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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
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 \_\_\_\_
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
Diabetes is the leading cause of: * ________ disease * Adult onset \_\_\_\_ * ________ amputations
Diabetes is the leading cause of: * End stage renal disease * Adult onset blindness * Lower extremity amputations
27
Diabetic classical triad of symptoms include:
Diabetic classical triad of symptoms include: * Polyuria * Polydipsia * Polyphagia
28
Combination of polyphagia (increased hunger) and weight loss suggest \_\_\_\_
Combination of polyphagia (increased hunger) and weight loss suggest _type 1 diabetes_
29
What causes polyuria and polydipsia in diabetics?
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
What explains polyphagia (increased hunger) and weight loss in diabetics?
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
Insulin deficiency can also cause decreased ________ which leads to hyperlipidemia
Insulin deficiency can also cause decreased _lipoprotein lipase_ which leads to hyperlipidemia
32
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
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
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
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
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 \_\_\_\_
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
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
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
What does MODY stand for and what is it?
**_M_**aturity **_O_**nset **_D_**iabetes of the **_Y_**oung Defects in glucose metabolism Note: just be aware of this for now, will go into more detail in future blocks
37
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 \_\_\_\_
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
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 \_\_\_\_
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
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 \_\_\_\_
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
Clinical/lab signs of diabetic ketoacidosis (common in type 1 diabtes)
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
Long term hyerglycemia leads to 4 main consequences:
Long term hyerglycemia leads to 4 main consequences: * AGE-RAGE binding * Protein kinase C * Polyols-oxidative stress * Hexosamine pathway
42
Clinical/lab signs of hyperosmolar coma (common in type 2 diabetes)
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
AGE-RAGE Binding is caused by long term ____ and leads to 2 main consequences:
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
Long term ____ leads to activation of ____ which leads to cytokine exretion and gene expression which leads to renal, retinal, neuronal, and vascular implications
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
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
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
Long term ____ leads to activation of the ____ pathway which leads to elevated plasminogen activator which increases risk of CVD
Long term hyperglycemia leads to activation of the _hexosamine_ pathway which leads to elevated plasminogen activator which increases risk of CVD
47
Macrovascular pathology is essentially \_\_\_\_ This is much worse in diabetics and can lead to (3 examples)
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
Diabetics may experience microvascular pathology with hyaline arterosclerosis which inolves (3 examples) ## Footnote **This underlies the conditions (3 examples)**
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
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
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
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
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
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
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
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
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
Insulin therapy overdose can cause ____ for which the symptoms include (5 examples)
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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