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Bio 144 > Glucose Homeostasis, Diabetes Mellitus > Flashcards

Glucose Homeostasis, Diabetes Mellitus Flashcards

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1
Q

Pancreas

A
  • Elongated organ posterior to stomach
  • Performs both exocrine and endocrine activities
  • 99% of cells are clustered acinar cells (exocrine)
    – Synthesizes digestive enzymes
    – Secreted through pancreatic ducts into small intestine
  • 1-2 million tiny clusters of cells form pancreatic islets (endocrine)
    – aka Islets of Langerhans
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2
Q

Pancreatic Islets

A
  • Alpha cells (17%) secrete glucagon
  • Beta cells (70%) secrete insulin
  • Delta cells (7%) secrete somatostatin
  • Pancreatic polypeptide (6%) cells secrete pancreatic polypeptide
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3
Q

GLUT-2

A

– Independent of insulin
– Pancreas
– Liver

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4
Q

GLUT-4

A

– Dependent on insulin
– Skeletal muscle
– Adipose tissue

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5
Q

Insulin

A
  • Secreted by beta cells
  • Stimulus: Increased blood levels of glucose
    – Humoral
  • Targets have a tyrosine kinase receptor (RTK)
    – Non-G-protein transmembrane receptor
  • Target: Liver
    – Action: Stimulates glycogenesis
  • Target: Skeletal muscle
    – Action: Glucose uptake
    – Action: Amino acid uptake
    – Action: Stimulates glycolysis
    – Action: Stimulates glycogenesis
    – Action: Stimulates protein synthesis
  • Target: Adipose tissue
    – Action: Glucose uptake
    – Action: Stimulates lipogenesis
  • Net effect: Decreased blood glucose levels
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6
Q

Absorptive (Fed) State

A
  • First four hours after a meal
  • Insulin stimulates enzymes needed for anabolism
    – Carbohydrates
    ▪ Glycogenesis: glucose is converted into glycogen
    – Lipids
    ▪ Lipogenesis: fatty acids are converted into triglycerides
    – Proteins
    ▪ Protein synthesis: amino acids are converted into proteins
  • Insulin inhibits enzymes needed for catabolism
    – Decreases glycogenolysis, lipolysis, proteolysis
  • Insulin inhibits gluconeogenesis
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7
Q

Growth Hormone

A

– Target: Skeletal muscle
▪ Decrease glucose uptake
– Target: Adipose tissue
▪ Stimulates lipolysis
– Target: Liver
▪ Stimulates gluconeogenesis

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8
Q

Excess GH causes hyperglycemia

A

– Results in increased insulin secretion
– May cause “beta-cell burnout”
– Called a diabetogenic effect

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9
Q

IGF

A

– Target: Skeletal muscle
▪ Increased glucose uptake
▪ Increase amino acid uptake
▪ Increased protein synthesis
– Target: Adipose tissue
▪ Increased glucose uptake

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10
Q

GH’s synergistic effects

A

– Works indirectly via IGF
▪ IGF has similar structure to insulin
▪ IFG receptor similar to insulin
receptor
– IGF increases glucose uptake
▪ Skeletal muscles and adipose tissue
– IGF increases amino acid uptake
▪ Skeletal muscles
– Protein Anabolism
▪ IGF stimulates protein synthesis

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11
Q

GH’s antagonistic effects

A

– Works directly on target cells
– Carbohydrate catabolism
▪ GH stimulates glycogenolysis
– GH decreases glucose uptake
▪ Skeletal muscle and adipose tissue
– GH stimulates gluconeogenesis
– Lipid catabolism
▪ GH stimulates lipolysis

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12
Q

Glucagon

A
  • Secreted by alpha cells
  • Stimulus: Decreased blood levels of glucose
    – Humoral
  • Targets have a Gs protein coupled receptor
  • Target: Liver
    – Stimulates glycogenolysis
    – Stimulates gluconeogenesis
  • Target: Adipose tissue
    – Stimulates lipolysis
  • Note: Glucagon does not have receptors on
    skeletal muscle
    – Skeletal muscle is NOT a target
  • Net effect: Increased blood glucose levels
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13
Q

Glucagon Hormonal Interactions

A
  • During nonemergent situations:
    – Glucagon & Insulin = Antagonistic
  • In response to physiological stresses:
    – Glucagon & Epinephrine = Synergistic
    ▪ Both glucagon and epinephrine stimulate adenylate cyclase pathway
    – Glucagon & Cortisol = Permissive
    ▪ Thyroxine increases number and sensitivity of glucagon receptors
    – Glucagon & Thyroxine = Permissive
    ▪ Thyroxine increases number and sensitivity of glucagon receptors
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14
Q

Postabsorptive (Fasting) State

A
  • More than 4 hours after a meal
    – Blood glucose levels fall as glucose leaves bloodstream to enter body cells while
    none is being absorbed from digestive tract
  • Glucagon stimulates enzymes needed for catabolism
    – Carbohydrates
    ▪ Glycogenolysis: glycogen is broken down into glucose
    – Lipids
    ▪ Lipolysis: triglycerides are broken down into fatty acids
  • Glucagon inhibits enzymes needed for anabolism
    – Decreases glycogenesis and lipolysis
  • Glucagon stimulates gluconeogenesis
    – New glucose molecules are formed from non-carbohydrate sources
    ▪ Amino acids and lipids
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15
Q

Diabetes Mellitus

A
  • Chronic condition in which pancreas does not produce sufficient
    insulin or body cells do not use insulin properly
  • Affects over 30 million people in the US
  • 4th leading cause of death, mainly due to damage to blood vessels
  • Leading cause of retinal blindness, kidney failure, and
    nontraumatic amputations in the United States
  • Associated with increased heart disease and stroke
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16
Q

Diagnosing Diabetes Mellitus

A
  • Expected values for normal fasting blood glucose concentrations is
    70 – 100 mg/dL
    – Fasting = no eating for at least 8 hours
  • Major hallmark of diabetes mellitus is hyperglycemia
    – High blood glucose levels
  • Prediabetes = blood glucose levels between 100 to 125 mg/dL
    – HbA1C between 5.7 – 6.4 %
  • Diabetes is diagnosed of patient has one of the following:
    – Fasting glucose ≥ 126 mg/dL on two separate occasions
    – Random plasma glucose > 200 mg/dL on two separate occasions
    – Symptoms of diabetes (e.g., polyuria, polydipsia, ketoacidosis) + random
    plasma glucose > 200
    – HbA1C > 6.5%
17
Q

Blood glucose meters (finger prick)

A

– Provide an instant, single time point of blood glucose level
– Using a lancet, a drop of blood is placed on a strip attached to a glucometer
– Fasting blood glucose test
▪ Measures blood glucose after an overnight fast
▪ Normal is 70-100 mg/dL
– Random blood sugar test
▪ Measures blood glucose at any time, with or without fasting
▪ Normal is about 70-180 mg/dL

18
Q

Glycosylated hemoglobin A1C (HbA1C) test

A

– Provides a measure of glucose control over a 2-3 month period
– Blood is drawn at a clinic/hospital and sent to a lab for testing
– Normal is less than 5.7%

19
Q

Continuous glucose monitoring (CGM)

A

– Provide a delayed, but continuous glucose levels
– Measures glucose in interstitial fluid (not blood)
– Sensor is placed on body and continuously detects glucose levels
– Sensor is connected to a device (usually wireless) that records readings

20
Q

Other symptoms

A

– Fatigue
▪ Cells are unable to make ATP without glucose
– Unexplained weight loss
▪ In the absence of glucose, body cells will metabolize fat and muscle for energy
– Glaucoma
▪ Hyperglycemia in eye prevents proper fluid drainage and leads to increased pressure on retina
– Cataracts
▪ Increased sugar in blood may create a cloudy buildup in the eye’s lens
– Irritability, trouble thinking clearly, anxiety
▪ Brain is most-energy demanding organ; without glucose
– Frequent infections and slow-healing cuts and sores
▪ Reduced white blood cell response and increased immune disfunction
– Ketone bodies in urine and ketoacidosis
▪ Ketones are a byproduct of fatty acid metabolism, which increases with diabetes

21
Q

Symptoms of Diabetes Mellitus

A
  • Polyuria (frequent urination)
    – Excess glucose lost in urine acts to pull fluid into urine by osmosis
    – Abnormal loss of fluid in urine; body is dehydrated
  • Polydipsia (increased thirst)
    – Hyperglycemia leads to hyperosmolarity (blood is hypertonic)
  • Polyphagia (increased hunger)
    – Cells are unable to normally absorb glucose into their cells
    – Increased proteolysis and lipolysis
22
Q

Acute Complications of DM (Hyperglycemic Crises)

A
  • Metabolic emergencies that may result in hospitalization and/or death
  • Increased gluconeogenesis results in hyperglycemia and hyperosmolarity of ECF
  • Both conditions show symptoms related to hyperglycemia
    – Polydipsia, Polyuria, Polyphagia
23
Q

Diabetic Ketoacidosis (DKA)

A

– Usually seen in DM type I
– Symptoms usually present within a few hours
– Without glucose, cells break down fatty acids for energy
▪ Ketones are produced as byproducts of fatty acid breakdown
▪ Ketones are acidotic and rapidly decrease blood pH (potentially fatal)
▪ Patients compensate low pH with deep fast breathing (Kussmaul breathing)

23
Q

Hypoglycemia

A

– Glucose levels below 60 mg/DL
– Numerous causes
▪ Insulin overdose, prolonged exercise, alcohol use, liver or kidney dysfunction
▪ Deficiency of glucocorticoids or growth hormone, genetics
– Brain cells are deprived of glucose needed to function effectively
– Symptoms include mental disorientation, convulsions, unconsciousness,
insulin shock, or death
– Glucagon given if individual unconscious and unable to eat
* Symptoms of hypoglycemia are similar to hyperglycemia
– Important to correctly identify cause of symptoms and treat appropriately
* Hyperinsulinism – most often occurs when diabetic injects too much insulin
– Stimulates secretion of epinephrine, glucagon, and growth hormone
– Main symptom is hypoglycemia (decreased blood glucose levels)

24
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A

– Usually seen in DM type II
– Symptoms present over days or weeks
– Beta-cells still produce insulin, but not enough to counter the target resistance
▪ No ketones produced as in DKA
– Dehydration and extreme hyperosmolarity causes encephalopathy (brain dysfunction)
▪ Confusion, delirium, slurred speech, memory loss, altered mental status

25
Q

Long Term Complications of DM

A
  • Macrovascular complications
    – Cardiovascular disease
    ▪ Diabetes can lead to atherosclerosis
    ▪ Increased risk of heart attack, stroke, coronary artery disease
  • Microvascular complications
    – Kidney damage
    ▪ Damage to blood vessels in kidney may impair ability to filter blood
    – Diabetic retinopathy
    ▪ Damage to retinal blood vessels can cause leaking or growth of abnormal new vessels on the retina’s surface, which may increase pressure in the eye
  • Neuropathy
    – Peripheral (diabetic) neuropathy
    ▪ Damage to nerves may lead to loss of sensations in lower extremities
    ▪ Increases risk of foot ulcers and infection
    – Gastroparesis (inability to move food through digestive tract)
    ▪ Nerve damage to digestive organs may cause muscles to slow or become dysfunctional, leading to nausea, heartburn, and bloating

Bio 144 (8 decks)

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