Labs: Carbohydrate Metabolism Disorders Flashcards
Is it possible that someone:
a) has glucosuria at a serum glucose concentration of 5 mmol/l?
b) does not have glucosuria at a serum glucose concentration of 15 mmol/l?
A: Yes. Failure to reabsorb glucose in prox conv tubule -> renal glucosuria. Seen in Fanconi syndrome (congenital) or heavy metal poisoning (acquired)
B: Yes. Other problems with kidney function can cause this: decreased GFR via renal artery obstruction or diabetic nephropathy
A 15-year-old girl has been losing weight in spite of having a good appetite, and she feels tired lately. She has been admitted to a hospital for vomiting, being dizzy and disoriented.
Laboratory findings: urine glucose: strongly positive ketone bodies: positive blood glucose: 28.5 mmol/l blood pH: 7.1 serum K+: 5.4 mmol/l What is your diagnosis, and what is to be done with her?
Diagnosis: DKA secondary to DM type 1. Can confirm diagnosis via C-peptide and antibodies against islet cells, insulin, or glutamic acid decarboxylase
Treatment: slow insulin + IV fluids. Monitoring K+ so that it doesn’t drop too much, probably giving K+ later (insulin stimulates Na/K ATPase, can reduce [K+]e.c. to hypokalemia.. but currently hyperkalemic so monitor it)
Slow drop in BGL is better for neuron function, 5mM/day reduction is safer. And and be careful about cerebral edema from high fluid intake.
A 56 year-old man who used to be healthy complains of polyuria.
Laboratory findings:
fasting blood glucose: 7.3 mmol/l,
fasting blood glucose a week later: 7.6 mmol/l.
What is your diagnosis, and what would you do with him?
Diagnosis: prob DM type II (but possibly LADA)
Treatment: BGL monitoring, oral antihyperglycemics (metformin, SGLT2 inhibitors, incretin mimetics)
Diet (reduced refined carb intake) + exercise
Monitor retinopathy, peripheral neuropathy, atherosclerosis, nephropathy.
A 60 year-old woman, weighing 90 kg. Fasting blood glucose concentration: 6.9 mmol/l. Neither glucose nor ketone bodies are found in her urine.
The results of oral glucose tolerance test:
fasting value: 6.4 mmol/l
2h value: 8.5 mmol/l
What is your diagnosis, and what would you advise to her?
Diagnosis: Impaired Glucose Tolerance (IGT) - Prediabetic. IGT because her 2 hour OGTT value > 7.8 but < 11.
Advice: reduce carbs + exercise (exercise stimulates GLUT4 expression), regularly check BGL.
Laboratory findings of a person:
fasting blood glucose: 6.2 mmol/l
Oral glucose tolerance test was performed on another occasion:
fasting value: 6.3 mmol/l
2h value: 6.5 mmol/l.
What is the diagnosis, and what is the clinical significance of it?
Diagnosis: Impaired Fasting Glucose (IFG) (below the 2 hour IGT range, which is 8-11 mmol/l)
IFG indicates risk of developing DM type II (something like 20-25%)
What are your options to check the glucose metabolism of your diabetic patient, to decide if the current treatment needs to be changed or not?
- Home glucose test strips
- Check-up every 3 months: fasting BGL (<6 mmol/L) + HbA1c (5-7% target). Alternatively, frucosamine can be used - like A1c but only last 2 weeks.
- Yearly check-up of diabetic complications: neuro, nephro, retinopathy
- DM type I: check C-peptide, antibodies, also A1c
A diabetic patient treated with insulin has a fasting blood glucose concentration of 6.4 mmol/l. No glucose was detected on the morning of the examination. The Hb-A1C level is 10 % (normal value: 3–6 %).
Do you think the control of glucose concentration was acceptable in the last 1–2 months?
No, the Hb-A1c is very high and the fasting glucose is also higher than 6 mmol/l. High A1c indicates hyperglycemia over last 3 months.
Risks: microangiopathy, atherosclerosis, diabetic food, silent AMI, neuropathy, etc.
A type 1 diabetic man has been eating very little for the last couple of days, due to a febrile illness, so he decided to stop administering his insulin. He checked his blood glucose, because he felt worse and worse, and was surprised to see, that it was more than 20 mM.
What is the explanation?
Because DM-I people cannot produce insulin, the insulin-stimulated cells starve and they react by performing gluconeogenesis to no benefit, and keep producing more and more glucose as the condition worsens.
Fever may also be accompanied by cortisol and cytokines that contribute to gluconeogenesis and hyperglycemia.
A diabetic man treated with insulin skipped his late evening meal before going to bed, without any change in his insulin administration. He has been sweating a lot during the night, and glucose has been detected in his urine in the morning.
What is the explanation for this?
Paradox/Somogyi Effect - no meal + insulin = hypoglycemia → sympathetic activation → sweating + ↑ insulin antagonist hormones (cortisol/glucagon/GH/catecholamines/T3/T4) → gluconeogenesis → hyperglycemia + morning glucosuria
A man with type 1 diabetes, cooperating very well with his physician, keeps his diet and insulin administration very precisely. He is an employee of a bank, and currently attends a team building training, a several-day-long survival tour causing significant physical exertion. The man, who is known to be reserved, starts shouting and quarreling with his coworkers, then he begins to sweat, quiver and develops cramps.
What do you think is the explanation of his behaviour?
Hypoglycemia: probably due to phys exertion consuming more E + lack of carbs. Maybe he took insulin and didn’t eat enough.
Hypoglycemia → symp activation → sweating
Hypoglycemia in CNS → agitation
A woman was admitted to the hospital with the complaint of recurrent seizures. Her fasting blood glucose level is 2.7 mmol/l.
What can cause these symptoms? What tests would you perform to establish the diagnosis?
If diabetic: over-administration of insulin without food
If not diabetic: insulinoma, excessive alcohol (via ↓ NAD for gluconeogenesis), fever, sepsis, Addison’s disease, hypothyroidism
Diagnosis: C-peptide low if insulin overdose but normal in insulinoma; imaging for insulinoma; ACTH test for Addison’s.
A breast-fed infant was admitted to the hospital with weight loss, vomiting and jaundice. Blood glucose level is somewhat low. Glucose is not, but a reducing substance is detectable in the urine.
What is the likely diagnosis?
Galactosemia: galactose-1-phosphate uridyltransferase deficiency
Can’t convert galactose to glucose -> weight loss
Fermenting of galactose in gut -> vomiting, distension, pain
Galactose metabolite build up in liver/spleen -> hepatosplenomegaly + jaundice
Needs low galactose diet (no milk)
A small boy gets regularly sick after eating sugar containing foods: he is sweating, feels dizzy, vomits. He does not eat sweets for this reason. These symptoms were shown to be caused by reactive hypoglycemia, on examination.
What is the likely diagnosis?
Fructose intolerance: lack of aldolase B
Fructose not fully metabolized, accumulates as F-1-P which depletes the supply of phosphates and inhibits glycogenolysis
