Chemical pathology Flashcards by Max Kam

What are common clinical problems that may require lab tests?
What emergency lab tests may be done?

Examples of common problems
– Abdominal pain
– Chest pain
– Coma
– Hypoglycemia
– SOB
– Chest infection
– Mental confusion
– ? Alcoholism
– Poisoning / over-dose
– Trauma

Tests
– ABG
– Amylase
– Cardiac markers (Troponin, CKMB)
– CXR/AXR
– ECG
– Glucose
– L/RFT/Ca/PO4
– CBC
– Urine Glucose / Ketones
– Osmolality
– Toxicology test, e.g. paracetamol, ethanol
– Urine pregnancy test

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What is metabolic acidosis and alkalosis for pCO2 and HCO3-?

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What is pCO2 and HCO3- in simple metabolic alkalosis with respiratory compensation
Simple metabolic acidosis with respiratory compensation

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Whta is the 1,2,3,4 rule in compensation for acute/chronic respiratory acidosis and alkalosis?

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How long does it take for respiratory or renal compensation to be in effect?

Respiratory response is quick
– Immediate, and max in 12 hours
Renal response is slow
– Takes 3 days to max

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What are the limits of respiratory and renal compensation?

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What is the diagnostic algorithm for normal pH?
Look at CO2, HCO3- and anion gap

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What is the cause of acidosis + high PCO2 + normal HCO3-?

Acute Respiratory Acidosis w/o metabolic compensation
CNS depression: trauma, infection, tumor, CVA, drug overdose
Neuromuscular: myopathy, GBS
Thorax: hydrothorax, pneumothorax, fail chest

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What is the cause of acidosis + high PCO2 + high HCO3-?

Chronic Respiratory Acidosis w/ partial metabolic compensation

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What is the cause of acidosis + high PCO2 + low HCO3-?

Mixed Metabolic & Respiratory Acidosis
* Cardiopulmonary arrest
* Respiratory failure with anoxia

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What is the cause of acidosis + low pCO2 + low HCO3-?

Simple metabolic acidosis with respiratory compensation

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What is the cause of acidosis + low pCO2 + low HCO3- + anion gap (high)?

High anion gap metabolic acidosis due to
* Renal failure
* Ketoacidosis: DKA, starvation, alcoholic acidosis
* Lactic acidosis
* Toxins: ethanol, methanol, ethylene glycol, salicylate

Anion gap = (Na+ +K) - (Cl- - HCO3-)
So many more measured anions over cations so anion gap will always be more than 0

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What is the cause of acidosis + low pCO2 + low HCO3- + anion gap (normal)?
What other to look at?

Look at plasma K if normal anion gap (acidosis +low pCO2 and low HCO3-)

HyperK normal anion gap hyperchloremic metabolic acidosis due to
* Type IV RTA (aldosterone deficiency receptor defect)
* Early uremic acidosis
* Obstructive nephropathy
* Mineralocorticoid deficiency
* Infusion/ingestion: HCl, NH4Cl, arginine HCL

HypoK normal anion gap (hyperCl) metabolic acidosis due to
* urine pH >5.5
* Distal RTA urine pH<5.5
* Proximal RTA, acute diarrhea, post hypocapnia, carbonic anhydrase inhibitors, uretero- intestinal conversion

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What is the pathophysio of HAGMA (high anion gap metabolic acidosis)?
What are causes?

Physiology
– 1. Normal unmeasured anions e.g. proteins
– 2. Presence of abnormal unmeasured anions, e.g. ketones, lactate
– 3. Unmeasured normal cations

5 common causes
* 1. Renal failure
* 2. Diabetic ketoacidosis
* 3. Alcoholic ketoacidosis
* 4. Lactic acidosis
* 5. Drugs / toxins

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F/34 yo, 32 wks pregnant
Long hx of alcohol abuse
C/o severe vomiting for 2 days
Admitted to a heavy alcohol intake prior to the onset of vomiting but did not take any after the vomiting started

pH, HCO3-, pCO2 all 3 low
HAGMA, what further tests done and how to interpret
what Tx

All 3 parameters low –> simple metabolic acidosis

Do plasma glucose, ketones, lactates and ketones (quantitative)
Beta-hydroxybutyrate 11.6mmol (<0.3)
Acetoacetate: 1.7mmol (<0.2)
Lactate 3.0mmol/L (<0.2)

Interpret the B-OHB: ACAC ratio
DKA: 3.1-5.1, alcoholic ketosis: 2.1-9.1. Ratio >5.1 suggest alcoholic ketoacidosis

This patient B-OHB: ACAC ratio was more than 5 indicating alcoholic ketosis (with history of alcoholism)
Requires immediate treatment of IV saline and dextrose infusion (will die within 4 hours with no treatment)

Starvation ketosis unlikely as severe ketosis in this disorder takes 1-2 weeks to develop.

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Acidosis, pCO2 low, HCO3- low

What can be the ddx?
What further ix needs to be done?

Causes of hypoK and NAGMA

Acute diarrhea
Drugs: carbonic anhydrase inhibitors (e.g. acetazolamide)
Urine diversions: uterosigmoidostomy, vesicocolic fistula
RTA: type 1, type 2

Requires urinary pH, Na, K, HCO3-, creatinine

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How to differentiate distal and proximal RTA by urinary pH (in hypoK and NAGMA)?
Why?
What is confirmatory test for proximal and distal RTA?

Proximal RTA (type 2): urinary pH (<5.5) as can excrete H+.
Use bicarbonate loading test. FEHCO3 >15%.

Distal tubule is responsible for excretion of H+. If affected unable to efficiently excrete H+. Hence in distasl RTA (type 1): high urinary pH (>5.5) while acidemic.
Do NH4Cl loading test to confirm

M/60y complains of
– increasing weakness of limbs for 3-4 wks (sat down
and could not stand up)
– polyuria and polydipsia for 2 weeks
P/E
– normal BP, well hydrated
– weakness of 4 limbs & decreased tendon reflexes.

HypoK and NAGMA
High urinary pH (>5.5) with FEHO3: 0.9%

High urinary pH (>5.5) while acidemic indicates distal RTA (type 1)

Sjogren syndrome complicated with distal RTA: common cause of distal RTA (can be confirmed with blood serology)

Toxicology screen
Blood: excess level of toluence
Urine: excess levels of hippuric acid and benzoic acid (which were metabolites of toluence)
What is dx?

HypoK with NAGMA (normal anion gap metabolic acidosis)
pH high (>5.5) with FeHCO3- relatively low –> distal RTA

Distal RTA secondary to toluene poisoning (thinner solution which is used for paint removal)

What Ix can be done for renal tubular acidosis?

Check urine pH
Fractional excretion of HCO3-

RTA already suspected when blood is hypoK and NAGMA

55/M COPD; Tx: thiazide diuretics

high pCO2: respiratory acidosis
high HCO3: metabolic alkalosis
normal pH –> mixed acid base disorder

HCO3- over the limit the compensation of primary respiratory acidosi asnd patient has hypoK and on thiazide diuretic therapy (causes of metabolic alkalosis).
Final dx: mixed respiratory acidosis and metabolic alkalosis

What are the causes of alkalosis + pCO2 low + HCO3- normal?

Acute respiratory alkalosis w/o metabolic compensation
* Anxiety/hysteria
* CNS: hypoxemia, infection, trauma, tumors, hepatic encephalopathy salicylate toxicity
* Lung: embolus, asthma, pneumonia, edema

What are the causes of alkalosis + low pCO2 + low HCO3- ?

Chronic respiratory alkalosis w/ partial metabolic compensation

What are the causes of alkalosis + low pCO2 + high HCO3- ?

Mixed metabolic & respiratory alkalosis
* Cardiac failure and vomiting
* Diuretics and hepatic failure
* Diuretics and pneumonia
* Vomiting and pneumonia
* Vomiting and hepatic failure

In alkalosis + pCO2 + high HCO3, what further investigation must you do?

Urine KCL By excluding diuretics and exogenous alkali can diagnosed mineralocorticoid excess without even doing serum aldosterone test. high urine K, high urine Cl (over 20mmol/L)

* F/18 admitted to hospital 3 times over 6 wk * C/o nausea, weight loss, muscle weakness, periods of ‘fainting’ * Denied having had any medication, vomiting or diarrhea alkalosis, pCo2- high, HCO3- high Urine Cl =5mmol/L, urine K = 68mmol/L

all 3 high = simple metabolic alkalosis ddx for hypokalemic alkalosis: diuretic therapy, vomiting, mineralocorticoid excess (conns syndrome or secondary casues), severe K depletion Dx: self induced vomiting (anorexia nervosa)

What is ddx for hypoK alkalosis

® Diuretic therapy ® Vomiting ®Mineralocortiocoid excess (Conn’s syndrome or secondary causes) ® Severe potassium depletion

What are the electrolyte abnormalities which may be seen in toxic alcohol poisoning?

Increase in osmolality (osmolar gap) Decrease in base excess Increase in methanol

What are the causes for pseudohyponatremia?

Normally 93% plasma, 7% solids (lipids and proteins) Hyperlipidemia and hyperproteinemia: replacement of a portion of the plasma water space with either lipid or protein (TP>150g/L or triglyceride >50mmol/L)

What is the use osmolality in hypoNa? How to differentiate true vs pseudohypoNa via serum osmolality?

* In true hyponatremia, measured serum osmolality is low (with normal urea). * In pseudohyponatremia, measured serum osmolality is normal in the absence of extra protein/lipids (with normal urea) * Osmolar gap is widened in pseudohyponatremia.

* Q. Does this patient has CO poisoning? * Do you think that she has hypoxia? * Q. Her COHb came back to be 30%. * How can you explain her normal SaO2 in CO poisoning?

if COHb was 30% --> expected SaO2 would be around 70% therefore there is systematic error with the pulse oximeter Pitfalls of SaO2 * Poor circulation * Prominent venous pulsation e.g. tricuspid regurgitation * Presence of other dyshemoglobins: COHb: normal SaO2, but poor tissue perfusion. MetHb: congenital methemoglobinemia, nitrate poisoning

If pulse oximeter has suspicious faulty readings what other POCT can be used?

Co-oximeter * Accurately quantify the proportions of HbO2 , Hb, COHb, MetHb and other dyshemoglobins * The amounts all Hb types are measured directly, co-oximetry gives a true picture of oxygenation in the presence of dyshemoglobinemias.

What is the degree of CO poisoning and clinical presentation What is treatment?

* F/9 days old with good past health * Presented with fever (38.6oC) and found central cyanosis with decreased responsiveness * Other P/E unremarkable * BP/P stable * SaO2 94% on room air pH normal, pCO2 normal, PaO2 normal, SaO2 normal Discrepency between clinical findings and oximeter reading and oxygen saturation. Methemoglobinemia suspected What is confiramatory Ix and treatment?

Faulty pulse oximetry * Co-oximetry measurement: – ↑MetHb: 20.2% (normal level <1%) – Oxygen saturation: 78.5% Patient was given "herbal powder" but instead gave sulfamethazine (antibiotics) which can lead to methaemoglobinemia. Treatment: IV methylene blue

What is appearance of methemoglobin in blood and skiin? Symptoms correlated to methemoglobin?

Oxygen carrying ferrous iron (Fe2+) of the heme group is oxidized to ferric state (Fe3+) Normal <1%: protective enzyme counteract MetHb formation. Excessive oxidative stress/defective enzyme cause methemoglobinemia Blood --> chocolate brown, skin --> blue skin * Methemoglobin does not bind oxygenà tissue hypoxia * Symptoms correlate to the Methemoglobin level: – < 10% - No symptoms – 10-20% - Skin discoloration – 20-30% - Headache, SOB on exertion – 30-50% - Tachypnea, palpitations, confusion – 50-70% - Coma, seizures, arrhythmias, acidosis – > 70% - Death

What is the etiology of Congenital Methemoglobinemia and Acquired Methemoglobinemia

Congenital methemoglobinemia * Defective protective enzyme system: – cytochrome b5 reductase deficiency * Hemoglobin variant: – Hb M variant Acquired methemoglobinemia * Oxidizing drugs or chemicals * Neonates are more susceptible due to immature protective enzyme system

What is tx?

Cyanide poisoning * Rapidly acting and lethal poison * Death within minutes ~ hours * Inhibit electron transport of cellular respiration * Rapid onset of coma * Metabolic acidosis * Anoxia without cyanosis * Antidote: sodium thiosulfate This is histotoxic hypoxia: defective cellular respiration

What are the types of hypoxia?

What are pitfalls in interpreting PaO2?

* Air bubble increases PaO2 * Leukemia/ infection, high WCC/platelets consume O2 * Oxygen therapy status not written down (i.e. if SaO2 97% but on 50% FiO2 than it is abnormal)

What is PaO2 What is SaO2 What is the 3 types of SaO2

PaO2 – oxygen dissolved in plasma SaO2 – oxygen saturation of Hb Three types of SaO2 1. Measured by pulse oximeter 2. Calculated from PaO2 by blood gas analyzer 3. Measured by co-oximeter (gold standard)

What is measured in POCT glucose meter test? What are products affecting the assay? What is dx below?

Measures GDH-PQQ therapeutic products affecting the assay * Icodextrin in peritoneal dialysis * D-xylose absorption test * IV solution containing maltose or galactose * IVIG Dx: Pseudo normohypoglycemia

Cause of positive pregnancy test and what further Ix?

Hx: age, LMP, contraception)) Further Ix (serum hCG level, FSH level, imaging, endometrial sampling, etc) When faint line always do further lab workup (do not miss a germ cell tumor/ectopic pregnancy) – Normal pregnancy – Abnormal pregnancy (ectopic pregnancy, miscarriage): will present as faint band --> requires lab workup – Gestational trophoblastic disease (including choriocarcinoma) – Germ cell tumours – Pituitary hCG (pituitary adenoma) – Ectopic hCG producing tumours (e.g. Ca lung) – Immunoassay interferences