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Clinical Chemistry > Carbohydrates and Diabetes > Flashcards

Carbohydrates and Diabetes Flashcards

1
Q

What type of carbohydrate/ (saccharide) does the body primarily use for energy utilization?
What are the three main sugars used?

A

Monosaccharides are the main carbs the body uses for energy. Examples are the reducing sugars:glucose, fructose, and galactose.

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2
Q

Disaccharides come from common food sources what are some examples?

A

Sucrose (glucose + fructose)
Lactose (glucose + galactose)
Maltose (2 glucose)

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3
Q

What is the size/length difference between oligo- and polysaccharides?

A

Oligosaccharides=3-10 monomer uniter

Polysacharrides= >10 monomer units

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4
Q

Starch and Glycogen are….?

A

Polysaccharides. Starch is sourced from plants and glycogen is sourced from animals.

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5
Q

What happens when monosaccharides are taken into the body?

A

Fructose and galactose are converted into glucose.

Glucose is then released in the bloodstream OR stored in the form of glycogen.

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6
Q

How are disaccharides and polysaccharides broken down in the body?

A

Disaccharidesa are cleaved by specific intestinal enzymes.

Polysaccharides are broken down by amylase.

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7
Q

What are the SIX MAJOR metabolic pathways in the body?

A 
Glycolysis (anaerobic)
Glycogenolysis
Gluconeogenesis
Glyconeogenesis
TCA cycle (aerobic)
Pentose Phosphate/HMP shunt
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8
Q 
In a nutshell what is happening in glycolysis?
Glycogenolysis?
Gluconeogenesis?
Glyconeogenesis?
TCA cycle?
Pentose Phosphate/HMP shunt?
A

Glycolysis: Glucose—–>PyruvateLactate
Glycogenolysis: Glycogen——–>Glucose
Gluconeogenesis: (non-carbs)——->glucose
Glyconeogenesis: Glucose—->Glycogen
TCA: Glucose->Pyruvate->CO2, H2O, & ATP

Pentose Phosphate:
Glucose——>Ribose,CO2, & NADPH

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9
Q

Name seven hormones responsible for the control/regulation of glucose?

A 
Insulin
Glucagon
Cortisol
Epinephrine
Growth Hormone (hGH)
Thyroxine (T4)
Somatostatin
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10
Q

Insulin is synthesized in in pancreatic beta-cells. What is first released and cleaved before to form insulin? What else is formed?

A

First, proinsulin is released and cleaved to form insulin and c-peptide which is biologically inactive.

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11
Q

What is the purpose of insulin and when is it released?

A

Insulin is released when blood glucose levels are high.
It signals cells (fat/muscle) to take up glucose, it inhibits glycogenolysis while increasing glycogenesis,glycolysis and lipogenesis.

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12
Q

What type of method is used to measure insulin? Why are the interpretations complicated?

A

Insulin is measured with the sandwich immunoassay to evaluate hypoglycemia, evaluate beta cell fnxnl reserve or insulin resistance.
Interpreting results can be a hassle because:
1) Assays are poorly standardized
2) Cross-reactivity with proinsulin (precursor to insulin)
3) antibodies to insulin interfere
4) cross reactivity with animal insulin
5) Hepatic metabolism

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13
Q

C-peptide is also measured with sandwich immunoassays.

Why may it be a better test at measuring hypoglycemia?

A

1) Insulinomas have normal insulin but high C-peptide levels
2 )No antibody effects
3) C peptide is not in exogenous insulin
4) No hepatic metabolism

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14
Q

Glucagon is made in pancreatic alpha cells. What is it’s function?

A

Secreted in response to low blood sugar and acts upon the liver to raise blood glucose, stimulates glycogenolysis and gluconeogenesis and ketogenesis.
Also stimulates lipolysis.
Also an immunoassay but rarely measured.

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15
Q

Action of Cortisol?

A

Stimulates gluconeogenisis, proteolysis, and lipolysis.

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16
Q

Action of Epinephrine?

A

Stumulates glucagon secretion, glycogenolysis, and gluconeogenesis, and inhibits insulin secretion.

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17
Q

Action of Growth hormone?

A

Stimulates gluconeogenesis and lipolysis.

Antagonizes insulin stimulated glucose uptake.

18
Q

What two hormones affect glucose but are not normally involved in glucose homeostasis?

A

Somatostatin and Thyroxine.
Thyroxine stimulates glycogenolysis and and increase intestinal absorption.
Somatoststin inhibits insulin glucagon and growth hormone secretion.

19
Q

Name three enzymes involved in glucose measurment.

A

Glucose dehydrogenase
Glucose oxidase-peroxidase
Hexokinase-G6PDH

20
Q

What happens to glucose in blood that has not been spun down?

A

Levels decrease 5-7%/hr

21
Q

What are the critical values for glucose?

A

> 500 mg/dL and

22
Q

What is the problem with gray top tubes for assaying glucose levels?

A

The specimen isn’t usable for 1-2 hrs due to inhibition of cellular enolase (urea in BUN), chelation of divalent cations and osmotically dilutes the sample.

23
Q

Why are glucose levels below 20-30 deadly?

A

Because the CNS is dependent on glucose and ketone metabolism.

24
Q

What causes hypoglycemia?

A

1) “reactive” hypoglycemia: overshoot after meal. If symptomatic test with 5 hr post meal test
2) Decreased gluconeogenesis: severe hepatic problem, Addison’s disease: hyperadrenalism: low cortisol
3) Increased uptake and use: over admin of oral hypoglycemic drugs, over admin of insulin, insulinomas

25
Q

What is the difference between type 1 and type 2 diabetes mellitus?

A
  • Type 1 is more symptomatic
  • Type 1 is prone to keto acidosis, Type 2 is not.
  • Type 2 more prevalent
  • Type 1 =insulin deficiency (insulinopenia). Type 2 = insulin resistance
  • Type 1 requires insulin replacement anf Type 2 typically does not.
26
Q

What is gestational Diabetes?

A

The first onset of diabetes/ or diagnosis during pregnancy. Due to insulin resistance =, maybe because preg hormones interfere with insulin cell signaling and glucose uptake.—->failure to compensate with increased insulin production?

27
Q

Gestational Diabetes can result in poat preg. diabetes as well. What effect on the fetus can gestational diabetes have?

A

Hypo calcemia
Hypoglycemia
Macrosomia

28
Q

Pathogenesis of DM1?

A

Autoimmune disease resulting in beta cell destruction. Can also be viral (rubella, mumps, Cox B), or genetic.

29
Q

Pathogenesis of DM2?

A
  • Insulin resistance (assoc. with metabolic syndrome).

- Beta cell dysfunction ( cant compensate for insulin resistance.

30
Q

Acute complications of DM are

due to what?

A

Due to current glucose deficit within cells.

-Ketoacidosis (Type 1)

-Hyperosmolar non-ketotic coma (Type 2)
Enough insulin to limit lipolysis and ketogenesis
Not enough to facilitate adequate uptake

31
Q

Chronic complications of DM are due to what?

A 
Glucose excess over long time:
Angiopathy
-CAD
-Stroke
-Necrosis & amputation
Nephropathy
Retinopathy
Neuropathy
Infection
32
Q

What is used as a diagnosis for diabetes?

A

Any one of the following is diagnostic :
1) Hemoglobin A1c ≥ 6.5%

2) Fasting plasma glucose ≥126 mg/dL
3) 2 hr plasma glucose ≥200 mg/dL during oral glucose tolerance test
4) Random plasma glucose ≥200 mg/dL with symptoms of hyperglycemia

33
Q

What is the (GTT) Oral Glucose Tolerance test?

A 
Test for ambulatory non-pregnant patients FASTING for at least 10 hours.
-≥150 gm/day carbohydrate intake for 3 days
-75 gm glucose ingestion 
-Diabetes if:
------Fasting sample: ≥126 mg/dL   OR
------2 hr sample: ≥200 mg/dL
Impaired glucose tolerance if:
-2 hr sample 140-199 mg/dL
Impaired fasting glucose if:
-Fasting glucose 101-125 mg/dL
34
Q

Diagnosis of gestational diabetes is done how?

A 
50 gm 1-hr GTT (NON-FASTING)
-(If 1-hr post 50 g glucose ≥140 mg/dL, then
3-hr post 100 g fasting GTT):
---FASTING: >/= 95 MG/DL
---1 HOUR:   >/= 180 MG/DL
---2 HOUR:  >/= 155 MG/DL
---3 HOUR:  >/= 140 MG/DL

Exceeding any two of four cutoffs signifies GDM

35
Q

What autoantibodies are involved in Type 1 DM?

A

1) Islet cell antibodies (ICA)
——-Indirect immunofluorescence
——-Labor-intensive, subjective interpretation
2) Anti-glutamate decarboxylase (GAD65)
——–Quantitative immunoassay
———-Found in 80% of DM1 patients at diagnosis
3) Anti-insulinoma antigen 2 (IA-2)
———–Quantitative immunoassay
4) Anti-insulin Abs
>90% of children under 5 yo,

36
Q

What are four ways diabetic control is monitored in a patient?

A

1) Self-Monitoring Blood Glucose (SMBG)
- –Fingerstick by patient, whole blood tested (≥3/day)
- –Real-time snapshot only

2) Hemoglobin A1c or glycated hemoglobin
3) Fructosamine or glycated protein
4) Urinary microalbumin
- —These tests monitor known diabetics to assess glycemic control or to predict disease sequelae.

37
Q

How is HA1c measured?

A

1) HPLC (ion-exchange chromatography)—reference method in US
2) Affinity chromatography (does not id hemoglobinopathies)
3) Immunoassay (does not id hemoglobinopathies)

38
Q

What is the goal HA1c measurement?

A

Monitoring recommended every six months if properly controlled, every three months if not
Goal of therapy = HbA1c 8.0%

39
Q

What are some interfering factors with HA1c measurment?

A

Situations of decreased rbc survival (e.g., hemolytic processes, hemoglobinopathies) underestimate average glycemic status due to 10-20% gives decreased glycation rate.

40
Q

What is the calculation for eAG?

A

28.7 x HA1c % - 46.7

Clinical Chemistry (9 decks)

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