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SU 17: Wine regions of South America > Endocrine Lecture 4: Pancreas & Diabetes > Flashcards

Endocrine Lecture 4: Pancreas & Diabetes Flashcards

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1
Q

The pancreas secretes insulin and glucagon which are vital in the regulation of:

A

glucose, lipid, and protein metabolism

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2
Q

Acini glands secrete:

A

digestive juices into the duodenum

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3
Q

Islet of Langerhans is composed of 3 types of cells:

A

Alpha cells

Beta cells

Delta cells

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4
Q

Islet of Langerhans:

Alpha cells secrete:

A

Glucagon

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5
Q

Islet of Langerhans:

Beta cells secrete:

A

Insulin

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6
Q

Islet of Langerhans:

Delta cells secrete:

A

Somatostatin and pancreatic polypeptie

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7
Q

Insulin is a hormone associated with energy abundance and storage of this excess energy. What are 4 specific functions of insulin in the body?

A
  1. Causes carbohydrates to be stored as glycogen in muscle and liver
  2. Excess carbohydrates that cannot be converted to glycogen are converted to fats and are stored in adipose tissue
  3. Causes fat storage in adipose tissue
  4. Insulin promotes uptake of amino acids and conversion to protein
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8
Q

Insulin release is stimulated by:

A
  • High blood glucose
  • Amino acids
  • Beta-keto acids
  • Glucagon
  • Acetylcholine, intestinal hormones
  • Insulin resistance: obesity
  • Sulfonylurea drugs (glyburide)
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9
Q

Insulin release is inhibited by:

A

-Low blood glucose
-Fasting
-Catecholamines -(alpha-agonists)
Somatostatin

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10
Q

Insulin circulates almost entirely ____ with plasma proteins and has a half-life of _ minutes.

A

UNboud to plasma proteins

6 minute half-life

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11
Q

The only cells permeable to glucose in the blood are in the ___. They do not require insulin for glucose uptake.

A

Neurons in the brain.

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12
Q

When insulin attaches to it’s very specific receptors ____ happens. Within seconds, adipose and muscle cells markedly increase their uptake of glucose. The cell membrane in creases in take of 3 other substances. What are they?

A

Endocytosis

Amino acids, Potassium, and Phosphate.

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13
Q

Anabolic effects of Insulin:

A

Storage of glucose for later use.

Increases muscle storage of glucose, fatty acids and amino acids
Increases glycogenesis (glycogen is storage form of glucose)
Inhibits glycogenolysis
Inhibits gluconeogenesis
Phosphorylates glucose (traps) for use in glycolysis, glycogenesis

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14
Q

Insulin facilitates entry of glucose into cells of all tissues except:

A

brain, kidney tubules, intestinal mucosa and RBCs

Increases hepatic uptake, storage, and use of glucose

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15
Q

Insulin effects the liver by:

A

Liver releases glucose between meals
Increases lipogenesis and protein synthesis in liver
Increases protein synthesis
Stimulates intracellular amino acid transport, increases translation of mRNA into proteins
Inhibits protein catabolism and depresses gluconeogenesis

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16
Q

Glucagon has effects that ____ the effects of insulin.

A

OPPOSE (Catabolic effects)

It increases blood glucose concentration and can cause hyperglycermia

Glucagon is secreted by the alphacells of the inslets of Langerhans when blood glucose levels fall.

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17
Q

Glucagon generally opposes insulin but stimulates ____

A

insulin release

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18
Q

Glucagon activates enzymes for ____.

A

Glycogenolysis

Glucagon responds to falling, fasting, or low blood glucose levels.

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19
Q

Glucagon increases the following processes:

A
  • Gluconeogeneses
  • glucogenoloysis
  • Lypolysis and ketogenesis (inhibits triglyceride storage in liver)
  • Increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis
  • also enhances heart strength, increases blood flow in some tissues, enhances bile secretion (inhibits gastric acid secretion)
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20
Q

Glucagon release is stimulated by:

A

-Fasting hypoglycemia
-Amino acids (protein meal)
-Beta-adrenergic stimulation
-Exercise
(Not associated with hypoglycemia, but may be a response to increased circulating amino acids)
-Cholecystokinin, gastrin and cortisol

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21
Q

Glucagon release is inhibited by:

A
  • High glucose levels
  • Somatostatin
  • Free fatty acids
  • Ketones
  • Insulin
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22
Q

Carbohydrate Metabolism:

Anabolic (synthesis) Phase: postprandial

A

Energy intake exceeds usage requirements

Energy is stored as glycogen, structural proteins and fat

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23
Q

Carbohydrate metabolism: post prandial

Insulin release begins at _____mg/dL of glucose and peaks at __-__mg/dL

A

100mg/dl

400-600mg/dl

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24
Q

After eating, plasma insulin concentration increases almost 10-fold in __-__ minutes due to dumping of preformed, stored insulin

A

3-5 minutes

Level decreases in 5-10 minutes

At 15 minutes, new insulin plateau is reached due to more release and synthesis

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25
Q

Shut-off of post prandial insulin bolus is in __-__ min after blood glucose level is under ___mg/dL.

A

3-5 minutes

80mg/dL

26
Q

Fasting Carbohydrate metabolism: Fasting

A

Needs met only by endogenous (internal) sources
Mediated by glucagon
Breakdown of glycogen, protein, triglyceride stores for energy supply: glucose, ketones.
Brain can function on glucose and ketones
12-24 hrs: liver glycogen sufficient for brain
24 hours: Gluconeogenesis uses AAs, glycerol and lactate to make glucose

27
Q

Ketones are produced by __?

A

Fat metabolism when other sources of fuel are unavailable.

28
Q

Fasting metabolism first stage:

What is broken down first to make glucose?

A

Amino acids from breakdown of muscle protein are a good source of glucose formation
Muscle wasting significant in first few days of fasting
Gluconeogenesis primarily in liver, some kidney

29
Q

Fasting metabolism later stages (2-4 days):

A

Fat stores broken down to free fatty acids for tissues, some glucose, but primarily ketones for brain.
Ketones formed in liver
At this point, most glucose used by CNS, protein loss minimized by fat loss
After weeks, brain uses primarily ketones
Measurable in urine

30
Q

What is Diabetes Mellitus (in general terms)?

A

A syndrome of impaired carbohydrate, fat, and protein metabolism caused by either a lack of insulin or a decreased sensitivity of the tissues to insulin

31
Q

What are the main characteristics of Type I diabetes?

A

Lack of insulin secretion.

Body Habitus: thin or normal

  • Ketoacidosis: common
  • Autoantibodies: usually present
  • Endogenous insulin: low or absent (death or inactivation of Beta cells)
  • Less prevelent than Type 2
32
Q

What are the main characteristics of type II diabetes mellitus?

A

Decreased sensitivity of target tissues to the metabolic effects of insulin (insulin resistance)

  • Gradual onset, mostly in adulthood
  • Body habitus: often obese
  • ketoacidosis: rare
  • autoantibodies: absent
  • endogenous insulin: normal, increased, eventually decreased due to cellular exhaustion), will become insulin dependent.

Most prevalent

33
Q

What are the effects of hyperglycemia on the kidneys?

A

Glucose is reabsorbed by kidney until about 180mg/dL.

Leads to osmotic diuresis, loss of Na, K, glucosuria
Hypovolemic hypotension, dehydration, polyuria, polydipsia, polyphagia (increased appetite from hypothalamus ventromedial nucleus)

34
Q

What are the effects of low insulin on the body?

A

Low insulin leads to muscle catabolism, increased fat

catabolism
Increases the release of keto acids (acetoacetic acid, beta-hydroxybutyric acid), causes an anion gap metabolic acidosis

35
Q

What are the 3 most common acute symptoms of Diabetes?

A
  1. Polyuria – osmotic diuresis
  2. Polydipsia – intravascular volume depletion
  3. Polyphagia and weight loss – protein catabolism

Additional symptoms:
-Confusion d/t hypertonic ECF leads to cell shrinkage.

-Visual disturbances – sorbitol formation in lens causes osmotic swelling, glycation leads to opacification
Microvascular disease affects perfusion of retina
Often present in 10-15 years

36
Q

What are some chronic symptoms and problems related to DM?

A

-Infection: depressed neutrophil and Macrocyte function d/t hyperglycemia.

-Macrovascular disease:
accelerated atherosclerosis
Causes CAD, PAD, AMI, CHF, CVA

  • Microvascular disease:
  • Nephrophathy – 1/3 of transplants, 50% develop CRF
  • Retinopathy – leading cause of blindness in US ages 20-65
  • Neuropathy – symmetric, sensory, stocking glove
  • Autonomic – orthostatic hypotension, delayed GI emptying
37
Q

What causes Type I diabetes?

A
  • Destruction of Beta islet cells results in loss of insulin release, caused by viral infections or autoimmune disorders
  • Heredity plays a role in determining susceptibility of beta cells to insults
  • Of note: Receptor and cellular mechanisms usually preserved
38
Q

What leads to development of Type II DM?

A
  • Caused by greatly diminished sensitivity of target tissues to metabolic effects of insulin
  • Plasma insulin is elevated in type II DM. Levels still insufficient for regulation, beta-cells become exhausted in some patients
  • Most patients with type II DM are obese
39
Q

How is DM diagnosed today?

A

Hbg A1C blood test
Reflects average blood sugar level over approximately 3 months (rbc lifespan). Glucose sticks to RBCs.

Normal level is between 4-5-5.6%

commonly used to gauge how well managed existing DM is managed.

40
Q

Perioperative implications of DM.

In addition to the Triad of Heart Disease, HTN, and Renal problems, what other problems does one need to be aware of when making a care plan for a patient with DM?

A

Of course: increased risk of heart disease and stroke (often silent MI in DM)

Increased risk of positioning injuries (microvascular issues and neuropathies)

-Increased risk of autonomic neuropathy and hemodynamic instability
IE: Inability to compensate for changes in volume and vascular tone
Increased risk of post-induction hypotension and sudden death

  • Increased risk of gastroparesis and pulmonary aspiration
  • Joints become stiff (TMJ, AA, cervical spine) resulting in difficulty with intubation
41
Q

Hyperglycemia causes increased incidence of:

A

-CHF
-18x mortality
-2x length of stay
-greatly increased risk of infection (suppression of action of neurtophils and Macrocytes)
-sepsis
-Acute Renal Failure
-illness related neuropathy
Increased (susceptibility to positioning injuries)
-CVA
-poor fetal outcomes

42
Q

Infection rate is 2.7x higher in diabetics if BG > ___

A

220

43
Q

What are the 3 distinct effects of glucose control?

A
  • Inhibits lipolysis and elevated FFAs which are assoc with cardiac arrhythmias
  • Insulin inhibits inflammatory growth factors important in acute MI, and general inflammatory responses
  • Decreased insulin leads to proteolysis, while insulin infusions lead to favorable alterations in myocardial and skeletal muscle metabolism
44
Q

Anesthesia and surgery interrupt regular meal and insulin schedules
Better glycemic control improves:

A
  • Decreased hospital/ICU length of stay
  • Decrease infection rates/improved wound healing
  • Improved outcome after strokes, MI
  • Decreased mortality after cardiac, carotid surgery
45
Q

Perioperative stress may increase serum glucose concentrations. how?

A

Increased release of cortisol (stress hormone) and catecholamines.

46
Q

Consensus that BS>___ perioperatively should be treated

A

200

47
Q

Perioperative guidelines for Diabetic Patients:

A
  • Plan surgery in diabetics as 1st case of the day to prevent prolonged fasting
  • Oral hypoglycemics are held day of surgery to prevent hypoglycemia until oral intake is restarted
  • Insulin therapy should balance adequate glucose control with the avoidance of hypoglycemia
  • Type I diabetics should continue basal insulin administration to avoid ketoacidosis
  • Patients on insulin pumps may be managed by continuing the pump for short operations or changing over to IV insulin infusions
48
Q

The primary features of DKA are:

A

Dehydration

Acidosis

Electrolyte depletion

49
Q

DKA Dehydration and electrolyte depletion:

A

Blood glucose rises without effective insulin leading to osmotic diuresis and lyte losses
Dehydration up to 4-6L
Loss of up to 10% body K+
Lesser degrees of Na, Mag, cl, phos losses

50
Q

DKA Acidosis:

A

Accelerated protein breakdown
Leads to increased liver gluconeogenesis, worsening hyperglycemia
Activation of B-oxidation of fatty acids
Insulin absence and catechols from volume depletion increase FAs
Ketogenesis results, which overwelms body’s buffer and results in ketoacidosis

51
Q

Symptoms of DKA:

A

Nausea/Vomiting, polyuria, polydipsia, polyphagia, anorexia, orthostatic changes, Kussmaul breathing, acetone halitosis
Level of consciousness related to pts osmolality, not acidosis

52
Q

Precipitating Events for DKA:

A
  • MI
  • trauma
  • etoh
  • infection
  • non-compliance
53
Q

Treatment of DKA:

A

Massive fluid resuscitation, electrolyte replacement, insulin therapy
Will present with often severe hyperkalemia in face of total body K depletion

Outcome:
3-10% mortality

54
Q

Nonketonic Hyperosmolar State:

A

Common in DM2, same precipitating events as DKA, but with very high glucose levels

55
Q

What are the primary features of nonketonic hyperosmolar state?

A
  • Severe hyperglycemia,
  • Dehydration
  • Severe hyperosmolar state (Na down 1.6/100 glucose)
  • lack of ketoacidosis
56
Q

S/S of nonketonic hyperosmolar state:

A
  • Thrombosis from hyperviscosity
  • focal neuro/reflex signs
  • global neuro signs, confusion, seizures, coma
57
Q

Treatment of Nonketonic Hyperosmolar state:

A

Fluid resuscitation
Add sugar to IVF when BG ~250 to avoid precipitous drop and cerebral edema
K+, phosphate, insulin if needed

Outcomes: 10-20% mortality

Note: Osmolarity = 2[Na+] + [Glucose]/18 + [ BUN ]/2.8

58
Q

Insulin excess= hypoglycemia. What are the physiological responses of the body to hypoglycemia?

A

Early response – liver glycogen breakdown
Glucagon response less important early, becomes increasingly important progressively

Late – Sympathetic stimulation, epi release

Very late – GH and cortisol secreted
Insulinoma – beta cell adenoma

Insulin shock: coma under 20mg/dl
Treat: glucose, (glucagon, epinephrine)

59
Q

Hypoglycemic shock develops in range of ___-___ mg/dl

A

20-50mg/dL

Progressive nervous irritability leads to fainting, seizures and coma
Brain uses only glucose if available, but can use fats/ketones with difficulty in times of stress
Treat with D50 + infusion of D5

60
Q

______ inhibits BOTH insulin and glucagon secretion.

A

Somatostatin

SU 17: Wine regions of South America (10 decks)

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