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Block 2 - Week 1 > Diabetes Pathophysiology > Flashcards

Diabetes Pathophysiology Flashcards

1
Q

Glucose metabolism is important because ____ and ____ are pivotal branch points in carbohydrate metabolism

A

Glucose metabolism is important because pyruvate and Acetyl-CoA are pivotal branch points in carbohydrate metabolism

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2
Q

Glucose metabolism is important for the production of ________ used for DNA and RNA synthesis

A

Glucose metabolism is important for the production of nucleic acid intermediates used for DNA and RNA synthesis

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3
Q

Glucose metabolism is important for the production of ________ for protein metabolism

A

Glucose metabolism is important for the production of amino acid intermediates/metabolism for protein metabolism

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4
Q

Glucose metabolism is important in ________ by providing important intermediates such as Acetyl-CoA and glycerol-3-phosphate

A

Glucose metabolism is important in fat synthesis and metabolism by providing important intermediates such as Acetyl-CoA and glycerol-3-phosphate

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5
Q

Endocrine glands secrete ____ into the ____

A

Endocrine glands secrete hormones into the blood

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6
Q

Exocrine glands secrete their products through ____

A

Exocrine glands secrete their products through ducts

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7
Q

The pancreatic ________ are the regions of the pancreas that contain its endocrine (hormone-producing) cells

A

The pancreatic islets of Langerhans are the regions of the pancreas that contain its endocrine (hormone-producing) cells

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8
Q

What are the 4 cell types of the Islet of Langehans and what do they produce?

A
  • Alpha (a) cells –> Glucagon
  • Beta (B) cells –> Insulin
  • Delta cells –> Somatostatin
  • PP cells –> Pancreatic Polypeptide
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9
Q

The Islet of Langerhans also has ____ input (adrenergic and cholinergic)

A

The Islet of Langerhans also has neural input (adrenergic and cholinergic)

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10
Q

The liver assists with glucose regulation through (3 examples)

A

The liver assists with glucose regulation through:

  • Glycogen Storage
  • Glycogenolysis
  • Gluconeogenesis
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11
Q

Fat tissues plays a role in glucose regulation through ________

A

Fat tissues plays a role in glucose regulation through TAG synthesis, storage, and release

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12
Q

Skeletal muscle plays a role in glucose regulation through ____ storage.

Skeletal muscle disposes of __% of a glucose load.

A

Skeletal muscle plays a role in glucose regulation through glycogen storage.

Skeletal muscle disposes of 80% of a glucose load.

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13
Q

The three main forms of glucose control are:

  • Regulatory ____
  • ________ utilization
  • ____ glucose output
A

The three main forms of glucose control are:

  • Regulatory hormones
  • Peripheral tissue utilization
  • Hepatic glucose output
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14
Q

GLUT __ is the only insulin-dependent transporter and is found on ________ and ________

A

GLUT4 is the only insulin-dependent transporter and is found on adipose tissue and skeletal muscle

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15
Q

GLUT__ is bidirectional and found on the ____, ____, ____,and ____

A

GLUT2 is bidirectional and found on the B islet cells, liver, kidney,and GI tract

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16
Q

How do B cells recognize glucose and trigger insulin release?

A
  1. Glucose uptake via GLUT2
  2. Glucokinase cell sensor
  3. ATP production
  4. ATP sensitive K+ channel closes –> depolarization
  5. Ca2+ to cytoplasm via ER voltage gated Ca2+ channels
  6. Ca2+ induces insulint vesicle fusion and insulin release
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17
Q

____ are hormones from the GI tract produced after a meal, and they facilitate ____ secretion

____ are metabolized by ________; an important one is ____

____ inhibitors are clinically available and prolong incretin biological effects

A

Incretins are hormones from the GI tract produced after a meal, and they facilitate insulin secretion

Incretins are metabolized by dipeptidyl dipeptidases (DPPs); an important one is DPP-4

DPP-4 inhibitors are clinically available and prolong incretin biological effects

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18
Q

Glucocorticoids are released from the ________ and have the following effects:

  • Enhance ____ catabolism to glucose intermediates
  • Increases ____
  • Are ____ (favor diabetes development)
A

Glucocorticoids are released from the adrenal gland and have the following effects:

  • Enhance protein catabolism to glucose intermediates
  • Increases gluconeogenesis
  • Are diabetogenic (favor diabetes development)

Note: virtually all cells have glucocorticoid receptors, and the receptors of glucocorticoids act as a transcription factor

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19
Q

Epinephrine effects glucose by:

  • Decreasing ____ in the liver
  • Increasing ____ in fat
  • Essentially blocking residual ____ effect

Epinephrine increases the availability of fatty acids which can be converted into ketones. Thus epinephrine can play a role in ____

A

Epinephrine effects glucose by:

  • Decreasing fatty acid synthesis in the liver
  • Increasing lipolysis in fat
  • Essentially blocking residual insulin effect

Epinephrine increases the availability of fatty acids which can be converted into ketones. Thus epinephrine can play a role in ketoacidosis

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20
Q

Insulin receptor pathway in muscle and fat

A

Insulin receptor pathway in muscle and fat

  • Insulint binds receptor
  • Receptor is a tyrosine-kinase type receptor –> phosphorylates tyrosine residues
  • Receptor phosphorylates IRS (insulin response substrate) –> GLUT4 moves to cell surface
  • Also activates MAP kinase pathway which favors cell growth and gene expression
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21
Q

Insulin promotes (5 examples)

Insulin inhibits (4 examples)

A

Insulin promotes:

  • Glycolysis –> Glycerol-3-phosphate –> lipogenesis
  • Glycolysis –> metabolic intermediates
  • Glycogenesis
  • Protein synthesis
  • Active glucose uptake (muscle and fat)

Insulin inhibits:

  • Lipolysis
  • Gluconeogenesis
  • Glycogenolysis
  • Protein catabolism
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22
Q

Glucagon promotes (4 examples)

Glucagon inhibits (3 examples)

A

Glucagon promotes:

  • Gluconeogenesis
  • Glycogenolysis
  • Fatty acid oxidation

Glucagon inhibits:

  • Glycolysis
  • Glycogen synthesis
  • Fatty acid synthesis
23
Q

____ diverts intermediates away from ketogenesis by:

  • Decreasing ________ activity –> decreasing available fatty acids for FA oxidation to make Acetyl-CoA
  • Decreasing ________ activity –> inhibiting the ketogenic pathway
  • Favoring ____ production which inhibits the CPT1 of the ____ shuttle
A

Insulin diverts intermediates away from ketogenesis by:

  • Decreasing hormone sensitive lipase activity –> decreasing available fatty acids for FA oxidation to make Acetyl-CoA
  • Decreasing mitochondrial HMG-CoA synthase activity –> inhibiting the ketogenic pathway
  • Favoring malonyl-CoA production which inhibits the CPT1 of the carnitine shuttle
24
Q

Insulin favors ____ production which inhibits CPT 1 in the ____ shuttle. Long chain fatty acids require this shuttle to get into the mitochondria to be used for ketone production, thus insulin plays a role in preventing ____.

A

Insulin favors malonyl-CoA production which inhibits CPT 1 in the carnitine shuttle. Long chain fatty acids require this shuttle to get into the mitochondria to be used for ketone production, thus insulin plays a role in preventing ​ketoacidosis.

25
Q

If complete insulin deficiency:

  • No ____ to regulate the carnitine shuttle –> free access of LCFAs to ketogenic machinery
  • Unregulated HSL –> increased ____ availability
  • Unregulated mitochondrial HMG-CoA synthase –> increased ____

All of this leads to ____

A

If complete insulin deficiency:

  • No Malonyl-CoA to regulate the carnitine shuttle –> free access of LCFAs to ketogenic machinery
  • Unregulated HSL –> increased fatty acid availability
  • Unregulated mitochondrial HMG-CoA synthase –> increased ketogenesis

All of this leads to ketoacidosis

26
Q

Diabetes is the leading cause of:

  • ________ disease
  • Adult onset ____
  • ________ amputations
A

Diabetes is the leading cause of:

  • End stage renal disease
  • Adult onset blindness
  • Lower extremity amputations
27
Q

Diabetic classical triad of symptoms include:

A

Diabetic classical triad of symptoms include:

  • Polyuria
  • Polydipsia
  • Polyphagia
28
Q

Combination of polyphagia (increased hunger) and weight loss suggest ____

A

Combination of polyphagia (increased hunger) and weight loss suggest type 1 diabetes

29
Q

What causes polyuria and polydipsia in diabetics?

A

Glucose is an osmolite (water follows it), thus increased blood glucose levels lead to increased fluid in blood which then gets excreted as urine

30
Q

What explains polyphagia (increased hunger) and weight loss in diabetics?

A

Diabetes causes protein catabolism which causes a negative energy balance (weight loss and polyphagia). Unintended weight loss combined with polyphagia is most often seen in type 1 diabetes.

31
Q

Insulin deficiency can also cause decreased ________ which leads to hyperlipidemia

A

Insulin deficiency can also cause decreased lipoprotein lipase which leads to hyperlipidemia

32
Q

Screening for diabetes:

  • Adults __-__ years of age should be screened for impaired gluocse (grade B evidence)
    • Especially patients with a BMI > __ plus 1 additional risk factor
  • Patients with 2 or more risk factors should be screened
A

Screening for diabetes:

  • Adults 40-70 years of age should be screened for impaired gluocse (grade B evidence)
    • Especially patients with a BMI > 25 plus 1 additional risk factor
  • Patients with 2 or more risk factors should be screened
33
Q

Diagnostic criteria for diabetes:

  • Random glucose: ____ is diabetes
  • 2 hour glucose tolerance: ____ is pre-diabetes and ____ is diabetes
  • Fasting blood glucose: ____ is pre-diabetes and ____ is diabetes
  • Hgb A1c: ____ is pre-diabetes and ____ is diabetes
A

Diagnostic criteria for diabetes:

  • Random glucose: >200 is diabetes
  • 2 hour glucose tolerance: 140-199 is pre-diabetes and >200 is diabetes
  • Fasting blood glucose: 100-125 is pre-diabetes and >126 is diabetes
  • Hgb A1c: 5.7-6.4% is pre-diabetes and >6.5% is diabetes
34
Q

Type 1 Diabetes

  • __% of diabetes cases; often present clinically or as ____
  • Autoimmune destruction of ________
  • Often ____ age group
  • Possible ____ trigger
  • Symptoms start at 70-90% loss of functional islet mass
  • Ultimate absolute ____ deficiency - important in ____
A

Type 1 Diabetes

  • 10% of diabetes cases; often present clinically or as ketoacidosis
  • Autoimmune destruction of pancreatic islets
  • Often younger age group
  • Possible infection trigger
  • Symptoms start at 70-90% loss of functional islet mass
  • Ultimate absolute insulin deficiency - important in ketoacidosis
35
Q

Type 2 diabetes

  • __% of diabetes cases; often detected in routine screening
  • A syndrome of ________ (relative ____ deficiency)
  • Strong ____ component
  • Associated with obesity, visceral fat accumulation, metabolic syndrome, and sedentary lifestyle
  • ____ production capcity remains (usually) to prevent ketoacidosis
A

Type 2 diabetes

  • 90% of diabetes cases; often detected in routine screening
  • A syndrome of insulin resistance (relative insulin deficiency); lower insulin affinity
  • Strong genetic component; first degree 5-10 fold risk
  • Associated with obesity, visceral fat accumulation, metabolic syndrome, and sedentary lifestyle
  • Insulin production capcity remains (usually) to prevent ketoacidosis
36
Q

What does MODY stand for and what is it?

A

Maturity Onset Diabetes of the Young

Defects in glucose metabolism

Note: just be aware of this for now, will go into more detail in future blocks

37
Q

Diabetes type 2

  • Decreased ____ (hormone stimulates FA oxidation)
  • Decreased ____ (hormone adequacy of fat stores)
  • Pro-inflammatory via ____ and _____
  • Insulin resistance through:
    • Failed ____
    • Failed expression of ____
A

Diabetes type 2

  • Decreased adiponectin (hormone stimulates FA oxidation)
  • Decreased leptin (hormone adequacy of fat stores)
  • Pro-inflammatory via inflammasome and IL-1
  • Insulin resistance through:
    • Failed signaling
    • Failed expression of GLUT4
38
Q

In type 1 diabetes there is no insulin which causes an increase in certain hormones and catecholamines such as ____ and ____ which increases ____ availability that can feed into ____

A

In type 1 diabetes there is no insulin which causes an increase in certain hormones and catecholamines such as glucagon and epinephrine which increases fatty acid availability that can feed into ketogenesis

39
Q

The lack of insulin in type 1 diabetes also blocks ____ synthesis, resulting in no ____ available to inhibit CPT1 which results in ____ going into the mitochondria via the carnitine shuttle to then be used for ____

A

The lack of insulin in type 1 diabetes also blocks FA synthesis, resulting in no Malonyl-CoA available to inhibit CPT1 which results in LCFAs going into the mitochondria via the carnitine shuttle to then be used for ketogenesis

40
Q

Clinical/lab signs of diabetic ketoacidosis (common in type 1 diabtes)

A

Clinical and lab signs of diabetic ketoacidosis:

  • Altered mental status/drowsy/coma
  • Increased anion gap
  • Arterial pH < 7.25
  • Plasma glucose > 250 mg/dL
  • Decreased serum bicarbonate
  • Positive urine or serum ketones
  • Positive urine glucose

Note: just have a general idea of the above

41
Q

Long term hyerglycemia leads to 4 main consequences:

A

Long term hyerglycemia leads to 4 main consequences:

  • AGE-RAGE binding
  • Protein kinase C
  • Polyols-oxidative stress
  • Hexosamine pathway
42
Q

Clinical/lab signs of hyperosmolar coma (common in type 2 diabetes)

A

Clinical/lab signs of hyperosmolar coma (common in type 2 diabetes):

  • Stupor/coma
  • Arterial pH > 7.3
  • Effect serum Osm > 320
  • Plasma glucose > 600
  • Bicarbonate > 15
  • Positive urine glucose

Usually occurs i the elderly with comorbid conditions; dehydration often involved

Note: just have a general idea of the above

43
Q

AGE-RAGE Binding is caused by long term ____ and leads to 2 main consequences:

A

AGE-RAGE Binding is caused by long term hyperglycemia and leads to 2 main consequences:

  • Cross linking of extracellular matrix –> amplifies vascular damage
  • Binding of RAGE receptors on T-cells/macrophages causing:
    • Cytokine release (inflammation)
    • ROS formation (tissue damage)
44
Q

Long term ____ leads to activation of ____ which leads to cytokine exretion and gene expression which leads to renal, retinal, neuronal, and vascular implications

A

Long term hyperglycemia leads to activation of protein kinase C which leads to cytokine exretion and gene expression which leads to renal, retinal, neuronal, and vascular implications

45
Q

Long term ____ leads to ________ which depletes NADPH in the aldose reductase reaction. NADPH not avaiable for reduction of oxidized glutathione –> deficient GSH –> oxidant stress, nerve damage, and peripheral neuropathy

A

Long term hyperglycemia leads to polyols and oxidatie stress which depletes NADPH in the aldose reductase reaction. NADPH not avaiable for reduction of oxidized glutathione –> deficient GSH –> oxidant stress, nerve damage, and peripheral neuropathy

46
Q

Long term ____ leads to activation of the ____ pathway which leads to elevated plasminogen activator which increases risk of CVD

A

Long term hyperglycemia leads to activation of the hexosamine pathway which leads to elevated plasminogen activator which increases risk of CVD

47
Q

Macrovascular pathology is essentially ____

This is much worse in diabetics and can lead to (3 examples)

A

Macrovascular pathology is essentially atherosclerosis

This is much worse in diabetics and can lead to:

  • Coronary artery disease –> which can lead to heart attack
  • Cerebral artery disease –> which can lead to stroke
  • Peripheral vascular disease –> which can lead to limb pain and gangrene
48
Q

Diabetics may experience microvascular pathology with hyaline arterosclerosis which inolves (3 examples)

This underlies the conditions (3 examples)

A

Diabetics may experience microvascular pathology with hyaline arterosclerosis which inolves:

  • AGE mediated crosslinking of matrix
  • Inductio of growth factors by signaling pathways
  • Leakage of plasma proteins into vascular wall

This underlies the conditions:

  • Nephropathy
  • Retinopathy
  • Some forms of neuropathy
49
Q

Renal disease is diabetics is caused by ____ hyaline arteriolosclerosis.

May also include nodular glomerulosclerosis (kimmeistiel-wilson disease)

Diabetes is a major cause of ESRD

Progression from microalbuminuria to ____ nephrotic syndrome

A

Renal disease is diabetics is caused by efferent hyaline arteriolosclerosis.

May also include nodular glomerulosclerosis (kimmeistiel-wilson disease)

Diabetes is a major cause of ESRD

Progression from microalbuminuria to nephrotic nephrotic syndrome

50
Q

Retinopathy in diabetics:

Non-proliferative retinopathy - early stage

  • ____ due to loss of pericytes
  • Increased vascular permeability

Proliferative retinopathy - late stage

  • Secondary to ____ and ____
  • Neovascularization under drive of ____
  • Late retinal hemorrhage
  • Can lead to vitreous ____ and retinal detachment
A

Retinopathy in diabetics:

Non-proliferative retinopathy - early stage

  • Microaneurysms due to loss of pericytes
  • Increased vascular permeability

Proliferative retinopathy - late stage

  • Secondary to ischemia and infarcts
  • Neovascularization under drive of VEGF
  • Late retinal hemorrhage
  • Can lead to vitreous hemorrhage and retinal detachment
51
Q

Peripheral neuropathy in diabetics:

  • Usually distal ____ neuropathy
  • Involves sensory function
  • ____ neuropathy is another variation which can include:
    • Fixed tachycardia
    • Orthostatic hypotension
    • Erectile dysfunction
    • Delayed bladder emptying
A

Peripheral neuropathy in diabetics:

  • Usually distal symmetric neuropathy
  • Involves sensory function
  • Autonomic neuropathy is another variation which can include:
    • Fixed tachycardia
    • Orthostatic hypotension
    • Erectile dysfunction
    • Delayed bladder emptying
52
Q

Insulin therapies can come in regular, ____ acting, and ____ acting forms

Some examples include:

____ which decreases insulin resistance

____ inhibitors which prolong incretin effects

GLP-1 analog and GLP receptor agonists

A

Insulin therapies can come in regular, short acting, and long acting forms

Some examples include:

Metformin which decreases insulin resistance

DDP-4 inhibitors which prolong incretin effects

GLP-1 analog and GLP receptor agonists

53
Q

Insulin therapy overdose can cause ____ for which the symptoms include (5 examples)

A

Insulin therapy overdose can cause hypoglycemia for which the symptoms include:

  • Palpitations
  • Diaphoresis
  • Light headedness
  • Anxiety/jitters
  • Syncope

Block 2 - Week 1 (9 decks)

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