Cardiogenic shock and Frank Starling

#KYJ - Cardiogenic Shock

Let’s unpack this common type of shock we see in our clinical deteriorating patient’s.

I edit, proof and English polish nursing and paramedic assignments as a side service to my seminar and cruise boat education sessions.

In many recent case studies, pathophysiology is a common theme that needs a bit of work to schmooze the passing paper in to an A Grade masterpiece.   The last 3 months was full of shock, and especially cardiogenic, so I thought I’d dedicate this episode of #KnowingYourJargon (KYJ) to this topic.

Let’s commence with nomenclature.  Cardio = heart.  Genic = to originate/create (think Genesis as the book of creation from Old Testament Judeo/Christian and Islam mythology) .

Shock- is fundamentally a state of imbalance between cellular oxygen demand vs delivery of oxygen to cells .   In a nutshell, shock is “relative global cellular hypoxia” (Timmings 2004) 

Then cardiogenic shock therefore means :

Global cellular hypoxia that originated from heart failure.

To unpack this further we need to understand heart pumping function, and it’s discourse- heart failure.

Given the adult heart pumps blood; the volume it pumps measured over a minute is termed Cardiac output.  Normally this equates to 4.2-7 litres/min which is pretty awesome given its size.

Now when there is injury, or death of heart muscle, or  degenerative changes occur with lifestyle challenges and the encroachment of the autumn years; the efficiency of the heart as a pump wanes.

This is called heart failure and can occur in with left or right heart or both, termed congestive heart failure (CHF)

These slow changes over years are called “chronic” , but after a cardiac event such as a myocardial infarction (commonly termed heart attack), or a traumatic injury to the heart eg stabbing, or blunt crushing trauma, then the cardiac failure is called Acute.  Irrespective of aetiology, a heart in failure wont pump adequate oxygenated blood around the body to meet the demand of cells-  this is shock. Cardiogenic shock.

Now read on if you are interested in diving deeper.

This is where you and I get our geeky on!!

Frank -Starling Mechanism(Law)

Otto Frank and Ernest Starling were a couple of turn of the century early 1900s geekoids that had a hankering for the dynamics of the heart pumping function- Otto loved playing with frogs, and Ernest was a Dog man, so armed with their work on Frogs n Dogs, they went and got a whole mechanism named after themselves.

Essentially what they asserted was two monumental principles.

First that a heart needs to fill up with blood before it can pump out any blood . . .

Yep, I know- crickets...

Their second assertion is that not only does the heart need to fill up with blood, but it’s chambers must actually be stretched a little to get a good strong elastic contraction.

I know these seem obvious, but in the world of medicine and cardiology especially, that fill up the heart till it’s a bit stretched like a balloon part is called “Preload”. You have to have preload the ventricles before an output from the pump will be efficient.

Think of a rubber band .

It’s elastic potential is only realised when you stretch it, and heart muscle is the same.  If you don’t pull back on a rubber band you can’t ‘feeyonnnng’ (real word*) it across the room at your loved one.

*ok that was t a real word- but you get it hey?   Stretch The rubber and whoosh there is a release of tension.

In cardiac ventricles this preload works like a partially inflated balloon.   Let it go and the elasticity causes the air you blew into the balloon to propel it across the room.

Hearts need to fill with blood and preload.

Now Frank and Starling also said that too much stretch (preload) is going to work against the pump.  Preload is a good thing but overload causes failure .

Like Tim Tams- some = good , but the whole packet = bad.

In heart failure the pump has lost its inotropy (force of contraction) so if the weak muscle can’t pump the reservoir of blood out efficiently= cardiogenic shock happens.

Likewise in MIs, or acute muscle injury.

A secondary mechanism is the hypoxia of heart muscles itself.  Muscle needs oxygen to pump (contract) but also to relax and fill.   So ischaemic (hypoxic) hearts are stiff and non compliant-  remember Starlings first principle ?   Heart has to fill up with blood first.

Well in stiff poorly filled hearts, output will drop.

Again - cardiogenic shock.

Are we done?

Credit: Robert Timmings 

#ECT4Health 

@ECT4Health 

#RobTimmings

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Irukandji syndrome

#KYJ - Irukandji Syndrome

They only live for about 6 months, they have 24 eyes, 4 stomachs, each with their own anus, and are no bigger than your thumb nail; but , they punch way above their weight by packing a sting that places them into the top 10 deadly venomous animals in the world.

Only a handful of deaths have been attributed to a collection of jellyfish stings known collectively as Irukandji, but the syndrome that their stings invoke always require hospital admission for analgesia, and cardiac monitoring. 

The most common offender Carukia barnesi, (identified in 1964 and named after its discoverer, Jack Barnes, is one of up to 16 species all thought to inflict the sting with venom causing what is now called Irukandji Syndrome.   There isn’t one “Irukandji jellyfish”, so with similar biology but different genetic features, it is tangible to see their venom effects can be difficult to pin down.

What is known is that these jellyfish uniquely have stinging cells (nematocysts) on not only their tentacles (of which there are four), but also in their Bell.  There is no safe place to handle them.

Their venom is thought to contain a nerve agent that acts to modulate sodium channels.  The effects cause rapid nerve firing .

Symptoms

5-30 minutes after a sting, the victim will experience severe generalised pain or cramps, 

GI symptoms of Diarrhoea, nausea and vomiting, 

Sympathetic symptoms localised or general sweating, restlessness, anxiety, headache,large muscle cramps and painful back spasms, and a classic sense of doom.

Pain from Irukandji can last weeks, and has been reported as the proverbial “10 out of 10”

Irukandji Syndrome can cause pulmonary oedema (likely cardiogenic) as acute hypertensive crisis is a frequent symptom, that has lead to stroke.

These stings hospitalise dozens of people world wide, and in Australia.  

The flourish in warm waters where hard coral is abundant (reefs). They are a family of jelly fish that actively hunt fish in the reef ecosystem, and are attracted to light.   What is sinister is that their annual blooms are being recorded as far south in the Australian east coast as Hervey Bay, and the southern migration each year correlated with warmer ocean currents.   The estimate from researcher is that their impact on the massive Gold and Sunshine Coast tourist industry will be inevitable as they march down our coast line.

Treatment.

Phase 1 - First aid

The first aid for suspected Irukandji stings is DRSABCD, and liberal dousing with vinegar.

While the vinegar does nothing for the pain or symptoms from stinging cells that have shot their load, the acid is thought to disable the unfired cells from further envenomation.

A few years ago Associate Professor Jamie Seymour from the Australian Institute of Tropical Health and Medicine (JCU in Cairns) reported that vinegar can actually cause discharge of stinging cells worsening the envenomation buy up to 50%, he stated "That's a big amount, and that's enough to make the difference, we think, between someone surviving and somebody dying."

That said, the Australian Resuscitation Council continues to recommend using vinegar.  So what to do?  More research is needed on the vinegar thing.

Phase 2- hospital management.

Pain and cardiovascular management is the priority.   Massive IV narcotic use and even sedation with ventilator support may be necessary.

There is no Antivenom or reversal agent.

Supportive use of Antihypertensives, and antihistamines are indicated.   Magnesium Sulphate is thought to be cardio protective and aids in the extreme haemorrhagic stroke risking hypertension.

These people go on to experience excruciating pain for days to weeks, so analgesia will be their friend.   Of the doom and dread and pain, one of my patients stated:

“For the first hour I was worried I would die, then for the next few hours, I was worried I wouldn’t!”

The jellies are coming more prevalent, and as more people are being stung in further southern parts of the coast, clinicians in places like south east Queensland will soon notch up their first Irukandji Syndrome patient in the annals of the reflective journals.

Written by Rob Timmings

@ECT4Health 

#Irukandji #ECT4Health 

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Spider bites and other creepy crawlers

#KYJ-  Spider bite.

In the last great act of defiance look at where this spider decided to sit.  We hear a lot about creepy crawleys in our area. Spiders, scorpions, ants, wasps and centipedes (and that is just my yard).

Recent east coast wet weather has produced a minefield of critters that can cause harm.

This KYJ is dedicated to terrestrial arthropod bites. 

These fall into two categories.  Insects (6 legged bugs) and arachnids like Scorpians, centipede and spiders.

With the exception of the infamous Funnel web spider, all critters listed above are treated the same. 

Wash the bite with soap and water, apply an ice pack for 10-20 minutes.

Rest the patient.

Paracetamol or ibuprofen for pain.

Funnel web spiders are potentially lethal. They can cause respiratory failure and are managed as snake bites using pressure immobilisation bandaging and antivenin.

Only male Sydney Funnel Web Spiders and Redback Spiders have caused human deaths, but none have occurred since antivenoms

were made available in 1981.

The Australian funnel-web spiders are among the deadliest spiders in the world, but while they can kill us, their venom has little effect on cats n dogs.  There are many species of funnel-web spiders in Australia but only males of the species is deadly. Despite an average of 40 bites per year from funnel webs, only 13 deaths have been recorded, and none for over 35 years.

Other large hairy spiders like Mouse spiders may have venom that is as toxic as that of some funnel-webs, and while people are bitten from time to time, no-one has been recorded as having died from the effects of a mouse spider bite. Antivenoms are available for both funnel-web and Redback Spider bites.

Red Back bites occasionally get antivenin, but this is a controversy.  In 2012 an Australian study concluded that there was little point, other than a mild, hit n miss analgesic effect.  Considering the fact that no one has died from Red Back spider bites for well over 60 years, many clinicians consider a wait n watch. That said, there is fierce debate among toxicologists (http://mobile.abc.net.au/news/2013-11-22/doctors-warned-to-keep-using-redback-anti-venom/5109838)

Typically spider bites cause an neurotoxic and cytotoxic responses.  

Neurotoxic symptoms include muscle rigidity, stiffness, myalgia and at its worst, weakness and paralysis (eg funnel web).

Cytotoxic effects cause local skin irritation and blistering.  A white hypo perfused area directly onthe bite, with a wide area of redness (inflammation) around the pale bite centre is common. Sweating around the bite site is a function of the neurotoxic effects. 

Some international spider bites (brown recluse) have been associated with necrosis and muscle breakdown but we don't see this in Australian spiders despite the mythical notion of the white tail spider.  It's now widely accepted that any infection post spider bite was not due to venom it was due to soil bacteria introduced at the time of the puncture.

First aid for spider bites remains rest, ice packs, analgesia and give it a good clean.  If the patient has not had a recent tetanus shot then this should be attended to.

Scorpions and centipede in Australia are not deadly. That said and anaphylactic reaction to any bite or sting is a life-threatening emergency.  Like spider bites scorpions and centipede bites I treated using basic first aid.

Whilst this post is focused on spider bites, is important to recognise that wasps and ants stings are also treated with ice packs although much success has been gained from rubbing the freshly cut surface of an onion straight onto a wasp or ant sting.

Personally I have had tremendous success with an onion. Instant pain relief. 

DOAC reversal

Reversing the new oral anticoagulants.

Till recently reversing the “Xabans” and the Direct Factor II inhibitor medications has been a challenge.   Unlike Warfarin which is reversed using Vitamin K, and Heparins which are reversed using Protamine Sulphate; the new direct oral anticoagulants (DOACs) don’t have a magic antidote.

In this post, I’ll unpack the way these new drugs work, and then discuss how they will be reversed if your patient is bleeding from trauma, or requires surgery.

If you’ve seen my YouTube then you will have a good understanding on the differences between blood clotting and blood coagulating (you should start there if you thought they were the same thing).

Fast forward to the #DOAGs section if you’re all over this coag cascade stuff.

Ok

Ultimately the solidification of blood to form a thrombus requires these two separate processes- clotting and coagulation which is the conversion of a cocktail of proteins (coag factors) in blood, from liquid state to a solid stringy strandy dental floss like product that, like string on a birthday parcel holds a parcel of clotted cells (RBC & Platelets) together.

That string is called FIBRIN

Here is where we start. 

If you can’t make fibrin, you can’t coagulate.   The complex cascade of chemical reactions in your blood which forms fibrin, is called coagulation.  Any drug that stops that chain reaction is called an Anti-coagulant.

Simple steps in the common coagulation pathway involve 4 players.

Vitamin K

Factor X (remember that ‘X’) though it’s pronounced “factor 10.”

Factors 2(Factor II) also called Prothrombin

Factor 1 (Factor I) also called Fibrinogen.

Now tissue injury and chemicals released from the platelets and vessel wall cells stimulate the coagulation chain reaction- think of a finger on dominoes.  This activates Factor X.  But this go button needs calcium and vitamin K to allow the cascade to start.

So Factor X activates now called Xa.

Xa activates Factor II Prothrombin 

Which is now called IIa (or Thrombin).

IIa activates factor I

which is technically Factor Ia (aka Fibrin).

Anticoagulants.

Warfarin deactivates vitamin K so the prices can’t start

Heparins/enoxaparin directly prevents the activation of FX into Xa and also stops Prothrombin (Factor II) activating into thrombin Factor IIa.

Now #DOACs 

Direct Oral AntiCoagulants inhibit one of two pathways.

The Xabans- (apixaban, rivaroxaban, edoxaban)

Their name with an “Xa” in indicates that they Ban the Xa-   They actually deactivate factor Xa.   

Remember once activated FX turns to FXa which converts Prothrombin FII.

The Xabans stop (ban) coagulation at that Xa step. 

Dabagatran (Pradaxa) is different.  It waits till Thrombin (IIa) forms then deactivates it so it can’t convert fibrinogen into strings of fibrin.

Now stopping these drugs is not possible, so to help the patient coagulate, we need to stimulate the Fibrinogen directly, or, in the case of Pradaxa, stimulates Prothrombin earlier in the chain reaction.

Now bleeding patients:

On warfarin we can reverse it giving a large bolts of Vitamin K.

Heparin is reversed using protamine.

DOACs are short acting (5-17 hour half lives) , so unless someone just took their dose today, reversal and severe bleeding is rare, making these anticoagulants quite safe.   But what if we don’t have that 5 hours?? 

If available, idarucizumab is recommended for reversal of anticoagulant effects for patients taking Dabigatran.

It is an antibody that binds to the drug blocking its effects on Thrombin.

For the Xabans, the reversal is harder, 

Many have tried and failed, and perhaps the fact that these drug are so short acting that motivating some research and development isn’t seen as worthwhile or profitable.  So we are left with few options; none of which are great.

Charcoal:

If taken inside 4-6 hours of last Xaban dose, activated charcoal orally can bind with Rivaroxaban and Apixaban.

Andexanet alfa, the first agent shown to reverse the anticoagulant effects of rivaroxaban and apixaban, has been approved by the FDA, according to statement from Portola Pharmaceuticals in early May 2018.  It is a factor Xa “decoy” molecule that acts by attracting and sticking to Xabans, thereby preventing them from interacting with actual factor Xa, but andexanet also has a short half life and hence the effect quickly reduces once treatment stops, so needs a complex infusion.

Factor VII - 4factor PCC

FEIBA 50 IU/kg (contains factors 2,7,9 an 10 in predominatly inactivated form as wellas activated factor 7 and 1-6 units of Factor VIII coagulant antigen (FVIII C:Ag) per mL)

Prothrombin-X

Current guidelines do not recommend use of prothrombin complex (Prothrombinex-VF in Australia) but it has been shown to normalise prothrombin time in a trial of 12 healthy male subjects at a dose of 50 IU/kg iv infusion (Eerenberg et al., 2011).

Tranexamic acid (TXA)

Not new, and scraping the bottom of the barrel, but TXA has been used in severe bleeding since Moses hunted Brontosaurus.   It is only used in bleeding patients with Xabans or Dabigatran, if bleeding is severe- ie trauma. Classified as a Plasminogen inhibitor, it really only helps you to maintain any coagulation you’ve been able to make already. So given that DOACs inhibit/slow down coagulation and don’t stop it completely, preserving any thrombus you’ve formed is what you want when you’re bleeding.  TXA does this by preventing body enzymes (plasminogen) dissolving the clots you already made.

Platelets , FFP and RBC 

Again, only if bleeding.   It stands to reason that as you bleed you also loose the DOAC drugs . So transfusions of unadulterated blood products acts to correct not only losses, but dilute the plasma bound DOACs.

Well that’s about it, so Q&A is open.

#RobTimmings #ECT4Health

This content is available in our #RustyPills pharmacology course, and #CardiacSeminars.
Find them all here Www.Ect4Health.Com.Au/whatsWww.Ect4Health.Com.Au/whats 

Bronchiolitis update 2018

#KYJ Bronchiolitis in 2018

Bronchiolitis
Dispelling the myths that we should do what we do because it’s the way it’s always been done.

Background.
The smallest airways are bronchioles. They connect the big airways (bronchi) with the air sacs (alveoli) where oxygen and CO2 do-si-do .

Bronchioles have mucous coated meaty walls with abundant smooth muscle .  They actually constrict and relax to change diameter and regulate air flow. Remember that pearl- we will use that later on.

When inflamed (Bronchiolitis) they swell and constrict, which results in restricted air flow, causing the person to have an increased work of breathing.   That is ok in mild bronchiolitis in fit older children or adults, but in babies or toddlers, these wee tikes get exhausted (the struggle is real).  Apnoea or respiratory arrest is the feared complication in severe bronchiolitis.

Now it comes in two flavours.   Allergic bronchiolitis, and infective bronchiolitis.  Both are swollen restricted airflow. Both cause increased work of breathing.

Infective Bronchiolitis is the most common reasons for babies to be admitted to hospitals in our region (Aust/NZ).  As the name implies, infective Bronchiolitis is caused by a pathogen, almost certainly viral, but far more rarely, bacteria.

With allergic Bronchiolitis the trigger is some substance other than a pathogen.  It might be milk, egg, pollen, dust mite, or any number of triggers.  This stimulates an immune response where histamine is released, swelling and mucous is produced, and unique to Allergic Bronchiolitis (Asthma by another name - but don’t call it that prior to the 3rd birthday), unique to this pathodrome is the feature of dominant bronchospasm.  Remember those smooth muscles?  Yeah, they constrict, strangling the bronchioles worsening air flow.

Ok...  still with me?

48% of infants admitted to Australian hospitals with bronchiolitis receive treatment that has no evidence of benefit (Davis , 2018).
You may know Tessa a Paediatrician who runs a great paeds SoMe called
#DontForgetTheBubbles

She writes that the PREDICT network have conducted a systematic review to produce Australia’s first bronchiolitis guideline .

Investigations
Recommended
•Urine M/C/S (if under 2 months old and febrile)
•Monitor Sats (spO2)
•Monitor work of breathing

Not recommended
•Routine blood
•Routine urine testing
•Viral swabs

Treatments
•Hydrate the kid.  Oral,NG or IV
•Oxygen in children sating at or below 91%

Not recommended
•Oxygen if Sats are >91% (prolongs stay)
•Salbutamol- May worsen
•Steroids eg Predmix
•Saline nebs
•Adrenaline nebs
•Nasal saline drops
•Antibiotics -more harm than good

 Now let’s look at these #CageRattlers.
A common feature of allergic bronchiolitis is bronchospasm, but that is not a common feature of chest infection, so salbutamol, adrenaline or other bronchodilators are not helpful.   In viral chest infection, antibiotics are only effective when it if the child gets an opportunistic bacterial infection on top.  And to suppress their immature immune system using steroids is asking for bacteria and thrush to come to the puffer-party.

So the key here is differentiating between an Asthma like presentation where steroids and salbutamol are indicated, and an infective bronchiolitis where they aren’t recommended as routine.

All in all an interesting summary with a bit of dogma busting along the way.

For a more comprehensive look
Click here: Davis, T. Bronchiolitis guidelines, Don't Forget the Bubbles, 2018. Available at:
http://doi.org/10.31440/DFTB.17023

Liver Falure blood tests

#KYJ - Transaminitis

Pesky liver enzymes.  You’ve had patients who have had blood tests looking at liver function.

When running biochemistry on patients suspected of being in liver failure, a number of enzymes and other proteins are measured.  In this knowing your jargon blog post I’ll take you through the basics in a way you’ll understand, and be able to share with your patients.

There are many, but the rock stars are:

ALT and AST

Albumin

Prothrombin Time or PT.

Let’s start with the Acute /current liver injury ones.

Alanine Transaminase (ALT) and Aspartate transaminase (AST).  These enzymes are in your liver cells.  Locked up like a prisoner in a cell.   There roles are complex and outside the scope of this post, and frankly unimportant for the purpose of measuring  acute liver disease.  

Let’s just say that they are inside liver cells and during acute damage, trauma, infections or cancer of liver tissue, they leak out like myoglobin from damaged muscle cells, or troponin from damaged heart cells.

It stands to reason that when you injure your liver with one too many Yager bombs or a wild night of Beer-pong, you can expect to have released some ALT/AST into your blood stream where it can be measured on biochem blood tests.

ALT/AST is a sensitive marker for acute damage where a big number of liver cells died.  In chronic liver failure, cells die off slowly, so these enzymes leak or leach slowly into the blood.  For this reason, ALT/AST is aun reliable in Chronic disease like cirrhosis or cancer.

An acute injury and subsequent inflammation is termed transaminitis rather than hepatitis which is usually associated with infective inflammation.  Both cause ALT/AST rise.

PT

Prothrombin time or PT is a measure of function of the liver’s role in coagulation.

You know that your liver makes proteins for coagulation. These are called Factors.  Factors 2,7,8,9,10 (and 1&5), all undergo manufacture and activation using Vitamin K .

In acute and chronic liver failure, these proteins (factors) are not made efficiently or in big enough quantities, so the TIME it takes for blood to coagulate is slower.

Measuring Prothrombin Time (PT) allows a measure of hepatic function on coagulation.  

If it normally takes 10 sec for a blood sample to convert Prothrombin into Thrombin, it may take 20seconds in someone in liver failure.

PT is also measured as a blood test called an INR.  It means International Normalised Ratio.

A way of standardising the measure of PT all over the world.

A PT of 10sec roughly equals an INR of 1.0.  PT of 20sec = INR of 2.0 and so on. 

Adequate vit K in the diet allows the liver the ingredients to make those coagulation factors .  Not enough VitK and coagulation (PT/INR) will get longer.  This is why warfarin (a VitK antagonist) makes it longer for people to coagulate.  So... in liver disease, coagulation suffers, and bleeding / bruising can complicate patient symptom sets.

Finally Albumin.

A hugely important protein called Albumin is made in a functioning liver and released into the blood.   It acts as a water magnet and carrier protein of many drugs and other substances in the blood.  After being secreted into the blood by the liver, it has a half life of about 20days. 

If you went into acute liver failure today, we wouldn’t really notice a change in your serum Albumin for a few weeks.  So Albumin reduction is a marker for chronic liver damage.

Well that is it.  A wordy but simplified overview of the stuff they are looking for in liver function tests. 

Raised ALT/AST = acute liver damage

Slowed PT = acute and chronic damage

Reduced Albumin= chronic damage.

More?? Consider coming to one of our fun nurseing/paramedic seminars.   We love our Jargon.

Courses:

Www.Ect4Health.Com.Au/whats 

#KnowingYourJargon

Urobilinogen in Urine

#KYJ - Urobilinogen.

Ward test urine is such a common nursing assessment.

Occasionally I go through some of the urine values seen in abnormal urine tests, but one often poorly understood urine value is urobilinogen.

To understand this substance in urine we need to go back to the origin.

Red blood cells are born in bone marrow, and after 120 days, they are killed off by your immune system.  Components of the dead RBC are recycled, and processed by the liver.

RBC bodies become unconjugated bilirubin, which is processed into bilirubin and further into Bile. There,  bile is secreted to the Gall bladder to be concentrated and stored, waiting for your next fatty meal.

Once fat in your meal is detected by your gut, bile is secreted into your duodenum to mix with food, assisting lipase enzymes to break the fat down into triglycerides for absorption.

The reminant bile passes with undigested food into the large bowel and is acted on by intestinal flora .

This bile is converted into stercobilin, a dark brown pigment that gives faeces it’s colour, and urobilinogen a water soluble waste that is reabsorbed from the faeces.

Now stay with me:

All gut reabsorption of urobilinogen passes into your liver where it is converted into urobilin, and released into the blood stream so the kidneys can excrete it.

It is a light yellow colour and gives the urine it’s hue.  The more urobilinogen and subsequent urobilin you have the yellower your pee.

So it’s in there and it’s normal.

But...

There is a limit! If urobilin on dip stick is reactive (too high) it can represent one of two things.

More bilirubin than the liver can metabolise or hepatic failure.

1- RBC destruction

Haemolysis is the break down of RBCs.  In gut bleeds, haematomas or haemolytic anaemia ; even after a blood transfusion (massive), the sheer numbers of RBCs that are being broken down, and producing bilirubin overwhelms the liver’s capacity to convert to bile, so the liver converts it directly to urobilinogen where kidneys excrete what it can.

2- Liver failure. 

In hepatitis, liver disease like cirrhosis or liver Cancer, or any other liver disease; the conversion of bilirubin fails.  It therefore fails to be utilised adequately, and must be renally excreted.

Symptoms to check your patient for, when there is positive urobilinogen in their WTU, include 

Jaundice or skin yellowing 

Itch, or pruritus. 

Yellowing of the sclera.

Pale/ fatty /offensive faeces

Altered Liver Function Tests.

Coagulation issues leading to bleeding/bruising.

It is not too often that we get a chance to review the little physiology tips and pearls .  So our KYJ (#knowingyourjargon) blogs are one small way I contribute to Free open access medical-education. (#FOAM).

Check them all out on our website. WWE.ect4health.com.au