Plasmids and antibiotic resistance

#KYJ -  Superbugs, Plasmids and Genetic mutation.

Make a note of " MCR-1 ".

It is a buzz term that you will hear more about.  We start our explanation of this, with a  a basic review of microbiology.... 

Hello.... Hello??  Are you still awake?  Stay with me.

Bacteria a living cells with cell walls made of carbohydrates (cellulose- a complex sugar).

Some have a fatty (lipid) membrane coating around the cell wall. 

Inside, are most of the goodies that other cells have, organelles like mitochondria, cytoplasm, lysosomes, and nucleus to name a small familiar sample.

Inside the nerve centre of the bacteria is genetic material (genes) arranged in to long protein strands called chromosomes.  This is where the bacteria gets its instruction to function and reproduce.  

Unlike animals and plants that must mate with a male/female combination to reproduce, bacteria are asexual; boring I know, but true none the less.  To divide into two identical copies of its self (producing offspring called Daughter cells), bacteria copies its chromosomes, then simply splits down the middle to form two new cells. 2 become 4 become 8 become 16 and so on ( look up you year 8 maths books , or have a chat to any Amway dealer to see how effective the power of duplication becomes.)

Anyhow I digress... 

Given that bacteria make absolute clones of them self, you would think they can't change.   But we know they do.   They become resilient, and adapt to new environments.  They mutate.

Enter the plasmid.

A plasmid is a rogue speck of genetic material that lives in the cytoplasm (watery juice) of the bacteria.  Plasmids are genetic coded proteins that can become altered when a bacteria is exposed to an antibiotic (that should have killed it) but survives.   Plasmids change, replicate on their own and translocate genetic information with genes inside the nucleus.

Now this surviving bacteria passes on this information to its daughter cells creating a bacteria that is now resistant to the antibiotic that previously would have killed its grand parents.

Are you still awake? 

Ok.  So plasmids don't just mutate and affect the host bacteria, but they can also share genetic information to other bacteria, even other species of bacteria.  A Strep can share its resistance recipe with a Staph, or an E.coli with an Enterococci, or a Bacillus with a diplococcus.

Frightened yet?

Recently, an E.coli strain was discovered in a urine sample of an American woman with a UTI.  This infection is resistant to every antibiotic.  EVERY ANTIBIOTIC.   

This drug resistant E.coli strain has a gene called MCR-1 which is harboured in the E.coli's plasmid.  

This E. coli bacteria with the mcr-1 gene could pass its plasmid and gene  to another superbug with other mutations-- creating a truly super-superbug that resists all known antibiotics.

The bio surveillance role that nurses and doctors have was always important, but this is going to have implications on infection control practices going forward.  

I'm off to wash my hands ... again! 

Adenosine

#KYJ.  Adenosine.
Have you ever given this IV drug to a patient?
It is used to cause a complete block through the AV node, in patients experiencing a Junctional Tachycardia (previously and more commonly called Supraventricular Tachycardia (SVT)).

Its use is common, and when given correctly it is very effective.  In the past you may have been taught to give it as a neat push IV.  But more recently it has become popular to dilute the required dose up to a 20ml volume and rapidly push in a largish (18g) IV cannula in the antecubital fossa, and quickly flush with a 10-20 ml saline

This drug has the effect of stopping the heart.  Thankfully it has a very short half life of 4-7 seconds (requiring the rapid push). Like a computer that is playing up, you get the sense that this drug is like a cardiac "Reset button", like someone said "have you tried turning it off, then on again?"

Vials come in 6 mg but it is very common (almost expected) that we start at 9mg.
A common regimen is
3 x 2 minutely doses starting at
9mg - 9mg - 12 mg.

If it works on dose 1, the other two are not needed.

Doses are expected to work in 5-10 seconds so as you give the push, the patient needs to be attached to the cardiac monitor.  You are watching for the SVT to deteriorate into a severe bradycardia or asystole (flat line).

Their heart stops.... Then in 3-5 seconds it automatically restarts, hopefully into a normal sinus rhythm .... It's a reset button.

Patients often experience fear, and altered consciousness as their brain oxygenation ceases for that few seconds.  Many describe a sense of doom, or near death phenomenon like a Tunnel of light, out of body experiences or a peaceful place of comfort and warmth.  Some report an experience of meeting their deity or previously deceased loved ones.  Rarely this experience is one of terror, and there are documented case reports of Post traumatic stress disorder.  This drug is excellent but has some issues.

Nurses should comfort the patient and prepare them for a sensation of "passing out". Tell them that you will stay with them and keep them safe.  Hold their hand.  They are often very frightened.

Have you had a patient on this drug?  Tell us your story.

#KYJ - HbA1c in Brief

Understanding HbA1c (#knowingyourjargon)

Smooth RBCs  are kind to your blood vessels, but sugary sticky ones damage the walls stimulating the inflammatory system that initiates cholesterol to be sent out from the liver to repair the damaged walls.

Red blood cells live 120 days.  During that time they slowly accumulate glucose and the haemoglobin protein (most famous for transporting oxygen) becomes glycated.

This glycated haemoglobin is measured as a percentage (old measurements) or in mmol/mol

The test for this stickiness of red blood cells is called HbA1c

As a percentage less than 6% is normal.
More modern tests measure in mmol/mol where less than 42 is considered normal.

Diabetes is commonly diagnosed with HbA1c levels above 6.5% or 48 mmol

Unlike a random BSL, the A1c test looks at glucose control over a period of 3 months, and is accurate as a control monitoring test for diabetics.

ACE inhibitors- why they cause cough

#KYJ - #KnowingYourJargon

ACE inhibitors and that nasty Cough.

With many classes of blood pressure drugs on the market, it can be a mind storm navigating them all as nurses.

A common first line antihypertensive is the humble ACE inhibitor.  It's main side effect is cough and it drives patients and their partners crazy.

... But why? 

How does it cause cough?

Well let's understand ACE.

Angiotensin Converting Enzyme.

ACE is created in lungs and there, it has a role in destroying inflammatory chemicals called Bradykinin and Substance P.   These pro-inflammation proteins cause lung tissue irritation- notably cough (tussis).

ACE also notably converts Angiotensin into a vasoconstrictor that raises Blood Pressure.  It stands to reason if I inhibit ACE then I can't convert Angiotensin.

Hence its valuable role as a blood pressure lowering drug.

BUT....

If you give an ACE inhibitor, and prevent the breakdown of bradykinin and substance P (Inflammatory chemicals), there is an accumulation of these protussive mediators (coughing stimulants) in the respiratory tract. 

This side effect is not dose-dependent and often precludes the use of all agents within the drug class.

Common offenders are Lisinopril, Perindopril, and a new one released after March and before May called April😆😆😆.

No seriously.  ACE inhibitors cause cough and often this means that the patient needs a new approach to BP control.

 

Polypharmacy and drug interactions

#KYJ - Polypharmacy
www.ect4health.com.au/rustypills/
Interesting term, but one we need to know more about.   Polypharmacy is defined as 4 or more concurrent medications.  The issue is drug to drug interactions that occur when a person takes two or more drugs that are metabolised by the same enzyme systems in the liver and other tissues.
Many medications use a system called Cytochrome 450 enzymes(P450).
If drug A and drug B are both metabolised at the P450, then metabolism of both drugs can be impaired or delayed, rendering both inactive or toxic.  These interaction can make one or both medicines overly potent.

The issue compounds with every extra medication a person takes. In fact if your patient takes 5 medications, there is a 50-80% chance of an adverse effect.  What's worse, is that the risk increases 12-15% for each extra drug in that little dosette box.

Take Lipitor (Atorvastatin) the worlds most prescribed drug.  It has over 250 drugs that interact with it to cause adverse effects.
Common medications  causing issues in combination with Lipitor include:
amlodipine
aspirin
atenolol
Cymbalta (duloxetine)
Fish Oil
gabapentin
hydrochlorothiazide (Enduron)
Lasix (frusemide)
levothyroxine
lisinopril
metformin
metoprolol
Nexium & omeprazole
Plavix (clopidogrel)
Synthroid (levothyroxine)
Vitamin D3 (cholecalciferol)

These drugs are hard to get our head around, but the issue of polypharmacy being linked to dementia, falls and muscle atrophy in elderly is one that is on the rise, and needs clinicians to be wary and hyper vigilant.

Our latest Rusty Pills seminar discusses this issue and many others.
Check out http://www.ect4health.com.au/rustypills/

Post concussive symptoms in children

Concussion in kids

Concussion is divided loosely into two categories.
Mild concussion is a bang on the head where the patient was not knocked out.

Classic concussion is when a person was knocked out.

When assessing patients after a closed head injury, nurses and doctors often use a multitude of tools and questions about the event.  On average about 30% of adults who receive concussions, go on to have persistent symptoms of headache and concentration loss, memory disturbances and dizzyness for months.   This is called Persistent post concussion syndrome (PPCS).
Predicting who will have PPCS is difficult, but one team of researchers in Canada have just published a paper that summarises the process in children.

They state that  "clinician prediction is no better than a coin toss".

In assessing long term risk of PPCS in children the research team found some surprising things.

Where we as clinicians have long thought that loss of consciousness and vomiting post head injury were somewhat prognostic for post concussion symptoms, these researchers consider these as less predictive.

Using a 12 point scoring system the researchers looked at some 3000 five to 18 year olds,
Higher scoring data (2 points) Included
Gender=female
Age >13
Fatigue

Points are also allocated for
Headache
Previous concussion
Slow to answer questions
Sensitivity to noise
History of Migraine
Poor balance
For

A score of 9-12 correlated with a 93% incidence of prolonged post concussion symptoms.

Ref:
Zemek et. al  2016
Clinical Risk Score for Persistent Postconcussion Symptoms among children with acute concussion in ED
JAMA. 2016;315(10):1014-1025.
 doi:10.1001/jama.
http://jama.jamanetwork.com/mobile/article.aspx?articleid=2499274

Breath Sounds -part 4. Ergophony and whispering Pectoriloquy

Breath Sounds -part 4

Whispering to a Goat??

Ergophony and Whispering Pectoriloquy.

In this short mini-series, we look at the basics of auscultation of lung sounds.

Few things are cooler than listening to a sick patient's chest and hearing the classic sounds that highly suggest a specific diagnosis.

Pneumonia (lobar consolidation), is one such diagnosis.  With alveoli collapsed and congested under the strain of pus, and other inflammatory debris, the way sound is transmitted becomes characteristically different.  If reading about this for the first time, you will be itching to give this a go.

Ergophony

Assume Mr Chester in bed 6 has a diagnosis of Right middle lobe pneumonia. He is admitted on the ward for IV antibiotics and supplemental oxygen.  As part of your routine assessment, you auscultate his lung sounds.  

You ask Mr Chester to repeat the letter E, over and over while you listen the the resonance of his voice, through your stethoscope, at different locations on his chest.  Across his left chest you hear the familiar sound of him chanting "Eeeee, Eeeee,Eeeee...." Over and over.

But as you place your stethoscope over the consolidated region of his right chest, the sound changes to a muffled "Aaaahhh, Aaaahhh, Aaaahhh..." sound.   It sounds to you like the bleat of a goat or sheep.   This is called Ergophony and literally means "voice of the goat".  It is caused by changes to the sound waves as they travel through different densities of lung. When transmitted through pus filled dense pneumonia lobes, the Eeee resonates to Aaahhh.

Whispering Pectoriloquy

Say it out loud :

"Peck - tor- rill- oh- Kwee"

Apart from being a cracking scrabble word, this funky phenomenon is another one that can be heard in patients with pneumonia.

Normally if I listen to your lung fields with my stethoscope while you are whispering, I wont hear your words.  The light air filled matrix of your ventilating lung filters out whispered sounds, rendering them inaudible on auscultation of a normal chest.  However, when Mr Chester has pneumonia and an area of consolidation, sound is transmitted well through more dense tissue.  

Start by asking your patient to sit upright and chant through the alphabet or count to 100 but only whispering.  As you listen to the healthy areas of his chest you'll not hear his whispers, but when the stethoscope is placed over pneumonia consolidation of lung masses, you will hear the whispered words through your stethoscope. This is called whispering pectoriloquy, and is a symptom of consolidation.

Well that is it for part 4 of our breath sounds .  Stay tuned for part 5 where we discuss some other adventitious noises.

If you missed our other KYJs in this series click them here.

Www.knowingyourjargon.blogspot.com

Please comment on and share these. I'd love to see you at one of my nursing seminars.  They can be found on our ECT4Health web page.