Chem Path Flashcards
If pt has a normal fasting glucose, but a OGTT (2hr reading) of 9mmol/L, what does this pt has?
This pt has impaired OGTT
Polyuria, polydipsia pt with fasting glucose of 9mmol/L but OGTT of 14mmol/L, what does hit pt has?
Fasting glucose is normal but OGTT meets requirements for diabetes. Hence this pt has T2DM.
This is probably a pregnant women or a patient with significant insulin resistance, where although the fasting glucose shows IFG, the 2h value in fact diagnoses diabetes.
Thus you can only diagnose IFG where the 2h value on a GTT is <7.8 (normal) or where a GTT is not done.
Cut off values for fasting glucose and OGTT for diagnosis of T2DM
Diabetes is diagnosed on the basis of history (ie polyuria, polydipsia and unexplained weight loss) PLUS
1) a random venous plasma glucose concentration >= 11.1 mmol/l
2) OR a fasting plasma glucose concentration >= 7.0 mmol/l (whole blood >= 6.1 mmol/l)
3) OR 2 hour plasma glucose concentration >= 11.1 mmol/l 2 hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT)
If pt is asymptomatic, repeat blood test
Ham’s test
The Ham test is a test used in the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH). The test involves placing red blood cells in mild acid; a positive result (increased RBC fragility) indicates PNH or Congenital dyserythropoietic anemia.[1][2] This is now an obsolete test for diagnosing PNH due to its low sensitivity and specificity.[3]
Anti-mitochondrial antibody
PBC
Characterised by chronic granulomatous inflammation leading to damaged inter lobular bile ducts. Chronic inflammatory process leads to cholestasis, cirrhosis and portal hypertension.
Patients are usually asymptomatic. Diagnosis made based on deranged LFTs and abnormal rise in serum ALP.
98% of pts are anti-mitochondrial antibodies (AMA) positive. ANA, SMA and ANCA may be positive but in low levels compared to AMA.
IgM may be raised.
TSH and cholesterol may be raised.
Anti-scl70
Systemic sclerosis
Multisystemic disease of unknown cause. May be limited to the skin and soft tissue in limited cutaneous systemic sclerosis (e.g hands, face and feet) or also involve the organs in diffuse cutaneous systemic sclerosis.
Raised levels of ANA, anti-centromere (limited cutaneous systemic sclerosis), anti-Ro, anti-topoisomerase antibodies are associated with systemic sclerosis. (SCL70)
What is Whipple’s triad
Defines hypoglycaemia
Initially used to describe insulinomas but also apply to all insulin resistance states
- Low glucose
- Symptoms of hypoglycaemia (adrenergic e.g. tremors, palpitations, sweating, hunger and neuroglycopaenic e.g. somnolence/sleepiness, confusion, incoordination, seizures, coma)
- Immediate relief of symptoms with glucose administration
Treatment for hypoglycaemia.
- Scenario 1: Pt is alert and orientated
- Scenario 2: Pt is drowsy/confused but intact swallow
- Scenario 3: Pt is unconscious/poor swallow
- Oral glucose and carbs
- rapid acting: juice and sweets
- long acting: sandwich/bread - Buccal glucose and IV access
- hypostop/glucogel - IV access
- 50ml of 50% glucose or 100m of 20% glucose
If deteriorating, refractory, insulin induced, difficult IV access consider IM glucagon (but only if the pt has glycogen stores i.e. not in anorexia nervosa)
Caution about high % glucose given via IV line - what can happen if the glucose do not go into the vein properly
This is called extravasation of IV glucose: irritant and cause phlebitis
How is glucagon administered? Route + dose. What precautions? What indications?
Indication: hypoglycaemia that is refractory to initial treatments e.g. oral, buccal glucose, IV glucose
Route: IM
Dose: 1mg
Caution: Danger of rebound hypo because release of glycogen stores as glucose may trigger insulin release
List some causes of non-diabetic reasons for hypoglycaemia?
- Fasting or reactive?
- Paediatric vs. adult
- Critically unwell
- Organ failure
- Hyperinsulinism
- Post gastric-bypass
- Drugs
- Extreme weight loss
- Factitious
Common reasons for hypoglycaemia in diabetics
• Commonest cause of hypoglycaemia • May be related to: o Medications o Inadequate CHO intake/ missed meal o Impaired awareness o Excessive alcohol o Strenuous exercise o Co-existing autoimmune conditions (sometimes, Addison’s diseases)
Schmidt’s disease
Diabetes + Addison’s disease
Also known as polyglandular autoimmune syndrome
What is carnitine deficiency? (from hypoglycaemia lecture)
Carnitine is a naturally occurring hydrophilic amino acid derivative, produced endogenously in the kidneys and liver and derived from meat and dairy products in the diet. It plays an essential role in the transfer of long-chain fatty acids into the mitochondria for beta-oxidation.
Form of fatty acid oxidation defect
Causes neonatal hypoglycaemia with suppressed insulin and C-peptide
Beckwith–Wiedemann syndrome
Beckwith–Wiedemann syndrome is an overgrowth disorder usually present at birth, characterized by an increased risk of childhood cancer and certain congenital features.
Common features used to define BWS are:[1]
- macroglossia (large tongue),
- macrosomia (above average birth weight and length),
- midline abdominal wall defects (omphalocele/exomphalos, umbilical hernia, diastasis recti),
- ear creases or ear pits,
- neonatal hypoglycemia (low blood sugar after birth).
- Hepatoblastoma
50 year old A&E regular, presents to A&E, appearing very unwell and intoxicated. Serum creatinine was 3x higher than that the average measured from his previous visits. Urine microscopy reveals calcium oxalate crystals.
Diagnosis?
Ethylene glycol poisoning
Ethylene glycol is the major ingredient of almost all radiator fluid products in the United States. It is added to prevent the radiator from overheating or freezing, depending on the season.
The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or anion ion gap acidosis is present in the blood.
The antidotes for ethylene glycol poisoning are ethanol and fomepizole.
Equation for creatinine clearance
Calculate the creatinine clearance for the following renal patient, following a 24 hour urine collection: urine volume 2litres; urine creatinine concentration 3mmol/l and plasma creatinine concentration 208 micro mol/l.
Creatine clearance = (creatinine’s urine concentration)* (Vol) / (plasma creatinine concentration) (note: the units have to match).
Ans: 20ms/min
The 3 forms of calcium in the body and which the most common form
- Free ‘ionised’ ~50% biologically active
- Protein-bound ~40% albumin
- Complexed ~10% - citrate/phosphate
Formula for corrected Ca2+
- Corrected Ca2+ levels adjusted for any deficient in albumin
- Serum Ca2+ + 0.02*(40-serum albumin in g/L)
- ^ the real level of Ca if albumin was normal at 40 g/L
Why does Ca2+ needs to be corrected in blood tests?
- Because calcium binds to albumin, if you have low albumin, the amount of protein-bound Ca decreases but the amount of free calcium stays the same, hence you get a ‘low’ Ca2+ on sampling
- Serum Ca2+ + 0.02*(40-serum albumin in g/L)
- If the corrected Ca is normal, means that the deficient in Ca was caused by albumin and free Ca (which is the biologically active/important component) is normal and is not of concern
What is the normal range for ionised Ca2+ and what kind of sample provide you with ionised Ca2+ readings
- Normal blood samples you cannot measure ionised Ca alone because the sample clots - hence ‘corrected Ca2+’ method
- But on blood gas machine, they measure ionised Ca2+ directly hence normal would be about ~1.1-1.3 mM
What is the corrected Ca2+ if a patient is septic and has a low albumin of 30? Plasma reading of Ca from a blood test is 2.2mM
Example of Ca calculation
* Pt septic, low albumin = 30, Measured calcium = 2.2
* Corrected calcium = 2.2 + 0.02 (40-30)
= 2.2 + 0.02(10)
= 2.4mM (normal)
* Serum Ca2+ + 0.02*(40-serum albumin in g/L)
When calcium is low you look at PTH. what are some causes of low calcium and high PTH
Vit D def - dietary, malabsorption, lack of sunlight CKD (1a hydroxylation of the kidney is impaired) PTH resistance (psuedohypoPTH)
When calcium is low you look at PTH. What are some causes of low calcium and low PTH
Surgical (post thyroidectomy)
Autoimmune hypoPTH
Congenital absence of parathyroids (e.g. DiGeroge syndrome - do not have thymus)
Mg deficiency (PTH regulation - Mg is required to make PTH)