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Clinical Chemistry > Carbohydrates > Flashcards

Carbohydrates Flashcards

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1
Q

An aldehyde, ketone, or a compound that yields either aldehyde or ketone after hydrolysis

A

Carbohydrates

*Phil setting: based on response of body based on insulin levels

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2
Q

General formula of monosaccharide

A

CnH2nOn

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3
Q

Aldoses and ketoses are

A

monosaccharides

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4
Q

Classifications of carbohydrates based on conromation

A

D and L Monosaccharides/
Fischer Projection
Haworth Projection

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5
Q

basis of fischer projetion

A

position of OH group (D or L)

*alpha-below beta-above (Haworth)

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6
Q

In the Embden-Meyerhoff Pathway, Glyceraldehyde-3-Phosphate is converted to?

A

Dihydroxyacetonephosphate (DHAP) or continue to the

Kreb’s Cycle

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7
Q

Glycolysis converts glucose to

A

pyruvate

*If body does not need sugar, glucose is shunted to PPP and etc

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8
Q

hormones from pancreatic beta cells (I of L) in fed state

A

insulin

*promotes cellular uptake of glucose (allowing transport of sugars from blood; anabolic)

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9
Q

How is proinsulin converted to insulin?

A

removal of C peptide (proinsulin: a + b + c peptides)

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10
Q

What are the requirements for insulin release?

A

− Glucose
− Other amino acids that can ramp up release of insulin
(Leucine, Arginine, Histidine, Phenylalanine)
− Sulfonylureas (tolbutamides)
− ACTH, GH
o As ACTH increases, cortisol increases which leads to an increase in glycolysis

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11
Q

What causes release inhibition of insulin?

A

− Thiazide diuretics (hypertensive drug)
− Dilantin (antiseizure)
− Human placental lactogen (diabetes of pregnancy)

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12
Q

What causes decreased tissue response to insulin?

A

− Glucocorticoids (Obesity)
− Estrogens (Inactivity)
− Progestins (Low carbohydrate diet)

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13
Q

Insulin INCREASES these metabolic pathways

A

lipogenesis
protein synthesis
glycogenesis

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14
Q

Insulin DECREASES these metabolic pathways

A

lipolysis
ketone formation
gluconeogenesis
glycogenolysis

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15
Q

hormones involved in unfed/fasting state

A

glucagon (from pancreatic alpha cells; catabolic)

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16
Q

What happens to glycogen in the liver? muscle?

A

liver: glycogen is converted to glucose, and released into the blood
Muscle: glycogen converted to glucose-6-phosphate, and remains in the muscle for its own energy needs

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17
Q

Its action is similar to glucagon and it is immediately expended

A

“Fight or Flight” epinephrine from adrenal medulla

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18
Q

Hormones involved in gluconeogenesis

A 
cortisol (hydrocortisone)- from adrenal cortex; inhibits glucose entry to muscle, connective and lymphoid tissue
Adrenocorticotropic Hormone (ACTH)- from anterior pituitary gland and stimulates prod of cortisol
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19
Q

Cortisols stimulates release of

A

gluconeogenic amino acids from the muscles

*also promotes conversion of amino acids into glucose by liver

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20
Q

What does cortisol stimulate in adipose cells?

A

lipolysis by releasing glycerol for conversion to glucose by liver

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21
Q

T or F: glycolysis stops in the sample once it is drawn

A

false
*Serum/plasma must be separated from cells soon after collection to avoid a falsely decreased glucose result
→ Ideally, processing must be done within 1 hour

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22
Q

What are the conditions of glucose reabsorption and glycosuria in PCT?
(renal threshold)

A

→ Reabsorbs all glucose if <180 mg/dL
→ Glycosuria results if blood glucose >180mg/dL
* >600 mg/dL in the kidney: greater than blood glucose threshold because of countercurrent mechanism

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23
Q

Increase in plasma glucose levels due to hormone imbalance

A

hyperglycemia

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24
Q

glucose reference ranges

A

74-106 mg/dL

increased if >110-120 mg/dL

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25
Q

Why does blood sugar increase at night?

A

fasting blood sugar (body undergoes gluconeogenesis at night to supply energy for the body’s organs)

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26
Q

How is fasting blood sugar counteracted?

A

insulin production so glucose enters cells and cortisol becomes active (basal metabolic rate) to increase blood sugar

27
Q

fasting blood sugar can have this effect on diabetics

A

somogyi effect

28
Q

Why shouldnt diabetics* take extra insulin shots before sleeping?

*in a constant catabolic state

A

Blood sugar goes down over the course of the night leading to hypoglycemia and a surge in cortisol from 4am-6am leads to hyperglycemia rebound leading to diabetic coma

29
Q

Immediate effects of hyperglycemia

A

increased extracellular osmotic pressure (increased glucose in plasma = water out of cells; dehydration)
acidosis (respiratory > metabolic)

30
Q

[Hyperglycemia effects] Results if glucos remains uncontrolled

A

acidosis

If patient’s cells are not able to take in glucose, fats are converted to fatty acids = keto acids

31
Q

[Hyperglycemia effects] hyperventilation of body to offset acidity

A

respiratory acidosis (not much change in pH)

32
Q

[Hyperglycemia effects] excess acids go to kidneys

A

metabolic acidosis (noticeable change in pH)

33
Q

physiological long term effects of hyperglycemia

A 
→ Heart attacks/stroke
→ Diabetic retinopathy (blindness)
→ Kidney failure
→ Neurological defects
→ Susceptibility to infections
34
Q

What chemical is formed as a long term effect of hyperglycemia (result of prolonged elevation of plasma glucose)?

A

glycosylated hemoglobin (HbA1c)

*more accurate parameter in gauging level of hyper/hypoglycemic state as it takes into acct average plasma glucose levels for past 30 days

35
Q

chronic hyperglycemia

A

diabetes

36
Q

four categories of diabetes accdg to WHO and ADA

A 
→ Type 1 Diabetes
• Most severe and potentially lethal
→ Type 2 Diabetes
• Affects the obese and those that are old and with poor diet
→ Other (Secondary Diabetes)
→ Gestational Diabetes Mellitus (GDM)
•Transient
•Unknown mechanism
37
Q

Physiologic abnormalities in diabetes

A

Hyperglycemia
Ketosis (from fat metabolism to ketonemia then ketonuria)
Hyperlipidemia
Decrease blood pH (metabolic acidosis)
Urine abnormalities (glycosuria, polyuria, loss of electrolytes-washed out with urine)

38
Q

most dangerous and potentially lethal type of diabetes

A

type 1 diabetes/ Insulin dependent diabetes mellitus (5-10% of cases)

39
Q

Pathology of type 1 diabetes

A

disease triggered by viral illness or environmental factors that destroys beta cells in pancreas which leads to absolute insulin deficiency (autoantibodies are present)

40
Q

Clinical symptoms of type 1 diabetes

A 
• Classical triad
→ Polyphagia – Increased food uptake
→ Polydipsia – Increased thirst
→ Polyuria – Increase urine production
• Other symptoms:
→ Mental confusion
→ Rapid weight loss or weight gain
→ Hyperventilation
→ Diabetic ketoacidosis
41
Q

Laboratory findings for type 1 diabetes

A
  • Hyperglycemia: plasma levels >110-120 mg/dL
  • Glycosuria: urine glucose >180 mg/dL
  • Decreased insulin
  • Increased glucagon leading to Chronic Gluconeogenesis and Increase Lipolysis (fat breakdown to produce ketones; main sourceS of type 1 DM)
  • Ketoacidosis
  • Decreased blood pH (acidosis)
  • ↓ Sodium, ↑Potassium, ↓ CO2
42
Q

Other names for type 2 diabetes (most common)

A

• Non-Insulin Dependent Diabetes Mellitus (NIDDM)
• Hyperosmolar Nonketotic Diabetes Mellitus
*relative deficiency of insulin and disorder in insulin resistance

43
Q

T or F: Type 1 DM patients take oral hypoglycemic meds

A

false, type 2

44
Q

Difference between lab findings of type 2 DM vs type 1 DM

A

• Insulin is present
• Glucagon is not elevated
• No gluconeogenesis, lipolysis and no ketoacidosis
• Excess glucose is converted to triglycerides (which yields higher plasma triglycerides)
• Normal or increased Na+ or K+
• Increased BUN and Creatinine
→ Due to dehydration
→ BUN:Creatinine ratio ≥ 20:1 indicates dehydration while 10:1 indicates renal tubular disorder
→ Leads to decreased renal function
• Hyperosmolar plasma from hyperglycemia

45
Q

T or F: type 2 DM develops gradually throughout years

A

true

46
Q

Type of diabetes where plasma glucose is unable to enter cells

A

type 2 DM

*Contributory factors:
→ Obesity
→ Lack of exercise
→ Diet
→ Genetics
→ Drugs (diuretics, psychoactive drugs like Dilantin and Tegretol)
→ Increases in hormones that inhibit/antagonize insulin (GH and cortisol)

47
Q

A genetic defect of beta cell and insulin function (genetic syndromes) and a pancreatic disease in alcoholics

A

secondary diabetes

*endocrinopathies and autoimmune diseases; drug or chemically induced

48
Q

type of diabetes associated with glucose intolerance assoc. with pregnancy’s hormonal and metabolic changes

A

Gestational Diabetes

49
Q

T or F: Although GD usually resolves after pregnancy, mother and infants are at increased risk for respiratory complications and hypoglycemia after birth

A

false, mothers= increased risk for diabets; infants only (macrosomic babies: >=4kg)

50
Q

Criteria for diagnosing diabetes

A

• Symptoms of Diabetes + Random Blood Glucose of >200mg/dL
(RBS: used in encephalopathic patients in ER; FBS: confined patient)
• 2-hour postprandial glucose >200mg/dL using oral glucose
tolerance test (OGTT) (low sensitivity)
• HbA1c >6.5%
*urine glucose testing = inaccurate (not used)

51
Q

definition of hypoglycemia

A

• Plasma glucose level falls <60 mg/dL

52
Q

When is glucagon released to inhibit insulin?

A

when plasma glucose <70 mg/dL

*other hormones to inhibit insulin: Epinephrine, cortisol, and growth hormone

53
Q

Why do hypoglycemic patients go into shock?

A

→ Body increases mean arterial pressure causing cerebral
edema
→ Death is caused by cerebral herniation

54
Q

General treatment of hypoglycemia

A

small, frequent meals (5-6x/day) that are low in carbohydrates, and high in proteins

55
Q

Symptoms of hypoglycemia

patient looks sleepy

A
  • Increased hunger
  • Sweating
  • Nausea
  • Vomiting
  • Dizziness
  • Shaking
  • Blurring of speech and sight
  • Mental confusion (Encephalopathic)
56
Q

laboratory finding of hypoglycemia which is secondary to profound hepatopancreatobiliary disease

A

Whipple’s triad
→ Symptoms of hypoglycemia
→ Low plasma glucose at time of symptoms
→ Alleviation of symptoms with glucose ingestion

57
Q

causes of HYPOGLYCEMIA (reactive process)

A
  • Insulin overdose
  • Ethanol ingestion (cytochrome p450 oxidase metabolizes ethanol; too much= enzyme depletion= increasing serum levels of ethanol)
  • Fasting
  • Insulin-producing tumors (ie Insulinomia)
  • Hepatic dysfunction
  • Sepsis
58
Q

This clinical test is still used for gestational diabetes diagnosis

A

Glucose tolerance test

normal diet: 3 days prior; no food after regular evening meal prior test; fasting blood, urine specimen

59
Q

When is serum taken for glucose tolerance test?

A

2 hours after drinking 100g glucose load within 5 minutes

*water ONLY during test

60
Q

Other conditions, tests associated with Diabetes Mellitus

A

White cell antigens (HLA types DR3, DR4, DQB1, *0302 checked to see if constant hypoglycemic state is genetic)
Lipid studies (increased triglycerides from hyperlipoproteinemia type IV)
Microalbuminuria
Microangiopathies (retinal, renal, neural probs)
(all involve alteration in genetic process)

61
Q

What are the diabetic resistant genes?

A

DR2, DQB1 *0602

62
Q

Why does microangiopathy happen?

A

In the blood vessels, the intima and media layers have bloodcapillary
barriers called capillary endothelial barriers. When the glucose is high, these barriers become leaky and the sugar enters, destroying nerve endings and ultimately weakening the blood vessels.

63
Q

(see management of DM and review qs)

A

(see management of DM and review qs)

Clinical Chemistry (9 decks)

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