KYJ 83 - Nitrogen in lungs
I was asked .... "In air we breathe, does nitrogen have a role"?
Let's recap. Air is 21% oxygen and 78% nitrogen (the other 1% is water, argon, and traces of many gases including CO2).
When we breath in, oxygen in air diffuses into the blood across the respiratory membrane. This occurs because blood in the lung is low in oxygen, so there is a one way flow from high oxygen concentration in alveoli, to low concentration in blood.
As arterial blood rich in oxygen perfuses tissues, cells consume oxygen depleting it. Hence it needs constant replacement.
Nitrogen is not consumed by tissues so it's blood concentration is consistent. It is called an "inert gas" meaning no physiological role.
Nitrogen in the alveoli doesn't diffuse into the blood because it's concentration in blood and in alveoli is the same. It is not being used by calls nor created by cells. The only way we can really remove it from blood is to reduce the concentration of it in the air we breathe... Remember that point.
Now back to the alveoli. That air sac with nitrogen and oxygen in it. Oxygen is leaking out, nitrogen is staying in the sac.
The sac collapses slightly. No big deal. Nitrogen's role in the lung is therefore to splint the alveoli open so they can't fully collapse but they do shrink a little.
Exercise: do this!
Take the deepest breath you can and hold it for 15 sec. At the 10-15second mark, just try and breathe in some more. ....
I bet you could. By loosing oxygen into your blood, you made a bit more space inside your lungs. Cool hey!!
Now, what do you suppose happens when you breathe in less nitrogen? We do this to a patient when we put on oxygen. Someone on a face mask at 8 lpm is breathing 50% oxygen, but by pure mathematics they are also breathing about 50% nitrogen.
Oxygen diffuses into blood, and as it does less nitrogen in the alveoli causes less splinting and more alveolar collapse- this is called atelectasis. The higher the O2 a person breathes, the greater is this atelectasis, and it can be bad.
As someone breathes high oxygen therapy, their blood nitrogen (now relatively higher than lung nitrogen), starts to drop. This off gassing of nitrogen is one of the mechanisms by which hyperbaric therapy works on divers with the Bends, but in others, the longer they breathe oxygen in high concentrations, the lower their blood nitrogen becomes.
Eventually you will take them off O2. Now both blood oxygen and nitrogen levels are reduced, meaning that when a person breathes in, the diffusion of both nitrogen and oxygen occurs... Collapsing the alveoli even worse than oxygen alone.
This is one reason that weaning off O2 slowly is needed. Widespread collapse leads to pneumonia.
Summary: the more oxygen you put on your patient, the more lung collapse you cause.
Oxygen is a potentially dangerous and, at times, toxic gas, use it wisely, never routinely.
Friday, 28 March 2014
82 - Pupil Response - neuro obs
KYJ 82. What do pupils add to a neuro assessment?
Consider a neurological assessment. It includes Glascow Coma Score, vital signs, a limb power assessment and pupils.
But what does the pupil check actually achieve? Response of pupils is actually a test of the second and third cranial nerve function (Optic & Occulomotor).
In a head injured patient. Or anyone with raised intracranial pressure, brainstem compression can reduce the efficiency of this pupil response to light either because they can't sense light (CN II) or they can't constrict to the stimuli (CN III). The sensitivity of pupil response is really only of importance in an unconscious patient when determining if the cause of altered consciousness is brain related.
When assessing pupil response we are looking for
- brisk pupil constriction to bright light
- consensual response (ie both eyes constrict irrespective of which eye the light is shone into)
- rapid return to a dilated state.
Size of the pupils ranges between people and ambient light. In a dark room everyone's pupils appear large, and in bright sunlight we have narrow pupils. The assessment of size is therefore essentially meaningless as there is no "normal" size. That said 75-80% of humans have pupils which are the same size. For the rest of the 20-25% of population a size difference of up to 1mm may be a variation of normal. This is called Anisicoria.
So let's take a patient who is unconscious, you assess pupils, and his right eye is size 5 and sluggish to light, left is size 5 and brisk to light. This is a sinister and abnormal finding, and it would lead to a high index of suspicion for a cerebral event (raised ICP, bleed or swelling).
The asymmetry in this scenario was the difference between light reflex briskness. Sluggish pupils mean pressure=bad.
At its worst, fixed dilated non reacting pupils are an indicator of severe raised intracranial pressure, and imminent brain death is probable.
Final practice tip. Use a dedicated pupil torch for this. Don't use that big red dolphin torch that you illuminate the ward on night shift with.
Pupil check is also used as part of a vision and eye test, in this instance the pupil should be clearly visible through a clear cornea, and no opacity in the lens would be a normal and expected finding.
Consider a neurological assessment. It includes Glascow Coma Score, vital signs, a limb power assessment and pupils.
But what does the pupil check actually achieve? Response of pupils is actually a test of the second and third cranial nerve function (Optic & Occulomotor).
In a head injured patient. Or anyone with raised intracranial pressure, brainstem compression can reduce the efficiency of this pupil response to light either because they can't sense light (CN II) or they can't constrict to the stimuli (CN III). The sensitivity of pupil response is really only of importance in an unconscious patient when determining if the cause of altered consciousness is brain related.
When assessing pupil response we are looking for
- brisk pupil constriction to bright light
- consensual response (ie both eyes constrict irrespective of which eye the light is shone into)
- rapid return to a dilated state.
Size of the pupils ranges between people and ambient light. In a dark room everyone's pupils appear large, and in bright sunlight we have narrow pupils. The assessment of size is therefore essentially meaningless as there is no "normal" size. That said 75-80% of humans have pupils which are the same size. For the rest of the 20-25% of population a size difference of up to 1mm may be a variation of normal. This is called Anisicoria.
So let's take a patient who is unconscious, you assess pupils, and his right eye is size 5 and sluggish to light, left is size 5 and brisk to light. This is a sinister and abnormal finding, and it would lead to a high index of suspicion for a cerebral event (raised ICP, bleed or swelling).
The asymmetry in this scenario was the difference between light reflex briskness. Sluggish pupils mean pressure=bad.
At its worst, fixed dilated non reacting pupils are an indicator of severe raised intracranial pressure, and imminent brain death is probable.
Final practice tip. Use a dedicated pupil torch for this. Don't use that big red dolphin torch that you illuminate the ward on night shift with.
Pupil check is also used as part of a vision and eye test, in this instance the pupil should be clearly visible through a clear cornea, and no opacity in the lens would be a normal and expected finding.
81 - Hepatic First Pass and Enterohepatic Recirculation
KYJ 81- Hepatic First Pass
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this episode, we look at the concepts of hepatic first pass, and a related term called enterohepatic recirculation.
Now let's go on a journey. You and I are an antibiotic (say Trimethoprim). It's 10pm and Sally the patient has been diagnosed this afternoon with UTI and Dr Tinkle prescribed a three day blast of Triprim, to be commenced tonight at bedtime.
Sally switches of "Gator people" the latest in classy reality TV shows to hit the small screen, has her last whoofy stinging wee for the night. Pops the Antibiotic and goes off to sleep.
As Sally swallows you, you dissolve almost immediately. Your transit through the stomach reduces you to mere particles in a slurry as you pass into the small intestine.
Here you are absorbed through the Villi, small finger like projections that line the rugated mucosa of the bowel. Absorbed into the blood supply, your very next port of call is the Liver. There you are metabolised into other molecular compounds. This movement from gut to liver is called Hepatic First Pass. It literally means that all ingested medicines are first passed through the liver before systemic circulation.
Now some drugs or their metabolites are released into systemic blood, where they exert their action by being transported to the sites of action. Some drugs or metabolites are secreted by the liver into Bile. This is manufactured in the liver and stored and concentrated in the Gall Bladder. During Sally's next meal, fat in her food will stimulate the Gall Bladder to contract and secrete bile into the duodenum to mix with the food bolus.
Many drugs, (eg antibiotics) after hepatic metabolism are bound to bile salts, where normal bowel bacteria release them for reabsorption. They again undergo hepatic metabolism and the cycle repeats until the drug is eventually eliminated.
This process of drug going round and round between gut and liver is called Enterohepatic Recirculation.
The drugs can be eliminated by many means, but that is a post for another day.
Hope these Pharmakokinetic KYJ posts are helping you hone your pharmacology knowledge.
If you are getting anything from these, let me know and tag a bunch of your nursing crew.
Share the love.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this episode, we look at the concepts of hepatic first pass, and a related term called enterohepatic recirculation.
Now let's go on a journey. You and I are an antibiotic (say Trimethoprim). It's 10pm and Sally the patient has been diagnosed this afternoon with UTI and Dr Tinkle prescribed a three day blast of Triprim, to be commenced tonight at bedtime.
Sally switches of "Gator people" the latest in classy reality TV shows to hit the small screen, has her last whoofy stinging wee for the night. Pops the Antibiotic and goes off to sleep.
As Sally swallows you, you dissolve almost immediately. Your transit through the stomach reduces you to mere particles in a slurry as you pass into the small intestine.
Here you are absorbed through the Villi, small finger like projections that line the rugated mucosa of the bowel. Absorbed into the blood supply, your very next port of call is the Liver. There you are metabolised into other molecular compounds. This movement from gut to liver is called Hepatic First Pass. It literally means that all ingested medicines are first passed through the liver before systemic circulation.
Now some drugs or their metabolites are released into systemic blood, where they exert their action by being transported to the sites of action. Some drugs or metabolites are secreted by the liver into Bile. This is manufactured in the liver and stored and concentrated in the Gall Bladder. During Sally's next meal, fat in her food will stimulate the Gall Bladder to contract and secrete bile into the duodenum to mix with the food bolus.
Many drugs, (eg antibiotics) after hepatic metabolism are bound to bile salts, where normal bowel bacteria release them for reabsorption. They again undergo hepatic metabolism and the cycle repeats until the drug is eventually eliminated.
This process of drug going round and round between gut and liver is called Enterohepatic Recirculation.
The drugs can be eliminated by many means, but that is a post for another day.
Hope these Pharmakokinetic KYJ posts are helping you hone your pharmacology knowledge.
If you are getting anything from these, let me know and tag a bunch of your nursing crew.
Share the love.
Monday, 10 March 2014
80 - Protein Binding (pharmacokinetics series)
KYJ 80 - Drug transport and Protein Binding
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In the last episode we looked at absorption. Once absorbed into the blood stream a drug is considered to be bioavailable.
Today we look at transport. Drugs travel in blood in 2 ways.
First of all they can be carried in their active state, or an inactive state needing to be converted in the liver to have an action.
Blood as a cocktail of cells and plasma (salts, water and protein).
Drugs are dissolved in the plasma water, or they bind to protein. While the most abundant drug carrier is Albumin, there are other proteins called globulins, glycoproteins, or lipoproteins that act as secondary transporters.
Think of a blood as being like a drug smuggler and their luggage, travelling to Bali. The dope is either bound to the boogie board (all taped up for later use) or in the smuggler's pocket, for quick access.
When bound to plasma proteins, the drug is not immediately usable, but when dissolved in the plasma water (in solution), it is available for immediate use. Given any absorbed drug, it is important to know that a drug's action is largely related to the fraction or percentage of a drug that is bound to protein vs the unbound fraction.
Some drugs have high protein binding eg Warfarin is about 98% protein bound, meaning only 2% is usable. In contrast morphine is about 25-30% protein bound, meaning that up to 75% of this drug is available to exert its effects.
If a drug is highly bound then we generally say it has a low volume of distribution and a long half life.
Suppose you gave me an antibiotic: "Robicillin" that was 60% protein bound.
You gave 1000mg
400mg is working at killing "Timmingsosis"
As the drug is used up or metabolised, it is being released from the plasma in proportion. At all times that drug is 60% protein bound and 40% is doing the work. The unbound vs bound fraction stays in balance. Thus the protein acts like a reservoir steadily releasing the drug. Eventually the concentration of unbound drug will dwindle requiring that another dose of the drug is administered to maintain effectiveness.
But if I had a medical condition where I had low albumin in my body (nephrotic syndrome, liver failure, malnutrition), then once all that albumin is saturated or bound to Robicillin, then it stays in the water of the plasma in a higher concentration. Effectively becoming toxic like being overdosed. Say I only had half my albumin. The drug normally 60% plasma protein bound (PPB) can now only bind half to protein (eg 30% PPB) meaning instead of 40% being available, now 70% or 700mg is exerting its action.
It is probable therefore that once a drug is given in a high enough dose, it has fully saturated the healthy person's plasma proteins, and is now toxic.
Toxicity can also occur when two drugs compete for plasma binding. If drug A is administered at the same time as drug B, then proteins could become saturated earlier giving rise to inadvertent potency or toxicity.
A common example is Warfarin and antibiotics (like Ciprofloxacin and clarithromycin). If these are given then the AB bind to plasma proteins reducing the PPB of Warfarin, hence more warfarin in solution increasing bleeding potential. Even Panadol, aspirin and other anti inflammatories, make this happen.
In this episode we touched on the issue of transporting drugs bound to plasma proteins. In summary the bound fraction of the drug is not used or active. Any situations that make more drug available in unbound form can potentate the drug, and some drugs will potentiate others as they compete to bind to plasma proteins.
Albumin is the principle plasma protein, and manufactured in the liver.
...
Time now to diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In the last episode we looked at absorption. Once absorbed into the blood stream a drug is considered to be bioavailable.
Today we look at transport. Drugs travel in blood in 2 ways.
First of all they can be carried in their active state, or an inactive state needing to be converted in the liver to have an action.
Blood as a cocktail of cells and plasma (salts, water and protein).
Drugs are dissolved in the plasma water, or they bind to protein. While the most abundant drug carrier is Albumin, there are other proteins called globulins, glycoproteins, or lipoproteins that act as secondary transporters.
Think of a blood as being like a drug smuggler and their luggage, travelling to Bali. The dope is either bound to the boogie board (all taped up for later use) or in the smuggler's pocket, for quick access.
When bound to plasma proteins, the drug is not immediately usable, but when dissolved in the plasma water (in solution), it is available for immediate use. Given any absorbed drug, it is important to know that a drug's action is largely related to the fraction or percentage of a drug that is bound to protein vs the unbound fraction.
Some drugs have high protein binding eg Warfarin is about 98% protein bound, meaning only 2% is usable. In contrast morphine is about 25-30% protein bound, meaning that up to 75% of this drug is available to exert its effects.
If a drug is highly bound then we generally say it has a low volume of distribution and a long half life.
Suppose you gave me an antibiotic: "Robicillin" that was 60% protein bound.
You gave 1000mg
400mg is working at killing "Timmingsosis"
As the drug is used up or metabolised, it is being released from the plasma in proportion. At all times that drug is 60% protein bound and 40% is doing the work. The unbound vs bound fraction stays in balance. Thus the protein acts like a reservoir steadily releasing the drug. Eventually the concentration of unbound drug will dwindle requiring that another dose of the drug is administered to maintain effectiveness.
But if I had a medical condition where I had low albumin in my body (nephrotic syndrome, liver failure, malnutrition), then once all that albumin is saturated or bound to Robicillin, then it stays in the water of the plasma in a higher concentration. Effectively becoming toxic like being overdosed. Say I only had half my albumin. The drug normally 60% plasma protein bound (PPB) can now only bind half to protein (eg 30% PPB) meaning instead of 40% being available, now 70% or 700mg is exerting its action.
It is probable therefore that once a drug is given in a high enough dose, it has fully saturated the healthy person's plasma proteins, and is now toxic.
Toxicity can also occur when two drugs compete for plasma binding. If drug A is administered at the same time as drug B, then proteins could become saturated earlier giving rise to inadvertent potency or toxicity.
A common example is Warfarin and antibiotics (like Ciprofloxacin and clarithromycin). If these are given then the AB bind to plasma proteins reducing the PPB of Warfarin, hence more warfarin in solution increasing bleeding potential. Even Panadol, aspirin and other anti inflammatories, make this happen.
In this episode we touched on the issue of transporting drugs bound to plasma proteins. In summary the bound fraction of the drug is not used or active. Any situations that make more drug available in unbound form can potentate the drug, and some drugs will potentiate others as they compete to bind to plasma proteins.
Albumin is the principle plasma protein, and manufactured in the liver.
...
Time now to diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
79 - Drug Absorption (Pharmacokinetics series)
KYJ 79- Drug Absorption
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this session: Absorption and transport of a drug in our bodies.
Consider three different drugs, orally ingested Warfarin. Intravenous Morphine and a topical tinea (ringworm/athletes foot) cream like Miconizole. All different drugs yet totally different routes of administration.
Absorption refers to the way that a drug gets from where we give it, to the site in the body where the drug will exert its influence. For most drugs, the drug is carried in the blood an exception would be a topical drug delivered directly to the site of action eg the tinea cream. When a person has a fungal lesion, Miconizole cream can be applied directly to affected skin where it exerts it's action topically. It is not absorbed into the blood stream.
Other examples include ear or eye drops, even salbutamol given by nebuliser or metered aerosol, is delivered topically at the site in smooth muscular bronchiole tissue, where is causes smooth muscle relaxation.
Systemic absorption
Some topical drugs are absorbed into the skin where it diffuses into the capillaries and enters the circulating blood. Examples include GTN (Transiderm) patches, Fentanyl and nicotine patches. Steroids like oestrogen, progesterone, hydrocortisone and non-steroid anti-inflammatory rubbing gels are systemically absorbed into the blood, eg Diclofenac (Voltaren Emulgel), and Ibuprofen.
When a drug is administered directly into the blood, it doesn't need absorption. These drugs are called parenteral drugs. Any drug given intravenously, intramuscular or subcutaneously fall into this category. Once injected, intravenous morphine is immediately into the blood stream and available to be carried to the brain where it binds to Mu receptors and exerts it's action centrally to inhibit pain sensation. In recent years other drugs eg Ondanzetron and Midazolam have been administered into the mouth or nose where they are absorbed directly into systemic blood through a dense network of blood vessels.
Other drugs are slower to be absorbed. When swallowed the medication packaged usually in a pill (sugar film coated) , capsule (protein film coated), or tablet (compressed powder), is swallowed, where it is broken down and digested. The drug is absorbed from blood vessels lining the stomach or most commonly the small intestine. Once entering the gut blood, this drug is transported directly to the liver and metabolised. This is called Hepatic First Pass (HFP). More on HFP in a later session.
For many drugs this HFP destroys the drug, making some drugs less active when taken orally (Pethidine, diazepam) or completely inappropriate for oral ingestion (eg insulin, heparin, GTN), for other drugs, this hepatic metabolism is necessary to metabolise a drug into an active chemical that exerts an action.
An example is Metronidazole (Flagyl) , paracetamol (Panadol), Enalpril and even codeine all need conversion into an activated new chemical to do their job.
Absorption is how a drug enters the blood stream. In our next episode, we will look at transportation and protein binding.
Now diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this session: Absorption and transport of a drug in our bodies.
Consider three different drugs, orally ingested Warfarin. Intravenous Morphine and a topical tinea (ringworm/athletes foot) cream like Miconizole. All different drugs yet totally different routes of administration.
Absorption refers to the way that a drug gets from where we give it, to the site in the body where the drug will exert its influence. For most drugs, the drug is carried in the blood an exception would be a topical drug delivered directly to the site of action eg the tinea cream. When a person has a fungal lesion, Miconizole cream can be applied directly to affected skin where it exerts it's action topically. It is not absorbed into the blood stream.
Other examples include ear or eye drops, even salbutamol given by nebuliser or metered aerosol, is delivered topically at the site in smooth muscular bronchiole tissue, where is causes smooth muscle relaxation.
Systemic absorption
Some topical drugs are absorbed into the skin where it diffuses into the capillaries and enters the circulating blood. Examples include GTN (Transiderm) patches, Fentanyl and nicotine patches. Steroids like oestrogen, progesterone, hydrocortisone and non-steroid anti-inflammatory rubbing gels are systemically absorbed into the blood, eg Diclofenac (Voltaren Emulgel), and Ibuprofen.
When a drug is administered directly into the blood, it doesn't need absorption. These drugs are called parenteral drugs. Any drug given intravenously, intramuscular or subcutaneously fall into this category. Once injected, intravenous morphine is immediately into the blood stream and available to be carried to the brain where it binds to Mu receptors and exerts it's action centrally to inhibit pain sensation. In recent years other drugs eg Ondanzetron and Midazolam have been administered into the mouth or nose where they are absorbed directly into systemic blood through a dense network of blood vessels.
Other drugs are slower to be absorbed. When swallowed the medication packaged usually in a pill (sugar film coated) , capsule (protein film coated), or tablet (compressed powder), is swallowed, where it is broken down and digested. The drug is absorbed from blood vessels lining the stomach or most commonly the small intestine. Once entering the gut blood, this drug is transported directly to the liver and metabolised. This is called Hepatic First Pass (HFP). More on HFP in a later session.
For many drugs this HFP destroys the drug, making some drugs less active when taken orally (Pethidine, diazepam) or completely inappropriate for oral ingestion (eg insulin, heparin, GTN), for other drugs, this hepatic metabolism is necessary to metabolise a drug into an active chemical that exerts an action.
An example is Metronidazole (Flagyl) , paracetamol (Panadol), Enalpril and even codeine all need conversion into an activated new chemical to do their job.
Absorption is how a drug enters the blood stream. In our next episode, we will look at transportation and protein binding.
Now diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
78 - Nitrites in urine
KYJ 78 - Nitrites on a urine test.
When we test urine using the colour coded dip stick there are many reagents that can indicate abnormality. One of the common illness to screen for is urinary tract infection (UTI). This problem is most common in women and relates to the simple fact that a female urethra is much shorter than a male's. It has been estimated that 50% of all women will experience a UTI at least once.
Bacteria and other flora can ascend the urethra and invade the bladder causing inflammation (cystitis) then, in severe cases, ascend the ureters, and infect the kidneys (pyelonephritis).
The most common organism is Escherichia coli or E.coli to his mates. This is a gram negative bacteria that normally lives in the bowel and are often referred to as "Normal Flora". They serve a good function of preventing "bad bacteria" proliferation and they manufacture Vit K.
Things turn nasty when they take leave from poo central, and migrate north to the sprinkle fields. Once invading the urethral meatus, the are usually flushed with every pee, but poor hydration, high sugar diet and other factors can provide the perfect environment to proliferate and cause inflammation.
As these bacteria multiply they attach to the bladder wall and secrete a gel that acts like a shield to hide from the immune system. Here they proliferate and overwhelm the immune defence causing symptoms of stinging, burning, frequency, urgency and offensive urine odour. Occasionally urine may be pink tinged, or cloudy in appearance. In severe pyelonephritis, it can almost look like pea-soup.
Diagnosis is usually clinically based on the history and these symptoms, but urine testing for blood, especially leukocytes (white blood cells WBC), and Nitrites is all suggestive of UTI.
As inflammation sets in, bladder capillaries engorge and become permeable to white and red blood cells leaching into the bladder. In infections this proliferation serves to cause more immune fighting neutrophils, and phagocytes to fight the bacterial invasion. This clouds the urine and pus is produced as dead WBC and bacteria accumulate.
Bacteria like E. coli secrete a chemical waste called Nitrite during their proliferative stage, and this accumulation of nitrites in urine is always a strong indicator of UTI. Long before leukocytes are seen on a dipstick test, nitrites will be present.
Occasionally the bacteria can turn the urine acidic which gives rise to the symptoms of stinging and burning during voiding. If you encourage water intake this has a soothing and acid dilution effect, as well as assisting to flush the bacteria away. Urinary alkalinisers are also effective for comfort, (Ural or Citravescent ) but don't kill the bacteria.
Treatment includes antibiotics, most commonly Trimethoprim taken once/day, at bedtime for 3 -7 days.
Trimethoprim is a bacteriostatic agent which doesn't kill E.coli, but prevents them from reproducing. They then die out or are flushed out.
Trimethoprim use is indiscriminate. It sterilises the E.coli in the UTI, but also affects all your good E.coli in the gut serving their important function. People on Trimethoprim, like other similar antibiotics should consider recolonising their gut simultaneously with a Probiotic (good bacteria) and /or a few tubs of yoghurt.
When we test urine using the colour coded dip stick there are many reagents that can indicate abnormality. One of the common illness to screen for is urinary tract infection (UTI). This problem is most common in women and relates to the simple fact that a female urethra is much shorter than a male's. It has been estimated that 50% of all women will experience a UTI at least once.
Bacteria and other flora can ascend the urethra and invade the bladder causing inflammation (cystitis) then, in severe cases, ascend the ureters, and infect the kidneys (pyelonephritis).
The most common organism is Escherichia coli or E.coli to his mates. This is a gram negative bacteria that normally lives in the bowel and are often referred to as "Normal Flora". They serve a good function of preventing "bad bacteria" proliferation and they manufacture Vit K.
Things turn nasty when they take leave from poo central, and migrate north to the sprinkle fields. Once invading the urethral meatus, the are usually flushed with every pee, but poor hydration, high sugar diet and other factors can provide the perfect environment to proliferate and cause inflammation.
As these bacteria multiply they attach to the bladder wall and secrete a gel that acts like a shield to hide from the immune system. Here they proliferate and overwhelm the immune defence causing symptoms of stinging, burning, frequency, urgency and offensive urine odour. Occasionally urine may be pink tinged, or cloudy in appearance. In severe pyelonephritis, it can almost look like pea-soup.
Diagnosis is usually clinically based on the history and these symptoms, but urine testing for blood, especially leukocytes (white blood cells WBC), and Nitrites is all suggestive of UTI.
As inflammation sets in, bladder capillaries engorge and become permeable to white and red blood cells leaching into the bladder. In infections this proliferation serves to cause more immune fighting neutrophils, and phagocytes to fight the bacterial invasion. This clouds the urine and pus is produced as dead WBC and bacteria accumulate.
Bacteria like E. coli secrete a chemical waste called Nitrite during their proliferative stage, and this accumulation of nitrites in urine is always a strong indicator of UTI. Long before leukocytes are seen on a dipstick test, nitrites will be present.
Occasionally the bacteria can turn the urine acidic which gives rise to the symptoms of stinging and burning during voiding. If you encourage water intake this has a soothing and acid dilution effect, as well as assisting to flush the bacteria away. Urinary alkalinisers are also effective for comfort, (Ural or Citravescent ) but don't kill the bacteria.
Treatment includes antibiotics, most commonly Trimethoprim taken once/day, at bedtime for 3 -7 days.
Trimethoprim is a bacteriostatic agent which doesn't kill E.coli, but prevents them from reproducing. They then die out or are flushed out.
Trimethoprim use is indiscriminate. It sterilises the E.coli in the UTI, but also affects all your good E.coli in the gut serving their important function. People on Trimethoprim, like other similar antibiotics should consider recolonising their gut simultaneously with a Probiotic (good bacteria) and /or a few tubs of yoghurt.
77- Brugada and SUDS
KYJ 77 - Brugada and SUDS
A recent image that went viral on the internet, showed an ECG that demonstrated a newish abnormality. Brugada syndrome is a genetically inherited ST elevation pattern in V1 and V2.
It was named after two brothers in the early 1990s who discovered the rhythm was associated with sudden unexplained death syndrome (SUDS).
Affecting boys and men with no other cardiac risk factors, Brugada strikes with no warning because, usually young fit men would have had no need to have an ECG previously. It is therefore diagnosed by accident or routine pre-op ECG in mining, military or other industries that require a rigid medical screening pre-employment. It is also seen post successful resuscitation of men who were "a near miss" for SUDS.
The course of illness manifests as collapse and sudden cardiac arrest (SCA) with victims found to be in ventricular fibrillation.
If detected, prophylactic use of an implantable defibrillator is often the treatment.
Brugada is perhaps the most common cardiac cause of sudden death in healthy men.
A recent image that went viral on the internet, showed an ECG that demonstrated a newish abnormality. Brugada syndrome is a genetically inherited ST elevation pattern in V1 and V2.
It was named after two brothers in the early 1990s who discovered the rhythm was associated with sudden unexplained death syndrome (SUDS).
Affecting boys and men with no other cardiac risk factors, Brugada strikes with no warning because, usually young fit men would have had no need to have an ECG previously. It is therefore diagnosed by accident or routine pre-op ECG in mining, military or other industries that require a rigid medical screening pre-employment. It is also seen post successful resuscitation of men who were "a near miss" for SUDS.
The course of illness manifests as collapse and sudden cardiac arrest (SCA) with victims found to be in ventricular fibrillation.
If detected, prophylactic use of an implantable defibrillator is often the treatment.
Brugada is perhaps the most common cardiac cause of sudden death in healthy men.
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