Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS VI Medicine > Chemical pathology > Flashcards

Chemical pathology Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
  • Respiratory response is quick
    – Immediate, and max in 12 hours
  • Renal response is slow
    – Takes 3 days to max
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the limits of respiratory and renal compensation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Chronic Respiratory Acidosis w/ partial metabolic compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Simple metabolic acidosis with respiratory compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • 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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acidosis, pCO2 low, HCO3- low

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

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

18
Q
  • 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%

A

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)

19
Q

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

A

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)

20
Q

What Ix can be done for renal tubular acidosis?

A
  • Check urine pH
  • Fractional excretion of HCO3-

RTA already suspected when blood is hypoK and NAGMA

21
Q

55/M COPD; Tx: thiazide diuretics

A

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

22
Q

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

A

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

23
Q

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

A

Chronic respiratory alkalosis w/ partial metabolic compensation

24
Q

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

A

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

25
Q

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

A

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)

26
Q
  • 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

A

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)

27
Q

What is ddx for hypoK alkalosis

A

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

28
Q

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

A

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

29
Q

What are the causes for pseudohyponatremia?

A

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)

30
Q

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

A
  • 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.
31
Q
  • 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?
A

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

32
Q

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

A

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.

33
Q

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

A
34
Q
  • 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?

A

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

35
Q

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

A

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
36
Q

What is the etiology of Congenital Methemoglobinemia and
Acquired Methemoglobinemia

A

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

37
Q

What is tx?

A

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

38
Q

What are the types of hypoxia?

A
39
Q

What are pitfalls in interpreting PaO2?

A
  • 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)
40
Q

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

A

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)

41
Q

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

A

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

42
Q

Cause of positive pregnancy test and what further Ix?

A

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

MBBS VI Medicine (92 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions