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MM Block 1 > Block 1- Carbohydrate Metabolism > Flashcards

Block 1- Carbohydrate Metabolism Flashcards

1
Q

Hyperglycemia:

  1. Mechanism
  2. Symptoms
  3. Treatment
A

Insulin defect

  1. Too little or improperly functioning insulin (autoimmunity vs insulin-producing beta cells in DM type I) leads to insufficient cellular intake of glucose
  2. extreme thirst (polydipsia), extreme hunger (polyphagia), excess urination (polyuria), shaking, headaches, hypotension, tachypnea (rapid breathing), ketoacidosis, confusion, seizures
  3. Insulin
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2
Q

Hypoglycemia

  1. Mechanism
  2. symptoms
  3. Treament
A

1.

  • 1-4 hrs post eating: excess insulin leads to excess uptake of glucose from blood; hereditary fructose intolerance
  • 4-24 hrs post eating: defects in liver glycogenolysis; defects in gluconeogenesis;
  • 12 hrs -40 hrs: defects in gluconeogenesis; defects in fatty acid metabolism without ketosis; ketotoic hypoglycemia
  1. extreme hunger (polydipsia), anxiety, tachycardia, tachypnea, ketoacidosis, dry mouth, cold clammy wet skin, lethargy, confusion, seizures
  2. glucose
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3
Q

Infant of Diabetic Mother:

  1. Mechanism
  2. Symptoms
  3. Treatment
A
  1. mother had consistent hyperglycemia during pregnancy. Insulin supply stays high, glucose supply does not.
  2. Fat baby, hypoglycemia, enlarged heart, seizure
  3. early and frequent feeding, IV glucose
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4
Q

Infant of malnourished mother

  1. Mechanism
  2. Symptoms
  3. Treatment
A
  1. Baby born with insufficient fat and glycogen stores, not much muscle mass for gluconeogenesis, leads to hypoglycemia. Lack of glycogen synthesis due to low substrate.
  2. wasting, signs of distress, sever hypoglycemia
  3. early and frequent feeding, IV glucose
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5
Q

Dietary Lactose Intolerance:

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Intestinal lactase deficiency
  2. osmotic diarrhea, bloating, overgrowth of intestinal bacteria w lactose consumption; could have hypoglycemia if only eating lactose
  3. Autosomal Recessive
  4. take lactaid, avoid lactose
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6
Q

Dietary Fructose Intolerance

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Defect in GLUT 5 (fructose transporter in intestine)
  2. Osmotic diarrhea, bloating, overgrowth of intestinal bacteria upon fruct. consumption. ; maybe hypoglycemic if only eating fructose
  3. AR
  4. avoid fructose
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7
Q

Glu-Gal Malabsorption:

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Defect in SLGT1 which absorbs glu and galactose in intestine with Na.
  2. diarrhea, acidosis, glucose in urine, kidney stones from damage to kidneys; hypoglycemia
  3. AR
  4. Ross carbohydrate formula+ fructose
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8
Q

Hereditary Fructose Intolerance

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Defect in F-1-P aldolase (aldolase B)–> can’t convert F-1-P to Glyceraldehyde-3-P/DHAP –> can’t convert fructose to glucose to enter glycolysis
  2. hypoglycemia after eating/drinking fructose, diaphoresis (excessive sweating), seizures, severe abdominal symptoms, liver faliure
  3. AR
  4. avoid fructose, responds well to IV glucose
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9
Q

Galactosemia

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Gal-1-P-Uridyl Transferase (GALT) deficiency–> can’t convert galactose to Gal-1-P for use for energy; galacitol accumulates
  2. cataracts, liver disease, neuronal disease, mental retardation; normoglycemia (glucose can be created from other sugars), but can become hypoglycemia if only galactose is eaten
  3. AR
  4. avoid galactose, especially dairy/breast milk. drink soy milk

most prevalent disorder of carbohydrate metabolism!

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10
Q

Von Gierke’s Disease (GSD 1)

  1. Mechanism
  2. Symptoms
  3. MOI
  4. Treatment
A
  1. Glucose-6-Phosphatase deficiency (can’t make glucose from G-6-P during glycogenolysis). This means can’t make glucose from glycogen in liver to give to other cells.
  2. hypoglycemia, cold, sweaty, lactic acidosis (high lactate b/c high G-6-P inhibits conversion from lactate to pyruvate in liver), lipid abnormality, doll-like faces, thin extremities, short stature, hepatomegaly
  3. AR
  4. frequent feeding, glucose, slow release sugar
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11
Q

Lactose Acidosis

  1. Mechanism
A
  1. Pyruvate carboxylase (pyruvate–> OAA) or pyruvate dehydrogenase (pyruvate –> acetyl CoA) deficiency leads to excess lactate production from fermentation. Fats broken down into ketone bodies, leading to acidosis
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12
Q

glucose sources with fasting:

  1. 1-4 hours post meal
  2. 4-16 hours post meal
  3. 16-32 hours post meal
  4. after 48 hours
A
  1. dietary glucose is consumed by all tissues, brain recieves glucose
  2. glucose derived from glycogen and gluconeogenesis is consumed in all tissues but the liver; brain eats glucose
  3. gluconeogensis (hepatic) and glycogen –> glucose provides glucose for the brain
  4. gluconeogenesis (heaptica and renal) for brain, blood, kidney. brain eats ketone bodies and glucose after 24 days??
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13
Q

SLGT1

A

an Na-glucose/galactose co-transporter at the apical membrane at the intestine.

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14
Q
  1. GLUT2:
  2. GLUT 4:
  3. GLUT 5:
A
  1. GLUT2 at intestine’s basolateral surface transports glucose and fructose.
  2. GLUT 4 is insulin sensitive
  3. GLUT 5 transports fructose into cells at apical membrane.
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15
Q

_____ breaks down sugars to dissacharides in the mouth; ____ furthers this, making maltose, isomaltose, and some trisaccharides. ____ digest disaccharides to monosaccharides like _____.

A

amylase digesting alpha 1,4-glycosidic linkages;

pancreatic amylase

brush border membrane

glucose, fructose

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16
Q
  1. Amylose
  2. Amylopectin
  3. Cellulose
A
  1. 1,4 linkages
  2. 1,4 and 1,6 linkages forming long chains
  3. structural rather than nutritional B1,4 linkages that can’t be broken down by mammals
17
Q

Glycogen Synthesis

A
  1. G-1-P + UTP = UDP-Glucose
  2. UDP-Glu is linked to primer molecule (glucogenin?)
  3. Glycogen Synthase (stimulated by insulin) adds more UDP-glucose via 1,4 linkages
  4. transferase moves blocks of 7 residues and creates 1,6 linkates to make branches
18
Q

Glycogenolysis

A
  1. Glycogen phosphorlyase releases Gluc-1-p (stops 4 residues from branch point)
  2. Transferase remodels
  3. Convert G-1-p to G-6-P
  4. In the liver, G-6-P is converted to free glucose
19
Q

Glycolysis

A

Occurs in the cytosol

  1. hexokinase traps gluc by phosphorylating it to G-6-P
  2. G-6-P –> Fruc 6-P
  3. Fruc-6-P –> Fruc 1,6-biP (committed step)
  4. Fruc 1,6 biP–> 2 glyceraldehyde-3-P via F-1,6-biP aldolase
  5. Glyc-3-P –> –> –> pyruvate +2ATP + 1 NADH
  6. aerobic: pyruvate enters TCA cycle
  7. anaerobic: pyruvate converted to lactate, liver converts lactate into glucose via gluconeogenesis
20
Q

Fructose Metabolism

A
  1. Fructose taken up by liver and converted to F-1-P
  2. F-1-P –> glyc-3-P/DHAP by F-1-P aldolase (defective in hereditary fructose intolerance)
  3. Gyc-3-P enters glycolysis
21
Q

Galactose Metabolism

A
  1. Galactose phospohorylated to Gal-1-P
  2. Gal-1-P combines with UDP-Glucose to make UDP-galactose and Glu-1-p
  3. Glu-1-p –> glu-6-p–> glycolysis and UDP-Gal–>UDP gluc
22
Q

Gluconeogenesis

A
  • lactate, AA, glycerol converted to glucose for use by brain and RBCs
  • 3 irreversible rxs that mostly occur int he liver.
  • Need 6 ATP to make 1 glucose from 2 pyruvate
  1. convert precursors to pyruvate
  2. pyruvate carboxylase gives pyruvate –> OAA
  3. PEP carboxylkinase converts OAA to phosphoenolpyruvate in cytosol –> Glyc-3-P –> F,1,6 biP
  4. fructose biphosphatase converts F-1,6,biP –> F-6-P
  5. F-6-P–> Gluc 6-P
  6. Gluc-6-P to glucose by gluc-6-phosphatase
23
Q

ETC/Ox.Phos.

A
  • NADH, FADH2 donate e- that are aultimately excepted by O2
  • complexes I, III, IV: energy derived from e- transfer pump H+ into intermembrane space to create H+ gradient
  • H+ flows down gradient from IMM to matrix ATP synthase to generate ATP
  • more ATP from NADH (3 ATP) b/c FADH (2 ATP) enters at Complex II

MM Block 1 (15 decks)

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