Pancreas Flashcards
1
Q
The pancreas is a glandular organ with both digestive ______ &______ functions
A
(exocrine) and endocrine
2
Q
The pancreas is about ___ inches long and rests in the back of the abdomen behind the stomach
A
6
3
Q
The pancreas secretes insulin and glucagon which are vital in the regulation of ____, _____, and _______ metabolism
A
glucose, lipid, and protein
The pancreas secretes other hormones with lesser and uncertain importance (e.g. amylin, somatostatin, pancreatic polypeptide)
4
Q
What is the Acini?
A
glands secreting digestive juices into the duodenum
5
Q
What are the 3 islets of Langerhans?
A
Alpha cells
Beta cells
Delta cells
6
Q
What do alpha cells secrete?
A
secrete glucagon
7
Q
What do beta cells secrete
A
secrete insulin
8
Q
What do delta cells secrete
A
secrete somatostatin and pancreatic polypeptide
9
Q
Insulin is a hormone associated with energy abundance and
A
storage of this excess energy
10
Q
Insulin causes carbohydrates to be stored as
A
glycogen in muscle and liver
11
Q
Insulin causes fat storage in
A
adipose tissue
12
Q
Insulin causes excess carbohydrates that cannot be converted to glycogen to be
A
converted to fats and are stored in adipose tissue
13
Q
Insulin promotes uptake of amino acids and
A
conversion to protein
14
Q
What is insulin stimulated by? (7)
A
High blood glucose Amino acids Beta-keto acids Glucagon Acetylcholine, intestinal hormones Insulin resistance: obesity Sulfonylurea drugs (glyburide)
15
Q
What is insulin inhibited by? (4)
A
Low blood glucose
Fasting
Catecholamines (alpha-agonists)
Somatostatin
16
Q
How is insulin circulating?
A
Circulates almost entirely unbound with plasma half-life of 6 minutes
(Circulates almost entirely unbound with plasma half-life of 6 minutes)
17
Q
Insulin: highly specific receptor leads to _______. Within seconds, adipose and muscle cells markedly
A
endocytosis
increase their uptake of glucose
18
Q
T/F: neurons in the brain respond differently to insulin as the rest of the body
A
true
19
Q
how do neurons in the brain respond to insulin
A
Neurons permeable to glucose
Normal blood glucose required to prevent hypoglycemic shock
20
Q
With insulin, the cell membrane increases intake of
A
amino acids, potassium and phosphate
21
Q
Storing glucose for later use is what type of effect?
A
anabolic effect
22
Q
Anabolic effects increases muscle storage of glucose, fatty acids and amino acids. What 4 things do these do?
A
Increases glycogenesis
Inhibits glycogenolysis
Inhibits gluconeogenesis
Phosphorylates glucose (traps) for use in glycolysis, glycogenesis
23
Q
anabolic effects of insulin facilitates entry of glucose into cells of all tissues except
A
brain, kidney tubules, intestinal mucosa and RBCs
24
Q
T/F: an anabolic effects of glucose is that it increases hepatic uptake, storage, and use of glucose
A
true
Liver releases glucose between meals
25
anabolic metabolism increases ________ and protein synthesis in the liver
lipogenesis
26
Does anabolic metabolism increase or decrease protein synthesis?
Increases protein synthesis
Stimulates intracellular amino acid transport, increases translation of mRNA into proteins
Inhibits protein catabolism and depresses gluconeogenesis
27
Does insulin increases fat synthesis and storage
YES
Increases formation of glycerol and fatty acids and the resulting triglycerides
Insulin promotes transport of glucose as well as
Conversion of excess glucose into fatty acids
Inhibits lipolysis enzymes
28
Des insulin increase protein synthesis and storage
YES
Increases amino acid uptake as well as glucose entry
Normally only slightly permeable to glucose, exercise and insulin increase permeability and uptake
Increases glycogenesis and protein synthesis
Used for energy if exercising
29
*** What is glycogen secreted by? and when does it happen?
alpha cells of the islets of Langerhans when the blood glucose falls
30
Glucagon has effects that ______ the effects of insulin
oppose
It increases blood glucose concentration and can cause hyperglycermia
31
What type of reaction os glucagon?
catabolic - generally opposes insulin but stimulates insulin release
32
info about glucagon
Activates enzymes for glycogenolysis
Increases gluconeogenesis
Increases lipolysis and ketogenesis
Inhibits triglyceride storage in liver
Increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis
33
What does glucagon enhance?
enhances heart strength, increases blood flow in some tissues, enhances bile secretion, and inhibits gastric acid secretion
34
What is glucagon stimulated by? (5)
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
35
What is glucagon inhibited by? (5)
```
High glucose levels
Somatostatin
Free fatty acids
Ketones
Insulin
```
36
For carbohydrate metabolism, what is the anabolic (synthesis) phase?
postprandial (after a meal)
37
During the anabolic phase, when energy intake exceeds sugar requirements, what is energy stored as?
glycogen, structural proteins and fat
38
What is anabolic phase mediated by?
insulin
Release begins at 100mg/dl glucose, peaks at 4-600mg/dl
After eating, plasma insulin concentration increases almost 10-fold in 3-5 minutes due to dumping of preformed, stored insulin
Level decreases in 5-10 minutes
At 15 minutes, new insulin
plateau is reached due to more release and synthesis
Shut off is in 3-5 min after level under 80 mg/dl
39
For carbohydrate metabolism, what is the catabolic phase?
Fasting
40
During the catabolic phase, how are body needs met?
What is this mediated by?
endogenous (internal) sources
glucagon
41
T/F: During the catabolic phase of carbohydrate metabolism, there is a breakdown of glycogen, protein, triglyceride stores for energy supply: glucose, ketones.
TRUE
42
Can the brain function on glucose and ketones?
YES
43
How long is liver glycogen sufficient for the brain?
At what time does gluconeogenesis uses AAs, glycerol and lactate to make glucose?
12-24 hours
24 hrs
44
Amino acids from breakdown of muscle protein are a good source of _____ formation
glucose
Muscle wasting significant in first few days of fasting
Gluconeogenesis primarily in liver, some kidney
45
when fasting, days 2-4 Fat stores broken down to free fatty acids for tissues, some glucose, but primarily ____ for brain.
ketones
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
46
What is the greek word diabetes mean
What mellitus latin for?
to pass through, a siphon
honey sweet (Thomas Willis)
47
What is the definition of DM
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
48
T/F: DM is the most common endocrinopathy
TRUE
49
What is type 1 DM caused by?
caused by lack of insulin secretion
50
What is type 2 DM caused by?
caused by decreased sensitivity of target tissues to the metabolic effects of insulin (insulin resistance)
51
how does insulin insufficiency lead to hyperglycemia?
decreased cell entry, increased gluconeogenesis, and glucose release from the liver
52
Glucose is reabsorbed by the kidney until about
180gm/dl
53
*** What does hyperglycemia lead to?
Leads to osmotic diuresis, loss of Na, K, glucosuria
Hypovolemic hypotension, dehydration, POLYURIA, POLYDIPSIA, POLYPHAGIA (increased appetite from hypothalamus ventromedial nucleus)
54
Low insulin leads to _____ catabolism, increased ___ catabolism
muscle, fat
Increases the release of keto acids
causes an anion gap metabolic acidosis
55
CNS acute symptoms
Polyuria – osmotic diuresis
Polydipsia – intravascular volume depletion
Polyphagia and weight loss – protein catabolism
CNS irritability/confusion – hypertonic ECF leads to cell shrinkage
Visual disturbances
56
how do visual changes happen with diabetes
sorbitol formation in lens causes osmotic swelling, glycation leads to opacification
Microvascular disease affects perfusion of retina
Often present in 10-15 years
57
Chronic symptoms of diabetes
```
Infection
Macrovascular disease (CAD, PAD, AMI, CHF, CVA)
Microvascular disease (nephropathy, retinopathy, neuropathy)
```
58
How does type 1 DM happen?
Destruction of Beta islet cells results in loss of insulin release
(responds well to insulin, just doesn’t have enough)
59
What is DM1 caused by?
Caused by viral infections or autoimmune disorders
| Heredity plays a role in determining susceptibility of beta cells to insults
60
What is DM 2 caused by?
Caused by greatly diminished sensitivity of target tissues to metabolic effects of insulin
61
are high levels of Keto Acids present in type 2
not usually
62
which type of DM is more common
2
63
How are plasma insulin levels in DM2?
Plasma insulin is elevated in type II DM
Levels still insufficient for regulation, beta-cells become exhausted in some patients
64
T/F: most patients with DM are obese
true
65
Was was DM historically diagnosed?
glucose tolerance test
| look at side 24 is you want to read more about this
66
Hgb A1C reflects average glucose over
3 months (RBC life span)
67
What is a normal Hbg A1C
4-5.6%
(the chart shows less than 6.5% still in the okay range)
The higher the HgbA1C, the higher the risks of developing complications related to diabetes
68
Majority of diabetics develop secondary disease in one of more organ systems. what are they are increased risk of>
Increased risk of CAD, HTN, CHF, perioperative MI (often silent), CVA
69
Increased risk of cerebral vascular, peripheral vascular, renal vascular, and microvascular disease with DM patients, what do you need to consider Intraoperative?
increased risk of positioning injuries, autonomic neuropathy and hemodynamic instability, gastroparesis and pulmonary aspiration
joints will become stiff resulting in difficult intubation
70
hyperglycemia causes increased
```
CHF
18x mortality
2x length of stay
greatly increased risk of infection
sepsis
ARF
illness related neuropathy
Increased susceptibility to positioning injuries
CVA
poor fetal outcomes
```
(look at slide 28 for stats)
71
Perioperative stress may increase serum glucose concentrations (cortisol and catecholamine release). When should glucose be treated?
>200
72
When should diabetes be scheduled for surgery?
1st case in the day
73
should oral hypoglycemics be given?
No, Oral hypoglycemics are held day of surgery to prevent hypoglycemia until oral intake is restarted
74
T/F:Type I diabetics should continue basal insulin administration to avoid ketoacidosis
true
75
In ketoacidosis, DM1, there is profoundly low insulin levels and elevated regulatory hormones (glucagon, cortisol, GH, catechols) that do what?
that render insulin ineffective
76
Primary features of DKA
Dehydration, acidosis, electrolyte depletion
77
In DKA, 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
78
DKA leads to accelerated protein breakdown that leads to
increased liver gluconeogenesis, worsening hyperglycemia
79
DKA leads to Activation of _______ of fatty acids
B-oxidation
80
Symptoms of pts in DKA
Nausea/Vomiting, polyuria, polydipsia, polyphagia, anorexia, orthostatic changes, Kussmaul breathing, acetone halitosis
(Level of consciousness related to pts osmolality, not acidosis)
81
What are precipitating factors in DKA?
MI, trauma, etoh, infection, non-compliance
82
treatment for DKA
Massive fluid resuscitation, electrolyte replacement, insulin therapy
Will present with often severe hyperkalemia in face of total body K depletion
83
Nonketotic hypersomolar state
in type 2 diabetics
84
primary features of HHNK
Severe hyperglycemia, dehydration, severe hyperosmolar state (Na down 1.6/100 glucose) and lack of ketoacidosis
85
symptoms of HHNK
Thrombosis from hyperviscosity, focal neuro/reflex signs, global neuro signs, confusion, seizures, coma
86
treatment for HHNK
Fluid resuscitation
Add sugar to IVF when BG ~250 to avoid precipitous drop and cerebral edema
K+, phosphate, insulin if needed
87
equation for osmolarity
2[Na+] + [Glucose]/18 + [ BUN ]/2.8
88
Hypoglycemia symptoms
Profound effects on CNS (confusion, convulsions, coma)
89
hypoglycemia
Early
Late
Very late
Early - liver glycogen breakdown
Glucagon response less important early, becomes increasingly important progressively
Late - Sympathetic stimulation, epi release
Very late - GH and cortisol secreted
90
What is insulinoma and how do you treat it?
beta cell adenoma
Insulin shock: coma under 20mg/dl
Treat: glucose, (glucagon, epinephrine)
91
hypoglycemic shock happens in what range
20-50
92
in hypoglycemic shock, the brain uses glucose if available, what else can it use
can use fats/ketones with difficulty in times of stress
93
how to treat hypoglycemia
Treat with D50 + infusion of D5
94
Prolonged hypoglycemia leads to
brain cell death and apoptosis
