue
Facial paralysis
Drooling
Breathing difficulty

Erythroblastosis fetalis

Rh-positive red blood cells in the fetus are attacked by antibodies from an Rh-negative mother. These antibodies make the Rh-positive cells fragile, leading to rapid rupture and causing the child to be born with serious anemia. This is in relation to the Rh factor of blood. The extremely rapid formation of new red cells to make up for the destroyed cells in erythroblastosis fetalis causes a large number of early blast forms of red cells to be released from the bone marrow into the blood.

Regards by
Dr.M M ADANAN
contact id:adnan_dani12@yahoo.com

Attention-deficit/hyperactivity disorder (ADHD)

is a chronic condition that affects millions of children and often persists into adulthood. Problems associated with ADHD include inattention and hyperactive, impulsive behavior. Children with ADHD may struggle with low self-esteem, troubled relationships and poor performance in school.

While treatment won't cure ADHD, it can help a great deal with symptoms. Treatment typically involves psychological counseling, medications or both.

A diagnosis of ADHD can be scary, and symptoms can be a challenge for parents and children alike. However, treatment can make a big difference, and the majority of children with ADHD grow up to be vibrant, active and successful adults.

Abreviations for Medical and Scientific terms

Some of the most frequently used abbreviations have been listed here. Notice that some have more than one interpretation.
It is important to know the abbreviations approved by your institution, use only those, and never make up your
own abbreviations. If there is any chance of confusion, write out the words.
ABC airway, breathing, circulation
ABG arterial blood gas
ABX antibiotics
ACh acetylcholine
ACTH adrenocorticotropic hormone
AD Alzheimer’s disease
ADH antidiuretic hormone
AIDS acquired immunodeficiency syndrome
ALS amyotrophic lateral sclerosis
ANS autonomic nervous system
ARDS acute respiratory distress syndrome
ARF acute renal failure (acute respiratory
failure)
ATP adenosine triphosphate
AV atrioventricular
BAL blood alcohol level
BBB blood-brain barrier
BMR basal metabolic rate
BP blood pressure
BPH benign prostatic hypertrophy
(hyperplasia)
BPM beats per minute
BS blood sugar (bowel sounds, breath sounds)
BUN blood urea nitrogen
CA cancer
CAD coronary artery disease
CAPD continuous ambulatory peritoneal dialysis
CBC complete blood count
CC creatinine clearance (critical condition,
chief complaint)
CCCC closed-chest cardiac compression
CF cystic fibrosis (cardiac failure)
CHD coronary heart disease (congenital heart
disease)
CHF congestive heart failure
CI cardiac insufficiency (cerebral infarction)
CNS central nervous system
CO cardiac output; carbon monoxide
COPD chronic obstructive pulmonary disease
CP cerebral palsy
CPR cardiopulmonary resuscitation
CRF chronic renal failure
C-section cesarean section
CSF cerebrospinal fluid
CT (CAT) computed (axial) tomography
CVA cerebrovascular accident
CVP central venous pressure
CVS chorionic villus sampling
D & C dilation and curettage
DM diabetes mellitus (diastolic murmur)
DMD Duchenne’s muscular dystrophy
DNA deoxyribonucleic acid
DNR do not resuscitate
DOA date of admission (dead on arrival)
DRG diagnosis-related group
Dx diagnosis
EBV Epstein-Barr virus
ECF extracellular fluid (extended care facility)
ECG (EKG) electrocardiogram
EDV end-diastolic volume
EEG electroencephalogram
EFM electronic fetal monitoring
EP ectopic pregnancy
ER endoplasmic reticulum
ERT estrogen replacement therapy
ESR erythrocyte sedimentation rate
ESRD end-stage renal disease
ESV end-systolic volume
FAS fetal alcohol syndrome
FBG fasting blood glucose
FOBT fecal occult blood testing
FSH follicle-stimulating hormone
FUO fever of unknown origin
Fx fracture
GB gallbladder
GFR glomerular filtration rate
GH growth hormone
GI gastrointestinal
HAV hepatitis A virus
Hb hemoglobin
HBV hepatitis B virus
HCG human chorionic gonadotropin
Hct hematocrit
HCV hepatitis C virus
HDL high-density lipoprotein
HLA human leukocyte antigen
HR heart rate
HRT hormone replacement therapy
HSV herpes simplex virus
HTN hypertension
Hx history
IBD inflammatory bowel disease
IBS irritable bowel syndrome
ICF intracellular fluid
ICP intracranial pressure
ICU intensive care unit
ID intradermal
IDDM insulin-dependent diabetes mellitus
Ig immunoglobulin
IM intramuscular
IV intravenous
LA left atrium
LDL low-density lipoprotein
LH luteinizing hormone
LLQ left lower quadrant
LUQ left upper quadrant
LV left ventricle
mEq/L milliequivalents per liter
MG myasthenia gravis
MI myocardial infarction
mL milliliter
mm3 cubic millimeter
mmHg millimeters of mercury
MRI magnetic resonance imaging
MS multiple sclerosis
MSOF multisystem organ failure
MVP mitral valve prolapse
NGU non-gonococcal urethritis
NIDDM non-insulin-dependent diabetes mellitus
NPN non-protein nitrogen
OC oral contraceptive
OTC over the counter
PE pulmonary embolism
PET positron emission tomography
PG prostaglandin
PID pelvic inflammatory disease
PKU phenylketonuria
PMN polymorphonuclear leukocyte
PMS premenstrual syndrome
PNS peripheral nervous system
PT prothrombin time (patient, patient
teaching, physical therapy)
PTH parathyroid hormone
PTT partial thromboplastin time
PVC premature ventricular contraction
RA right atrium
RBC red blood cell
RBM red bone marrow
RDA recommended daily allowance
RDS respiratory distress syndrome
REM rapid eye movement
RE(S) reticuloendothelial (system)
Rh Rhesus
RIA radioimmunoassay
RLQ right lower quadrant
RNA ribonucleic acid
RUQ right upper quadrant
RV right ventricle
Rx prescription
SA sinoatrial
SC subcutaneous
SCID severe combined immunodeficiency
SF synovial fluid
SIDS sudden infant death syndrome
SLE systemic lupus erythematosus
SPF sun protection factor
S/S (sx) signs and symptoms
STD sexually transmitted disease
SV stroke volume
T3 triiodothyronine
T4 thyroxine
TIA transient ischemic attack
TMJ temporomandibular joint
t-PA tissue plasminogen activator
TPN total parenteral nutrition
TSH thyroid-stimulating hormone
TSS toxic shock syndrome
Tx treatment
UA urinalysis
URI upper respiratory infection
US ultrasound
UTI urinary tract infection
UV ultraviolet
VPC ventricular premature contraction
VD venereal disease
VS vital signs
WBC white blood cell
WNL within normal limits

What is Pulmonary Edema?

Pulmonary oedema is a condition in which fluid accumulates in your lungs,  caused by back pressure in the lung veins.



Pulmonary oedema is a complication of:

a heart attack;


cardiac dysfunction;


a disease of the valves in your heart, (called "mitral or aortic valve disease") ;


exposure to high altitude.

Fluid overload is a common cause in infants.

Fluid backs up into the veins of the lungs. Increased pressure in these veins forces fluid out of the vein and into the air spaces (alveoli). This interferes with the exchange of oxygen and carbon dioxide in your lungs.

Can pulmonary oedema be prevented?

In severe cases, this condition can not be prevented. However, pulmonary oedema associated with less severe disease can be prevented by appropriate treatment. The risk can be reduced by prompt treatment of cardiac disorders.

What are the symptoms of pulmonary oedema?

You may experience:

shortness of breath;


a feeling of "air hunger" or "drowning";


"grunting" sounds with breathing;


wheezing;


anxiety;


restlessness;


cough;


excessive sweating;


pale skin.



Best regards by:
Dr.M M ADNAN
contact id:adnan_dani12@yahoo.com

Hypoxia

Hypoxia


Hypoxia is a state of oxygen deficiency in the body which is sufficient to cause an impairment of function. Hypoxia is caused by the reduction in partial pressure of oxygen, inadequate oxygen transport, or the inability of the tissues to use oxygen.


In brief, is kind of the same as being exposed to high altitude. In both cases, oxygen to your brain and muscles is reduced.

Types of Hypoxia

Hypoxic Hypoxia is a reduction in the amount of oxygen passing into the blood. It is caused by a reduction in oxygen pressure in the lungs, by a reduced gas exchange area, exposure to high altitude, or by lung disease. [This is the hypoxia that is a hazard to aviators.]


Hypemic Hypoxia is defined as a reduction in the oxygen carrying capacity of the blood. It is caused by a reduction in the amount of hemoglobin in the blood or a reduced number of red blood cells. A reduction in the oxygen transport capacity of the blood occurs through blood donation, hemorrhage, or anemia. A reduction in the oxygen carrying capacity of the blood occurs through drugs, chemicals, or carbon monoxide. [This hypoxia usually experienced by smokers.]


Stagnant Hypoxia is an oxygen deficiency due to poor circulation of the blood or poor blood flow. Examples of this condition are high "G" forces, prolonged sitting in one position or hanging in a harness, cold temperatures, and positive pressure breathing. [This hypoxia usually experienced when sitting for hours in a boring class.]


Histotoxic Hypoxia is defined as the inability of the tissues to use oxygen. Examples are carbon monoxide and cyanide poisoning. Certain narcotics, chewing tobacco, and alcohol will prevent oxygen use by the tissues. [This hypoxia usually experienced after drinking too much.]



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Dr.M M ADNAN
Contact id:adnan_dani12@yahoo.com

Alzheimer's Disease

Also called: AD

Alzheimer's disease (AD) is the most common form of dementia among older people. Dementia is a brain disorder that seriously affects a person's ability to carry out daily activities.
AD begins slowly. It first involves the parts of the brain that control thought, memory and language. People with AD may have trouble remembering things that happened recently or names of people they know. Over time, symptoms get worse. People may not recognize family members or have trouble speaking, reading or writing. They may forget how to brush their teeth or comb their hair. Later on, they may become anxious or aggressive, or wander away from home. Eventually, they need total care. This can cause great stress for family members who must care for them.
AD usually begins after age 60. The risk goes up as you get older. Your risk is also higher if a family member has had the disease.

No treatment can stop the disease. However, some drugs may help keep symptoms from getting worse for a limited time.





Regards by Dr.M M ADNAN
Contact id:adnan_dani12@yahoo.com

Hemophilia

is a bleeding disease thata occurs almost exclusively in males.In 85 percent of cases, it is caused by an abnormality or deficiency of Factor VIII; this type of hemophilia is called hemophillia A or classic hemophilia.

About 1 of every 10,000 males in the United States has classic hemophilia.In the other 15 percent of hemophilia patients , the bleeding tendency is caused by deficiency of Factor IX.Both of these factors are transmitted genetically by way of the female chromosome.Therefore, almost never will a woman have hemophilia because al least one of her two X chromosomes will have the appropriate genes.If one of her X chromosome is deficient, she will be a hemophilic carrier , transmitting the disease to half of her male offspring and transmitting the carrier state to half of her female offspring.

The bleeding trait in hemophilia can have various degree of severity, depending on the character of the genetic deficiency. Bleeding usually does not occur except after trauma, but in some patients, the degree of trauma required to cause severe aand prolonged bleeding maay be so mild that it is hardly noticeable.For instance, bleeding can often last days after extraction of a tooth.

Factor VIII hs two active components, a large component with a molecular weight in the millions and a smaller component with a molecular weight of about 230,000. The smaller component is most important in the intrinsic pathway for clotting and it is deficiency of this part of Factor VIII that cause classic hemophilia.Another bleeding disease with somewhat different characteristics, called von Willbrand's disease, results from loss of the large component.

When a person with classic hemophilia experiences severe prolonged bleeding, almost the only therapy that is truly effective is injection of purified Factor VIII. The cost of Factor VIII is high, and its availability is limited because it can be gathered only from human blood and only in extremely small quantities.

Treatment of hemophilia

ECG

What is ECG?

When impulses passes through heart the electrical current also spreads to the surrounding tissue and to surface of body.When electrodes are placed on the surface then it can record the electrical activity.This is known as ECG


ECG Paper:
ECG Paper: contains small and large squares.

Each small squares is 1mm and large square is 5mm

Time is measured along horizontal line and each small square is 0.04s and each large square is 0.2s.

Voltage is measured along vertical line and 10mm is equal to 1mV.

ECG paper moves at 25mm/s speed i.e. 1500sq/min



ECG leads
3 types of leads:

(HORIZONTAL PLANE LEADS)

1.Chest leads/precordial leads:V1,V2,V3,V4,V5, and V6.

(FRONTAL PLANE LEADS)

2.Bipolar leads/standard/Einthoven's Leads: I II III.

3.Augmented Unipolar leads: aVR, aVL ,aVF.


PLACEMENT OF LEADS

Augmented Leads:

aVR: Right arm

aVL: Left arm

aVF: Left foot


Chest leads:

V1: in 4th ICS at right sternal border .

V2:in 4th ICS at left sternal border .

V3:Mid way between V2 and V3

V4:5th ICS in left MCL (mid clavical line)

V5:Anterior axillary line in 5th ICS

V6:Mid axillary line in 5th ICS .....

ECG

What is ECG?

When impulses passes through heart the electrical current also spreads to the surrounding tissue and to surface of body.When electrodes are placed on the surface then it can record the electrical activity.This is known as ECG

ECG Paper:

ECG Paper: contains small and large squares.

Each small squares is 1mm and large square is 5mm

Time is measured along horizontal line and each small square is 0.04s and each large square is 0.2s.

Arthritis

What is arthritis? What causes arthritis?

Arthritis is a joint disorder featuring inflammation. A joint is an area of the body where two different bones meet. A joint functions to move the body parts connected by its bones. Arthritis literally means inflammation of one or more joints.

Arthritis is frequently accompanied by joint pain. Joint pain is referred to as arthralgia.

There are many types of arthritis (over 100 and growing). The types range from those related to wear and tear of cartilage (such as osteoarthritis) to those associated with inflammation resulting from an overactive immune system (such as rheumatoid arthritis). Together, the many types of arthritis make up the most common chronic illness in the United States.

The causes of arthritis depend on the form of arthritis. Causes include injury (leading to osteoarthritis), metabolic abnormalities (such as gout and pseudogout), hereditary factors, infections, and unclear reasons (such as rheumatoid arthritis and systemic lupus erythematosus).

Arthritis is classified as one of the rheumatic diseases. These are conditions that are different individual illnesses, with differing features, treatments, complications, and prognoses. They are similar in that they have a tendency to affect the joints, muscles, ligaments, cartilage, and tendons, and many have the potential to affect other internal body areas.

Symptoms of arthritis include pain and limited function of joints. Inflammation of the joints from arthritis is characterized by joint stiffness, swelling, redness, and warmth. Tenderness of the inflamed joint can be present.

Many of the forms of arthritis, because they are rheumatic diseases, can cause symptoms affecting various organs of the body that do not directly involve the joints. Therefore, symptoms in some patients with certain forms of arthritis can also include fever, gland swelling (lymph node), weight loss, fatigue, feeling unwell, and even symptoms from abnormalities of organs such as the lungs, heart, or kidneys.

Who is affected by arthritis?

Arthritis sufferers include men and women, children and adults. Approximately 350 million people worldwide have arthritis. Nearly 40 million people in the United States are affected by arthritis, including over a quarter million children!

More than 27 million Americans have osteoarthritis. Approximately 1.3 million Americans suffer from rheumatoid arthritis.

More than half of those with arthritis are under 65 years of age. Nearly 60% of Americans with arthritis are women.

regards by
Dr.M M ADNAN
contact id:adnan_dani12@yahoo.com

Parkinson's disease

(also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills, speech, and other functions.

Parkinson's disease belongs to a group of conditions called movement disorders. It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia) and, in extreme cases, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive.

PD is the most common cause of chronic progressive parkinsonism, a term which refers to the syndrome of tremor, rigidity, bradykinesia and postural instability. PD is also called "primary parkinsonism" or "idiopathic PD" (classically meaning having no known cause although this term is not strictly true in light of the plethora of newly discovered genetic mutations). While many forms of parkinsonism are "idiopathic", "secondary" cases may result from toxicity most notably of drugs, head trauma, or other medical disorders. The disease is named after English physician James Parkinson, who made a detailed description of the disease in his essay: "An Essay on the Shaking Palsy

Signs and symptoms

Parkinson's Disease affects movement (motor symptoms). Other typical symptoms include disorders of mood, behaviour, thinking, and sensation (non-motor symptoms). Patients' individual symptoms may be quite dissimilar and progression of the disease is also distinctly individual

Motor symptoms:

The cardinal symptoms are:

• Tremor: normally 4-6 Hz tremor, maximal when the limb is at rest, and decreased with voluntary movement. It is typically unilateral at onset. This is the most apparent and well-known symptom, though an estimated 30% of patients have little perceptible tremor; these are classified as akinetic-rigid.
• Rigidity: stiffness; increased muscle tone. In combination with a resting tremor, this produces a ratchety, "cogwheel" rigidity when the limb is passively moved.
• bradykinesia/Akinesia: respectively, slowness or absence of movement. Rapid, repetitive movements produce a dysrhythmic and decremental loss of amplitude.
• Postural instability: failure of postural reflexes, which leads to impaired balance and falls.

Sleep:

• Excessive daytime somnolence
• Initial, intermediate, and terminal insomnia
• Disturbances in REM sleep: disturbingly vivid dreams, and rapid eye movement behavior disorder, characterized by acting out of dream content — can occur years prior to diagnosis.

Perception

• Impaired visual contrast sensitivity, spatial reasoning, colour discrimination, convergence insufficiency (characterized by double vision) and oculomotor control
• Dizziness and fainting; usually attributable orthostatic hypotension, a failure of the autonomic nervous system to adjust blood pressure in response to changes in body position
• Impaired proprioception (the awareness of bodily position in three-dimensional space)
• Reduction or loss of sense of smell (hyposmia or anosmia) - can occur years prior to diagnosis
• pain: neuropathic, muscle, joints, and tendons, attributable to tension, dystonia, rigidity, joint stiffness, and injuries associated with attempts at accommodation

Autonomic:

• Oily skin and seborrheic dermatitis^[10]
• Urinary incontinence, typically in later disease progression
• Nocturia (getting up in the night to pass urine) — up to 60% of cases
• Constipation and gastric dysmotility that is severe enough to endanger comfort and even health
• Altered sexual function: characterized by profound impairment of sexual arousal, behavior, orgasm, and drive is found in mid and late Parkinson disease. Current data addresses male sexual function almost exclusively.
• Weight loss, which is significant over a period of ten years.

Levodopa:

Stalevo for treatment of Parkinson's disease

The most widely used form of treatment is L-dopa in various forms. L-dopa is transformed into dopamine in the dopaminergic neurons by L-aromatic amino acid decarboxylase (often known by its former name dopa-decarboxylase). However, only 1-5% of L-DOPA enters the dopaminergic neurons. The remaining L-DOPA is often metabolised to dopamine elsewhere, causing a wide variety of side effects. Due to feedback inhibition, L-dopa results in a reduction in the endogenous formation of L-dopa, and so eventually becomes counterproductive.

Carbidopa and benserazide are dopa decarboxylase inhibitors. They help to prevent the metabolism of L-dopa before it reaches the dopaminergic neurons and are generally given as combination preparations of carbidopa/levodopa (co-careldopa) (e.g. Sinemet, Parcopa) and benserazide/levodopa (co-beneldopa) (e.g. Madopar). There are also controlled release versions of Sinemet and Madopar that spread out the effect of the L-dopa. Duodopa is a combination of levodopa and carbidopa, dispersed as a viscous gel. Using a patient-operated portable pump, the drug is continuously delivered via a tube directly into the upper small intestine, where it is rapidly absorbed. There is also Stalevo (Carbidopa, Levodopa and Entacapone).

Tolcapone inhibits the COMT enzyme, thereby prolonging the effects of L-dopa, and so has been used to complement L-dopa. However, due to its possible side effects such as liver failure, it's limited in its availability. A similar drug, entacapone has not been shown to cause significant alterations of liver function and maintains adequate inhibition of COMT over time.^[35]

Dopamine agonists:

The dopamine agonists bromocriptine, pergolide, pramipexole, ropinirole , piribedil, cabergoline, apomorphine, and lisuride are moderately effective. These have their own side effects including those listed above in addition to somnolence, hallucinations and/or insomnia. Several forms of dopamine agonism have been linked with a markedly increased risk of problem gambling. Dopamine agonists initially act by stimulating some of the dopamine receptors. However, they cause the dopamine receptors to become progressively less sensitive, thereby eventually increasing the symptoms.

Dopamine agonists can be useful for patients experiencing on-off fluctuations and dyskinesias as a result of high doses of L-dopa. Apomorphine can be administered via subcutaneous injection using a small pump which is carried by the patient. A low dose is automatically administered throughout the day, reducing the fluctuations of motor symptoms by providing a steady dose of dopaminergic stimulation. After an initial "apomorphine challenge" in hospital to test its effectiveness and brief patient and primary caregiver (often a spouse or partner), the latter of whom takes over maintenance of the pump. The injection site must be changed daily and rotated around the body to avoid the formation of nodules. Apomorphine is also available in a more acute dose as an autoinjector pen for emergency doses such as after a fall or first thing in the morning. Nausea and vomiting are common, and may require domperidone (an antiemetic).

regards by
Dr.M M ADNAN
contact id:adnan_dani12@yahoo.com