Bilirubin results interpretation made Simple

Before entering this post, you must first understand the process of Bilirubin Metabolism...

Here I attach a diagram which hopefully would help, you can refer to various tutorials and materials online to understand its metabolism...

Basically, in urinalysis, we can only see one thing in urine in normal condition, which is the urobilinogen. If there is abnormal condition, we will see the second thing, which is conjugated bilirubin, cB because it is water soluble so it is able to escape into urine from renal blood flow.

so you want to look at the uB amount and sometimes cB in the bloodstream and the urobilinogen and the cB amount in the urine.

i. Prehepatic (Pre- the prefix indicated there is already a problem before coming to the liver)

An example of problem would be hemolytic anemia, meaning the body keep breaking down red blood cells due to various reasons and so there would be increase in the breakdown product namely heme which then was converted to uB. Thus, bilirubin, uB will increase in plasma. But because other parts of the metabolism, in which the liver function and excretion of bilirubin are normal, and so when these plenty of uB converts to cB, they will be sent as usual to the small intestine and converts to plenty of urobilinogen. Therefore , an increase in uB would result in increase of urobilinogen which maybe excreted through feces, reuptake into the bloodstream or excreted in urine (which you would agree if you had study the bilirubin metabolism I told you to). So the result is, in plasma, uB would increase and in urine, urobilinogen would increase. However, there would be no uB found in the urine because they are water insoluble, they bind to the albumin and could not pass through glomerulus filtration barrier. (GLOMERULUS: NO ENTRY). And cB is not found as well in the urine because it was continuously converted to urobilinogen in the small intestine.

ii. Hepatic (Liver, you've got TROUBLE!)

There were 3 type of problems which our Mr. Liver might have.

1. He might not be able to uptake the uB from the plasma. 

2. He might not be able to conjugate the uB that was uptaken into cB. (What was that enzyme again?)

3. He might not be able to send the conjugated cB into bile canaliculi. (Delivery man problem)

First problem if occur, because there was no uptake, uB in plasma continuously being produced (as breaking down old (they called it senescent) red blood cells was part of the normal process in our bodies. So, there would be increase of uB in plasma but no cB found in the urine.

For second problem, Mr. Liver couldnt conjugate the uB this time, and so uB in plasma will stay in high amount, however there was no cB in the urine. 

For the third problem, the cB that was produced via conjugation by the liver was not sent to the bile canaliculi. And so, cB escaped into the systemic circulation and was excreted directly into the urine through renal blood flow, thus for this case you will see cB appearing in the urine. 

Urobilinogen amount in a hepatic cause of jaundice would be either normal or increased. Reason for its increase is that hepatic disease would usually affect the enterohepatic circulation in which less urobilinogen would be re-uptaken into the liver and was excreted in urine instead. 

iii. Post Hepatic (there's a roadblock set after the liver)

Usually this was due to a obstruction that impede the bile flow along the way from the point immediately after the liver all the way to the small intestine. 

Thus, the cB was not able to be sent to the small intestine via bile flow. Thus cB will escape to the systemic circulation and being excreted in the urine.

So, you would wonder what about urobilinogen.

Well, if the roadblock (obstruction) is complete, then no cB is able to pass through thus no conversion, so zero urobilinogen!

If the obstruction is partial, meaning there is still some cB able to pass through, the urobilinogen amount would be either normal or less than normal... 

So conclusion, if you see an increase of urobilinogen in the urine, usually the problem was pre-hepatic.

If there was increase in cB, it would be either hepatic or posthepatic.

And an increase of uB or cB in the bloodstream exceeding certain amount would result in JAUNDICE (a sign you can see in patient...THE YELLOW MAN! in which the yellow discolouration occur in skin and sclera).

Electrical and Mechanical Properties of Heart (revision)

Before understanding how ECG works:

Electrical Properties of heart:

1. Autorhythmicity
The ability to generate action potentials without external stimulus
•spontaneous pre-potential (pacemaker potential) followed by action potential.
•Pacemaker tissue (sino atrial node, atrio ventricular node, atrio ventricular bundle and purkinje fibers) can initiate repetitive action potentials.
•Pacemaker tissue is characterized by unstable resting membrane potential because of its continuous change in membrane permeability.





Pre-potential:
Slow decrease in K+ efflux while permeability of other ions remain constant (through ‘h’ channels and transient ‘T’ Ca2+ channels).

Depolarization:
Ca2+ influx through long lasting Ca2+ channels ( ‘L’ )

Repolarization:
K+ efflux.

Rate of Impulse (per min):
SA node--70-100
AV node--40-60
Atrial and atrial pathway--20-40
Purkinje fibers--20-40

2. Excitability:
Cardiac muscle is excitable tissue
-->it forms a wave of depolarization in response to a stimulus(generation of AP)

0: Rapid depolarization.
Opening of Na+ channels causes increase in Na+ influx.

1: Rapid initial fall in membrane potential (initial rapid repolarization)
Inactivation of Na+ channels.

2: Plateau phase.
Slow opening of Ca2+ channels causes Ca2+ influx.

3: A rapid fall in membrane potential (repolarization phase)
Opening of K+ channels causes rapid K+ efflux.

4: Polarised state.
Ionic composition is restored by activation of Na+K+ATPase pump

3. Conductivity
the ability of cardiac muscle fibers to conduct the cardiac impulses that are initiated in the SA node.

• Impulse from SA node spread quickly to AV node via atrial (internodal) pathway.
• Time delay (0.1 s) occurs as impulses pass through AV node.
• Impulse conduction increases as spread to Purkinje fibers at a velocity of 4 m/s.
• Ventricular contraction begins 0.1-0.2 s after contraction of the atria. (important for ventricular filling phase)
• LBB starts before RBB, as LV wall is thicker so the impulse needs more enough time to reach. Accordingly both ventricles will contract together.

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Electrical activity of the heart:
1. Depolarization and origin of cardiac impulse at the SA node. (if SA node doesnt work, AV will take place of being the pacemaker)

2. Conduction of the impulse to all parts of the atria through atrial muscle (there may be some special pathways that conduct impulse fast ie. have a higher conduction velocity). The impulse also spreads to the AV node along the atrial muscle. (Atrial fibrillation occurs when the atrial ms contract independently and continuously bombard AV node with depolarizing waves of varying strength, and depolarization spreads at irregular intervals down the Bundle of His)

3. The impulse will not pass from atrial muscle to ventricles directly as they are not in contact (fibrous tissue separates them). (thus if AV node is blocked, and impulse from SA node couldnt reach ventricle, ventricular muscle will initiate its own impulse as it also has autorhythmicity, eg. seen as AV dissociation on ECG)

4. AV node has a low conduction velocity and thus the impulse takes sometime to travel across it. It eventually travels across it and reaches the upper end of the bundle of His.

5. Bundle of His has a high conduction velocity. It conducts the impulse through its branches to the Purkinje fibre network just under the endocardium of the ventricles. (In a normal conditionn where impulse is able to be transmitted from AV node to Bundle of His, impulse created by ventricular muscle itself doesnt cause muscle contraction as the impulse hits the absolute refractory period--all/none law of the action potential of cardiac muscle that is stimulated by normal conduction system's impulse)



*atrial repolarization not seen on ECG as it was masked by the stronger ventricle depolarization

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Mechanical Properties of the heart:

1. Contractility
---when an action potential occurs in the muscle it responds by contraction.
During excitation-contraction coupling the ER releases some Ca++ ,but to have sufficient calcium for contraction there must be influx through the sarcolemma. Hence the importance of the plateau phase of the action potential.

• For cardiac muscle, the amount of stretch of the muscle before a contraction has special significance and is called preload (Starling Law).
• Protected from tetanus because of its long ARP
• No recruitment of cardiac muscle fibers.
• Strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the ECF

2. All or None Law

• Action potential of cardiac muscle is an all or none law response to a stimulus.
• If the stimulus is sub-threshold (inadequate), no action potential is produced.
• If the stimulus reaches threshold, a full-fledged action potential is produced.
• Further increase in the intensity of a stimulus produces no increment in the amplitude of AP.

Absolute refractory period:

• The excitability of cardiac muscle is completely lost during this period, i.e. doesn’t respond to 2nd stimulus.
• Occupies the whole period of systole.

Relative refractory period:

• The excitability of cardiac muscle is partially recovered during this period, i.e. stronger stimuli than normal are required to excite the muscle.
• Occupies the time of diastole.
• Can be affected by the heart rate, temperature, vagal stimulation, sympathetic stimulation & drugs.

******************************************************
Factors affecting heart rate:

1. Sympathetic stimulation

Act via β1-adrenergic receptors -->increase cAMP-->Increases heart rate by opening of Ca2+ channels--> increase Ca2+ influx-->increase rapidity of the depolarization phase--> increase heart rate (positive ‘chronotropic’ effect)

2. Vagal stimulation

Acts via M2 muscarinic receptors -->decreasing cAMP-->Decreases heart rate by opening of K+ channels and slows the opening of Ca2+ channels --> increase K+ efflux of nodal tissues -->hyperpolarization --> decrease slope of pre-potentialp--> decrease firing rate--> decrease heart rate (negative ‘chronotropic’ effect)

3. Temperature

Arise in body temperature by 1 °C increases the heat rate by 10 beats/minute.

The rise in body temperature increase the heart rate by increasing the permeability of the membrane to Ca++ during the pacemaker potential.

4. Sinus arrhythmia

Variation in R-R interval during deep inspiration.

During deep inspiration, lung stretch--> inhibits cardio-inhibitory center-->decreases tonic vagal discharge -->increases HR.

5. Ion concentration in ECF

K +

-the early effect of mild hyperkalemia on myocyte function is to increase myocyte excitability by shifting the resting membrane potential to a less negative value and thus closer to threshold potential; but as potassium levels continue to rise, myocyte depression occurs and Vmax continues to decrease.

A plasma potassium of >6.5mmol/L (normal 3.5-5.5) is an emergency, myocardial hyperexcitability--> ventricular fibrillation--> cardiac arrest

5.5-6.0 mEq/L - Mild


6.1-7.0 mEq/L - Moderate


7.0 mEq/L and greater - Severe

Sx: fast irregular pulse, chest pain, weakness, palpitation, and light-headedness

ECG: Tall tented T wave, small p wave, wide QRS complex

Causes:

Decreased or impaired potassium excretion - As observed with acute or chronic renal failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)


Additions of potassium into extracellular space - As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)


Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)


Fictitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis

Management:

Urgent:

• Stabilize Cardiac membrane with 10ml 10% calcium gluconate
• drive K+ into cell with 10 units actrapid in 50ml 20% glucose

Non-urgent: (K+ not >6.5, no myocardial hyperexcitability)

• Treat underlying causes.
• Polystyrene sulfonate resin 15g/8h PO

Ca2+ ion in ECF

• Increase in Ca2+ concentration --> increase cardiac contractility
• Decrease in Ca2+ concentration --> decrease cardiac contractility

6. Blood flow

Insufficient blood flow--> decreased oxygen and nutrient supply--> decreased heart conductivity and metabolism

7. Drug

Sympathomimetic drug--> increased HR 

parasympathomimetic drug--> reduce HR

Principle of CT scan

Principle of CT scan, good to know.

Complete/Incomplete Spinal Cord injury, Neurological Examination and Asia Chart

Spinal shock can occur and last for about 24-72 hours after spinal cord injury and a/w complete motor and sensory loss, hypotension and bradycardia. (monitor Bp with vasopressor to prevent fluid overload)

Bulbocarvenosus reflex: 
If present, Squeezing of penis/clitoris/pulling of Foley catheter would cause contraction of anal sphincter muscle.

The reflex is spinal mediated and involves S2-S4.

Presence of reflex indicates ends of spinal shock.
(Sometimes absence of reflex could be due to cauda equina syndrome instead of spinal shock)

Sacral Sparing Test was done after ends of spinal shock to determine complete or incomplete spinal injury:
1. flexion of big toe present
2. anal reflex present
3. perianal sensation present (S3-5)

Sacral sparing indicates incomplete spinal cord injury

(pinprick sensation predicts better prognosis of motor function: as lateral spinothalamic is near to lateral corticospinal tract)

spinal cord anatomy:


TYPES OF INJURY:
Central Cord Syndrome


Anterior Cord Syndrome


Brown Sequad


Posterior Cord Syndrome



Determine Level of Spinal Cord Injury/Lesion by using Asia Chart

Difference in level of nerve exit:

Cervical nerve exit above vertebra level, example C4 nerve exit above C4 vertebra and below C3 vertebra

Thoracic nerve exit below vertebra level, example T4 nerve exit below T4 vertebra and above T5 vertebra

Loss of sensation at the dermatomal area and power at myotomal area at C4 spinal cord level would indicates injury at C3 vertebral level. Likewise a radiograph of C3 vertebra injury is expecting sensory and motor impairment to C4 spinal cord level.

In PID (Prolapsed Intervertebral Disc), the location of herniated disc in after level of conus medullaris (L1 vertebra) would determine different type of lesion.

Example, centrally herniated disc would affect nerve of the next vertebral level, lateral herniated disc would affect nerve of the same vertebral level. (Refer diagram below)

ASIA chart impairement score:

Motor power determine grade of impairment:

Summary:

In acute spinal injury (emergency case):
-check patient vitals, bulbocarvenosus reflex to rule out spinal shock, if shock present, manage the shock
-then sacral sparing test to determine complete or incomplete injury
-then neurological examination to determine type and level of injury

1. Neurological Examination (usually exam will specify either upper limb/lower limb):
a. Sensory, dermatome (Light touch, Pin Prick)
b. Motor, (Tone, Power, Reflex)
*always compare both side

2. Determine Type of  Injury:
a. Pure sensory loss
b. Pure motor weakness
c. Combined motor and sensory loss
d. Unilateral/Bilateral

3. Determine Etiology:
Acute: Fracture(burst) 
Gradual: PID, spinal stenosis

4. Confirm diagnosis with special test
eg. Straight leg raising test in PID, perianal sensation to rule out cauda equina syndrome (usually caused by large midline disc herniation or extrusion, emergency and need surgical decompression if patient had urinary retention)

Remedial O&G Group 1 teaching with Dr. Rahimah [note to myself]

Dr. Rahimah stressed on knowing definition of gravida, parity and knowing how to count LMP and EDD. In case patient is USOD, we can give roughly estimated LMP by subtracting 40 weeks from REDD.

eg if this is patient 5th pregnancy, she had a molar, ectopic, a miscarriage and an IUD so it should be?

G5P1+3 (where there is 1 molar, 1 ectopic and 1 miscarriage)

In a case of SGA/IUGR, I put 'or' because a SGA case(suspected constitutionally small because of smaller mother's size with previous hx of small fetus) must be managed as TRO IUGR as if causes failed to be identified and patient was discharged and if a IUGR was not detected and managed, it will lead to IUD.

3 important factors lead to IUGR:
1. Placental insufficiency, which could be caused by
-pre-eclampsia (usually early onset which start to affect during formation of placenta)
-chronic medical illness which affect placenta formation
-smoking
-autoimmune disease such as SLE
-placenta previa, as placenta attach to lower segment of uterus with thinner myometrium--> less blood supply--> less nutrients--> baby smaller
(thats why we opt for lower segment c-sec as lesser blood supply there)

2. fetal infection
rule out TORCHES

3. fetal anomalies
oligohydramnios suspect renal agenesis

symmetrical IUGR: early onset, caused by Chromosomal anomalies, infection
asymmetrical IUGR, late onset, caused by placental insufficiency, thus have head-sparing

GDM will cause fetal macrosomia
however pre-existing DM in mother more likely --> congenital anomalies--> fetal microsomia

as this patient has a previous hx of small baby, ask if there is oligohydramnio in the previous pregnancy, chances are the patient has intrauterine infection in the previous pregnancy which continue to the next...

find out about percentile on growth chart for SGA, IUGR

if at district hospital, need to refer to tertiary centre if there are two abnormal plotted growth charts
usually the gap between 2 serial scans is about 1 week

however normal growth scan is 2 weeks

1 previous scar is already a criteria for admission

If Doppler U/S is abnormal, need to do CTG daily

If leaking of liquor, need to do U/S every 1w or 3d

HOPI for IUGR must rule out any CX such as
abnormal CTG, reduced fetal movement,doppler u/s findings, leking of liquor any PV discharge

Also diet hx to assess whether mother malnourish

VE assess Bishop score, if cervix favourable, deliver
if not, do induction, however previous scar, so do not do Induction as risk of uterine rupture...
if fetal distress, abnormal CTG, doppler, then c-sec
if no fetal distress, opt for vaginal delivery

Plan and management:
1. monitoring
2. timing of delivery
3. mode of delivery

investigations:
1. Blood: anemia, TWC, torches screening, group screen hold, High vaginal swab if leaking of liquor
2. U/S doppler: fetal BPP, placenta (any redding calcification), head and abd circumference, any fetal anomalies such as renal agenesis
3. CTG daily, fetal heart monitoring,

what to revise:
growth chart
causes and mx of IUGR
fetal BPP
torches
redding calcification

Remedial O&G CT3 & 6 [note to myself]

CT 6 teaching with Dr. Hoo

Pt is a 32y/o lady G2P1 came in with Placenta Previa Type III Posterior for observation at 34w + 5d.
She had previous hx of Placenta Previa Type IV in her first pregnancy and had done elective Cesarean section at 2013 which is 3 years ago. She also had a past surgical history of cystectomy at 2012 which is 4 years ago. She denied any APH such as PV bleed or abd pain. The dx was made based on ultrasound findings at 30w.

In this pt, the risk factor for her recurrent PP in second pregnancy is previous C-sec.
To clerk history of a previous C-sec, must exclude cx such as any blood transfusion? any injury to bladder, bowel, ureters? any post-partum hemorrhage? any wound infection? endometritis? UTI?
Importance is to detect any presence of placenta accreta in her next pregnancy...as C-sec is a risk.

C-sec is also planned for her second pregnancy.
Must know how to plan a C-sec,
Inform and get consent,
Large bore IV access, catheterize bladder,

Pre-op: Take blood for FBC (ensure Hb level >10g/dl), PT/PTT, GXM (4-6units of blood), urea/creatinine.
consider ECG/CHEST XRAY

Neutralize gastric contents to prevent aspiration pneumonia if GA is used.
Elective C-sec, NBM + Ranitidine

Emergency C-sec: sodium citrate and metoclopromide

Thromboprophylaxis
low-risk: early mobilization, hydration
moderate: IV heparin and TED stockings
high: IV heparin until 5-d post-op and TED stockings

Antibiotic prophylaxis
IV cefazolin. given after cord is clamped

Also don't forget to revise all the risk factors that could cause PP.

Learning Point:
C-sec cx and planning
GXM and GSH difference
PP type, risk factors, mx
Rubella=german measles, effect on fetus?
ATT to prevent emergency delivery at non sterile environment
Hepatitis B vaccine? can be given during pregnancy or not?
Primary vs secondary dysmenorrhea
Pap smear done because need to remove pre-malignant lesion if there is.
Find out about Diabetic diet and ensure GDM mother follow
Results for MOGTT 5.6-7.8

CT3 with Dr. Fauziah

Know what is abnormal progress of labour, the hour...
Know partogram, and how to detect abnormal progress by partogram and how to mx to avoid fetal distress

what can a 1st U/S tell us?
-viability,
-dating
-location of gestational sac (ectopic: abdomen, cervix, broad ligament)
-fetal number, MCDA, DCDA
-Pregnancy of unknown location need beta-hCG test
-exclude uterine abnormalities
-exlude fibroid, ovarian mass

Ovarian cyst in pregnancy, cystectomy can only be done less than 18w, more than 18w might cause abortion, so planned cystectomy only after delivery

MOGTT HOW TO DO, RESULTS, WHEN TO DO, RISK FACTOR

Remedial O&G Fetal events during labour

AP diameter:
Suboccipitobregmatic 9.5 cephalic (well-flexed)

Transverse diameter:
Biparietal: 9.5cm
Bitemporal: 8cm



Internal rotation probably occurs as the fetal head meets the muscular sling of pelvic floor, it is often not accomplised until presenting part has reached the level of ischial spine (zero station) and is therefore engaged.

engaged= 2/5 palpable on abdomen = zero station descent at ischial spine.