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Patho II > Pancreas I > Flashcards

Pancreas I Flashcards

1
Q

The exocrine pancreas is composed of ?

What does it secrete?

Where do these secretions head to ?

A

These digestive enzyme need to be activated

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2
Q

The endocrine pancreas is composed of what type of cells?

What do these cells secrete?

A

Composed of the islets of Langerhans that
secrete:

  • insulin by β cells
  • glucagon by α cells
  • somatostatin by δ cells
  • PP cells secrete pancreatic polypeptide
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3
Q

Excrine pancreas diagrams

A
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4
Q

Diabetes Mellitus can be defined as a group of metabolic disorders sharing the commone feature of hyperglycemia…Hypergycemia in diabetes is caused by?

A
  • defects in insulin secretion
  • insulin action
  • or, most commonly, both
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5
Q

Chronic hypergycemia and associated metabolic dysregulation might cause?

A

secondary damage in multiple organ systems, especially the kidneys, eyes,
nerves and blood vessels

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6
Q

After a meal, Insulin in normal subjects does what two things in normal people?

A
  1. It decreases liver glucose production by decreasing both glycogenolysis and gluconeogenesis
  2. It increases glucose uptake by skeletal muscle and adipose tissue by
    translocating glucose transporters
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7
Q

What counter-regulatory hormones increases within the earliest stages of hypoglycemia ?

What type of natual behaviors occur during a hypoglycemic state?

What happens to the plasma glucose concetration levels?

A

Relation between insulin and glucagon:

  • In the earliest stages (within minutes):
    • decreased insulin increased glucagon

Behavior defenses:

  • The initial symptoms of sweating, anxiety, palpitations, hunger and tremor
    • plasma glucose concentration falls below 55 mg/dL
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8
Q

There is a direct relationship between overnight blood glucose and the cause of the following morning hyperglycemia glucose level… What are they?

A

the cause of morning hyper glycemia is …nocturnal growth hormone secretion and hypoinsulinemia

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9
Q

How can exercise affect someone with insulin-deficient diabetes?

A

increases glucose utilization
by muscle can cause
hypoglycemia in patients with
insulin-deficient diabetes

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10
Q

Hypoglycemia-Associated Autonomic Failure (HAAF) in Diabetes is defined as ?

What is the Hypoglycemia-Associated Autonomic Failure (HAAF) mechanism?

A
  • the clinical syndromes of defective glucose counter-regulation and hypoglycemia unawareness
  • hypoglycemia, even if asymptomatic, causes a vicious cycle of recurrent hypoglycemia

HAAF mechanism:
-reducing the sympathoadrenal response to subsequent hypoglycemia due to:

  • changes in hypothalamic functions
  • increase in cortisol
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11
Q

What is the most important stimulus for insulin synthesis and release?

A

glucose itself

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12
Q

How does glucose get inside the cells?

A
  • Glucose enters beta cells via the glucose transporter, GLUT2, which causes the release of insulin into the blood stream to bind to insulin receptors
  • Insulin stimulates glucose uptake by skeletal muscle and fat by GLUT-4
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13
Q
  1. GLUT-2 acts on?
  2. GLUT-3 acts on?
  3. GLUT-4 acts on?
A
  1. GLUT-2 acts on– Beta cells, liver cells
  2. GLUT-3 acts on– All tissues, central nervous system
  3. GLUT-4 acts on?– Skeletal muscle, fat cells
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14
Q

Effect of insulin on metabolism of:

  • Glucose?
  • Fat: ?
  • Protein: ?
A
  • Glucose
    • Prevens liver from forming new glucose - inhibits gluconeogenesis
      • Increases uptake by skeletal/fat cells
  • Fat: decrease lipolysis
    • Causes storage of triglycerides in fat cells
      • decrease lipolysis means less fatty acids go to liver leads to decrease production of glucose
  • Protein: inhibits breakdown
    • decreases catabolism
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15
Q

Effects of insulin on:

  • Adipose tissue
  • Straited muscle
  • Liver
A
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16
Q

Where does glycated hemoglobin come from?

What is the Clinical test to estimate blood glucose control?

What does this test reflect ?

A
  • measurement of glycated hemoglobin (also called A1C, hemoglobin A1C, glycohemoglobin, or HbA1C)
    • Goal is less than or equal to 7% blood glucose
  • A1C reflects mean blood glucose over
    the entire 120-day lifespan of the red blood cell, but it correlates best with mean blood glucose over the previous 8 to 12 weeks
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17
Q

Describe type I and type II diabetes?

A
  • Type I
    • an autoimmune disease characterized by pancreatic β cell
      destruction      and anabsolute deficiency of insulin
      • Islet destruction by endogenous β-cell antigens
  • Type II
    • caused by a combination of peripheral resistance to insulin action and an inadequate secretory response by the pancreatic β cells (“relative
      insulin deficiency”)
18
Q

What are the etiologies of type I and type II

A
19
Q

You are genetically susceptibility to aquiring type I diabetes who are heterozygous for high-susceptibility genes in what region?

A
  • HLA region
    • group of genes on chromosome six that encode for the MHC
      • protein that is extemely important for helping the immune system recognize foreign molecules along with maintaing self tolerance
20
Q

What is the immunologic response that leads to the islet cell destruction?

A
  • The Beta cell antigens binds to MHC Class II this leads to T-Cell activation. These T-cells don’t recognize our own bodys own cells and caus autoimmune injury to the pancreatic beta cells →less insulin →less glucose entering cells so blood glucose increases
    • (These rogue T-cells are knwon as Islet cell autoantibodies (ICAs))
  • Costimulatory proteins further increase T Cell activation
21
Q

How do “people” measure the risk of type I diabetes?

A
  • It is asses in the amount of islet autoantibodies
  • The presence of two or more of these islet autoantibodies leads to increase risk of type I diabetes
    • Insulin
    • Glutamic acid decarboxylase (GAD)
    • Insulinoma associated antigens 2 (alpha and beta)
    • ZnT8 (zinc transporter)
22
Q

Clinically evident type 1 diabetes does not occur until….?

A

Clinically evident type 1
diabetes does not occur until
there has been a much greater
loss of functioning beta cell
mass = >50% destruction

23
Q

When does type I diabetes appear if there are genetic markers for it versus immune markers?

A

• Genetic markers: present from birth
• Immune markers: first appear at the time of the
environmental triggering events

24
Q

Is Diabetic ketoacidosis (DKA) & hyperosmolar hyperglycemic state (HHS) related to type I or II ?

A

DKA - type I

HHS-type II

25
Q

Diabetic ketoacidosis (DKA) & hyperosmolar hyperglycemic state (HHS) in
patients with uncontrolled diabetes:

  1. HHS is when glucose ….?
  2. What is the pathogenesis of HHS?
  3. DKA pathogensis?
A

1.) When glucose exceeds 1000 mg/dL (56
mmol/L)

2.)Pathogenesis:
• Insulin deficiency and/or resistance
• Glucagon excess.

3.) Ketoacidosis if formed by lipolysis (leads to increased FA’s)→ synthesis of ketones from free fatty acids in the liver

-ketone bodys can be used by the cells as energy but they also increase the acidity of the blood( this can lead to increase potassium in the blood as Hydrogen ions will rush into the cells to try to decrease the acidity of the blood also insulin maintains the sodium potassium pump so with a lack of insulin sodium will stay inside the cell and potassium will stay ouside the cell in the blood due to the lack of exchange)

*Processing the body’s fat is a key job for the liver. Once the liver is full of glycogen, it starts turning the glucose it absorbs from the blood into fatty acids, for long-term storage as body fat.

26
Q

What are the multifactorial “factors” that are involved with type II DM?

A

Definition:
• Complex disease that involves an
interplay of genetic and environmental
factors and a pro-inflammatory state

27
Q
  1. Is type II DM autoimmune related?
  2. Type II DM is characterized by?
  3. What is hyperglycemia’s affect by itself on pancreatic beta cells?
  4. Metabolic syndrome is defined as ?
A
  1. NO evidence of an autoimmune basis
  2. Characterized by hyperglycemia, insulin
    resistance and relative loss in insulin
    secretion
    1. Sometimes there is a genetic abnormality with the GLUT-2 transporter so it doesn’t even get expressed to bring glucose into the beta cells to let them know to secrete insulin
  3. Hyperglycemia itself can damage pancreatic
    beta-cell function and magnify insulin
    resistance, causing a vicious cycle of
    hyperglycemia
  4. Definition of metabolic syndrome:
    • co-occurrence of metabolic risk factors for both type 2 diabetes and CVD
28
Q

What are the most important risk factors for Diabetes type II?

A

obesity and lack of exercise

29
Q

What are the three metabolic defects in type II diabetes ? describe them

A
  • Insulin resistance
    • Target cells of insulin is not working properly (due to insulin-receptor mutations) and not responding to the insulin (resistant to the insulin)
  • Inadequate insulin secretion:
    • → Due to the genetic alteration affecting GLUT-2 expression
  • Impaired insulin processing:
    • → The processing of proinsulin to insulin in the beta cells is impaired in type 2 diabetes (so there is less insulin)
30
Q

What are the major organs associated with insulin resistance?

What are the consequences of insulin resistance?

A

Major organs associated with insulin resistance:

• Liver, skeletal muscle and adipose tissue

Consequences of Insulin resistance:
• Failure to inhibit gluconeogenesis →high
fasting blood glucose levels

• Failure of glucose uptake and glycogen
synthesis → high post-prandial blood
glucose level

• Failure to inhibit lipoprotein lipase → FFAs
→ amplify the state of insulin resistance

31
Q

Describe lipotoxicity

A

-When we eat a meal the extra carbs are going to be stored as triglycerides in the fat cells, what happens when we fast is we have increased lipolysis so free fatty acids will be stored in other organs too.

If stored in heart –>there is increased risk of CVD

If stored in pancreas –> insulin resistance and destruction of beta cells

If stored in liver–> steatosis –> nash–> fibrosis/cirrhosis

32
Q

Insulin resistance BEGINS in the ________ and leads to…….

A

Insulin resistance BEGINS in the hypothalamus and leads to imbalance of satiety and hunger signals

33
Q

Obesity gives rises to what three components that cause Insulin resistance?

A

Adipokines = cytokines produced by the fat cells themselves

34
Q

How is inflammation linked to insulin resistance?

A
  • Proinflammatory mediators are increased due to dyslipidemia (which means increase in free fatty acids) and Hyperglycemia
  • Pro-inflammatory factors directly lead to inflammatory syndrome which leads to two things:
    • Insulin resistance in peripheral tissues b/c of inflammation
    • Beta cell dysfunction & cellular apoptosis → decreased insulin secretion
35
Q
  • explain the classic symptoms of hyperglycemia?
  • Explain how the symptom polydipsia occurs?
A

Classic symptoms of hyperglycemia:

  • Asymptomatic
  • polyuria,
    • increased thirst
  • polydipsia,
    • increased urination
    • Polyuria occurs when the serum glucose concentration significantly above 180 mg/dL (10 mmol/L)
  • nocturia,
    • urination during the night
  • blurred vision, and,
  • infrequently, weight loss
  • Glycosuria causes osmotic diuresis (ie, polyuria) and hypovolemia ⇒polydipsia
    • glucose is a solute so it cannot get into cell membrane by itself obvi its needs insulin so increased level in the blood is going to cause water to rush out of cells to dilute solutes leaving the cells dehydrated. This is going to increase thirst level →increase fluid intake→frequent urination
36
Q

Explain the short term and long term effects of muscle metabolism in Nondiabetics?

A

Once you start exercising the glycogen stores in muscles will be broken down to be used as energy

37
Q

Effects of exercise in type I and type II DM

→short term vs. long term effects of both types?

A

DM type I person who diabetes isn’t undercontrol starts exercising…. the amount of ketone bodys will be increased due to increase of lipolysis (increase of FFA that is producing the ketone bodies

38
Q

The morbidity associated with longstanding diabetes
of either type is due to damage induced in?

Macrovascular disease causes accelerated
atherosclerosis in diabetics?

The effects of microvascular disease are most
profound in the?

A

The morbidity associated with longstanding diabetes
of either type is due to damage induced in:
• diabetic macrovascular disease - associated with atherosclerosis in big vessel

• diabetic microvascular disease-small vessels

Macrovascular disease causes accelerated
atherosclerosis in diabetics:
• increased risk of myocardial infarction

  • stroke
  • lower extremity ischemia

The effects of microvascular disease are most
profound in the:
• Retina →diabetic retinopathy

  • Kidneys → diabetic nephropathy
  • Peripheral nerves → diabetic neuropathy
39
Q

Describe the Pathogenesis of Long-term Complications of Diabetes and how it leads to mirco/macro vascular complications?

A
40
Q

What is the clinical significance of Advanced Glycosylation End Products (AGEs) in diabetes?

A

Patho II (12 decks)

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