Pancreas Flashcards
(136 cards)
1
Q
Pancreas characteristics
A
gladular organ with both digestive (exocrine) and endocrine function. It is about 6 inches longand rests behind the stomach
2
Q
Two major hormones the pancreas secretes
A
insulin and glucagon
3
Q
Islet of Langerhans - Alpha cells secrete ________
A
Gucagon
4
Q
Islet of Langerhans - Beta cells secrete _______
A
insulin
5
Q
Islet of Langerhans - Delta Cells secrete _________
A
somatostatin and pancreatic polypeptide
6
Q
Glands secreting digestive juices into the abdomen
A
acini
7
Q
Insulin is a hormone associated with _______ abundance and _______ or this excess energy
A
energy / storage
8
Q
Insulin causes carbohydrates to be stored as __________ in muscle and liver
A
glycogen
9
Q
Insulin causes fat storage in _______ tissue
A
adipose
10
Q
Excess carbohydrates that cannont be converted to ______ are converted to ______ and are stored in adipose tissue
A
glygcogen / fats
11
Q
_________ promotes upatake of amino acids and conversion to protein
A
insulin
12
Q
**Insulin is stimulated by what?
A
High blood glucose, amino acids, beta-keto acids, glucagon, acteylcholine, intestinal hormones, sulfonyurea drugs (glyburide), insulin resistance (obesity)
13
Q
**Insulin is inhibited by what?
A
Low blood glucose, Fasting, catecholamines (alpha-agonists), somatostatin
14
Q
Insulin circulates almost entirely _______ with plasma half-life of ___ min
A
unbound / 6 min
15
Q
_______ degrades unused insulin in liver, some degraded by kidney and muscles
A
insulinase
16
Q
Highly specific ______ leads to endocytosis
A
receptor
17
Q
Within seconds adipose and muscle cellls markedly _______ their _______ of glucose
A
increase / uptake
18
Q
Do neurons in the brain respond to insulin in the same way as muscles and other cells?
A
No, because neurons are permeable to glucose. Normal blood glucose is required to prevent hypoglycemic shock
19
Q
The cell membrane increases intake of amino acids, potassium and _____
A
phosphate
20
Q
Anabolic effects of inuslin is basically what?
A
storing glucose for later use
21
Q
Anabolic effects of insulin - Insulin ________ glycogenesis (glycogen is storage form of glucose)
A
increases
22
Q
Anabolics effects of insulin - Insulin _______ glycogenolysis
A
inhibits
23
Q
Insulin ________ gluconeogenesis
A
inhibits
24
Q
Inuslin ________ glucose (traps) for use in glycolysis, glycogenesis
A
phosphorylates
25
Insulin fascilitates entry of ________ into cells of all tissues except _______, _______, _____, _____
gluose / brain, kidney tubules, intestinal mucosa, and RBCs
26
Insulin ________ hepatic upatake, storage and use of glucose
increases
27
The liver releases glucose between ______
meals
28
Insulin increases ____ and protein ______ in the liver
lipogenesis / synthesis
29
Insulin increases protein synthesis by stimulating amino acid _________ and inhibits protein ________ and depresses ________
transport / catabolism / gluconeogenesis
30
Insulin will increase ______ synthesis and storage
fat
31
Insulin increases formation of glycerol and fatty acids and the resulting ___________
triglycerides
32
Insulin promotes transport of glucose as well as conversion of excess glucose into _____ _____
fatty acids
33
T/F Insulin inhibits lipolysis enzymes
TRUE
34
Insulin will increase protein _____ and ______
synthesis and storage
35
Insulin increases amino acid _____ as welll as glucose ______
uptake / entry
36
Normally cells only slightly permeable to glucose, what increases permeability and uptake
exercise and insulin
37
Inuslin can increase glycogenesis and protein synthesis which can be used for energy if _______
exercising
38
_______ is secreted by alpha cells of the islets of Langerhans when glood glucose levels FALL
glucagon
39
Glucagon has effects that _______ the effects of insulin
oppose
40
Glucagon increases blood glucose concentration and can cause _______
hyperglycemia
41
Glucagon has a catabolic effect, generally OPPOSES inuslin but stimulates ______ release
insulin
42
Activates enzymes for glycogenolysis
glucagon
43
Increases gluconeogenesis
glucagon
44
Increases lipolysis and ketogenesis which inhibits triglyceride storage in liver
glucagon
45
T/F Glucagon increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis
TRUE
46
Enhances heart strength, increase blood flow in some tissues, enhances bile secretion, and inhibits gastric acid secretion
glucagon
47
Glucagon is stimulated by
fasting hypoglycemia, amino acids (protein meal), Beta-adrenergic stimulation, exercise, cholecystokinin, gastrin, cortisol
48
T/F Exercise is not associated with hypoglycemia, but may be a response to increased circulating amino acids
TRUE
49
Glucagon is INHIBITED by
high glucose levels, somatostatin, free fatty acids, ketones, insulin
50
Carbohydrate metabolism Anabolic (synthesis) Phase: Postprandial -If energy intake exceeds usage requirements energy is stored as what?
glycogen, structural proteins and fat
51
Carbohydrate metabolism Anabolic (synthesis) Phase is mediated by _________. Release begins at 100 mg/dl glucose, peaks at 400-600 mg/dl.
insulin
52
After eating, plasma insulin concentration increases almost ___ fold in 3-5 minutes due to dumping of performed, stored insulin. Level decreases in 5-10 minutes
10
53
At 15 minutes postprandial, new insulin plateau is reached due to more ______ and _____
release and synthesis
54
Insulin is shut off in 3-5 min after level under ____ mg/dL
80 mg/dL
55
Carbohydrate metabolism: Catabolic phase (fasting) - Needs met only by ________(Internal) sources and is mediated by _______
endogenous / glucoagon
56
During the catabolic phase you have breakdown of glycogen, protein, triglyceride stores for energy supply which produces ____ and ____
glucose and ketones
57
T/F The brain can function on glucose and ketones
TRUE
58
Fasting 12-24 hrs
liver glycogen is sufficient for brain
59
Fasting >24 hrs
Gluconeogenesis uses amino acids, glycerol and lactate to make glucose
60
Amino acids from breakdown of muscle protein are a good source of _______ formation
glucose
61
______ _______ significant in first few days of fasting
muscle wasting
62
Gluconeogenesis is primarily in the ______ but also some happens in the _______
liver / kidney
63
Days 2-4 fasting: Fat stores broken down to free fatty acids for tissues, some glucose, but primarily _____ for the brain
ketones
64
Ketones are formed in the ______. At this point, most glucose used by CNS and protein loss is minimized by _____ loss. After weeks, brain uses primarily ______ which are measurable in the urine.
liver / fat / ketones
65
Diabetes greek meas what?
to pass through, a siphon
66
Diabetes is a disorder of __________ causing excessive thirst and the production of large quantities of ________
metabolism / urine
67
Mellitus is latin for
honey sweet
68
In diabetes insipidus the urine is dilute and has no _____. Whereas in mellitus the urine is _____
taste / sweet
69
Thomas Willis in 1675 added mellitus to the word diabetes to coin the term
diabets mellitus
70
DM is a syndrome of impaired carbohydrate, fat, and protein metabolism caused by what?
Either a lack of inuslin or a decreased sensitivity of the tissues to insulin
71
Type I DM
caused by lack of insulin secretion and is less prevalent
72
Type II DM
caused by a decreased sensitivity of target tissues to the metabolic effects of insulin (insulin resistance)
73
Insulin _______ leads to hyperglycemia from decreased cell entry, increased gluconeogenesis, and glucose release from the ________
insufficiency / liver
74
Glucose is reabsorbed by kidney until about ____ mg/dL. High blood glucose leads to _____ diuresis, loss of Na, loss of K, and glucosuria
180 / osmotic
75
T/ F High blood sugar can lead to hypovolemic hypotension, dehydration, POLYURIA, POLYDIPSIA, POLYPHAGIA
TRUE
76
Polyphagia is an increased appetite from _______
hypothalamus ventral nucleus
77
Low insulin leads to muscle ________ and increased fat _________
catabolism / catabolism
78
Low insulin increases the release of _____ acids which causes an ____ ____ metabolic acidosis
keto / anion gap
79
Diabetes acute symptoms
Polyuria, polydipsia, polyphagia
80
Polyuria results in
osmotic diuresis
81
Polydipsia occurs from
intravascular volume depletion
82
Polyphagia and weight loss occurs from
protein catabolism
83
CNS irritability/confusion in diabetes is related to _______ ECF that leads to cell ______
hypertonic / shrinkage
84
Visual disturbances from diabetes occurs from _____ formation in lens that causes osmotic swelling and glycation leads to opacification
sorbitol
85
Microvascular dz affects perfusion to ______, and this often is present in 10-15 years
retina
86
Chronic symptoms of DM
infection, macrovascular dz, microvascualr dz
87
Chronic symptoms of DM - Infection: Why are diabetics more prone to infection
decreased PMN phagocytosis
88
Chronic symptoms of DM - Why does macrovascular dz happen?
accelerated atherosclerosis / Think CAD, PAD, AMI, CHF, CVA
89
Chronic symptoms of DM - Microvascular dz: Nephropathy
1/3 of transplants, 50% develop CRF
90
Chronic symptoms of DM - Microvascular dz: Retinopathy
leading cause of blindess in US ages 20-65
91
Chronic symptoms of DM - Microvascular dz: Neuropathy
symmetric, sensory, stocking glove. Autonomic issues include orthostatic hypotension and delayed gastric emptying
92
Destruction of beta 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. Receptor and cellular mechanisms usually preserved
Type I DM
93
Caused by greatly diminished sensitivity of target tissues to metabolic effects of insulin. High levels of keto acids are not usually present. Far more common than Type I. Formerly known as adult onset DM but obese children can develop as well.
Type II DM
94
Plasma insulin is _______ in type II DM. However, levels still insufficient for regulation, beta-cells become ______ in some patients
elevated / exhausted
95
Most patients with Type II DM are ____
obese
96
Read slide 24
historical DM diagnosis
97
HgbA1c is used to diagnose ___ and how well it's managed
DM
98
Normal HgbA1C
4-5.6%
99
The higher the HgbA1C, the higher the risks of developing complications related to ____
diabetes
100
T/F DM patients are at increased risk of CAD, HTN, CHF, perioperative MI (often silent), CVA
TRUE
101
Increased risks with DM patients
increased risk for all of this: positioning injuries, autonomic neuropathy, hemodynamic instability, inability to compensate for changes in volume and vascular tone, post-induction hypotension and sudden death, gastroparesis, pulmonary aspiration, stiff joints (TMJ, AA, c-spine) resulting in difficulty with intubation
102
Hyperglycemia causes increased:
CHF, 18x mortality, 2x LOS, increased risk of infection, sepsis, ARF, illness related to neuropathy, positioning injuries, CVA, poor fetal outcomes
103
TKA infection rate for diabetics
7% infection / 12% wound complication / 15% UTI
104
CVA and abdominal ssurgery infection rate is 2.7x higher if BG >
200
105
Mortality for ICU patients with DM is at 8% if BG is between ____ and ___
180-200
106
3 Distinct effects of gluose control: Inhibits lipolysis and elevated FFAs which are associated with ______ ______
cardiac arrhythmias
107
3 Distinct effects of gluose control: Insulin inhibits ________ growth factors important in acute MI, and general inflammatory responses
inflammatory
108
3 Distinct effects of gluose control: Decreased insulin leads to _________, while insulin infusions lead to favorable alterations in myocardial and skeletal muscle metabolism
proteolysis
109
Perioperative stress may increase serum glucose concentrations due to _____ and _____ release
cortisol and catecholamine
110
BS greater than _______ should be treated
200
111
Perioperative glucose control guidelines
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 admnistration to avoid ketoacidosis. Patients on insulin pumps may be managed by continuing pump for short operations or changing over to IV insulin infusions.
112
DKA can happen in Type I diabetics with profoundly low ____ levels. Elevated counterregulatory hormones (glucagon, cortisol, GH, catechols) render insulin _______
insulin / ineffective
113
Primary features of DKA
dehydration, acidosis, electrolyte depletion
114
In DKA, blood glucose rises without effective insulin leading to _____ diuresis and ______ losses
osmotic / electrolyte
115
Dehydration in DKA can result in ___ to __ L fluid loss and loss of up to ____ body K+
4-6 / 10%
116
T/F In DKA, accelerated protein breakdown leads to liver gluconeogenesis which worsens hyperglycemia
TRUE
117
Activation of B-oxidation of fatty acids in DKA leads to what?
ketogenesis results, which overwhelms body's buffer and results in ketoacidosis
118
DKA symptoms
N/V, polyuria, polydipsia, polyphagia, anorexia, orthostatic changes, Kussmaul breathing, acetone, halitosis, altered LOC
119
T/F LOC in DKA is related to patient's OSMOLALITY not ACIDOSIS
TRUE
120
Precipitating events for DKA
MI, Trauma, infectioin, non-compliance
121
Treatment for DKA
Massive fluid resuscitation, electrolyte replacement, insulin therapy
122
T/F DKA will often present with severe hyperkalemia in face of total body K depletion
TRUE
123
Mortality for DKA
3-10%
124
Nonketotic hyperosmolar state has same precipitating events as _____ with a very high _____
DKA / blood glucose
125
Primary features of Nonketotic Hyperosmolar State
severe hyperglycemia, dehydration, severe hyperosmolar state and lack of ketoacidosis
126
Symptoms of Nonketotic hyperosmolar state
thrombosis from hyperviscosity, focal neuro/reflex signs, global neuro signs, confusion, seizures, coma
127
Treatment for Nonketotic hyperosmolar state
fluid resuscitation. Dextrose should be added to IVF when BG is 250 to avoid precipitous drop and cerebral edema. Provide K+, phos and insulin if needed.
128
Mortality for nonketotic hyperosmolar state
10-20%
129
Osmolarity formula
2[Na] + Glucose/18 + [BUN]/2.8
130
Hypoglycemia (inuslin excess) has profound CNS effects including
confusion, convulsions, coma
131
Early response to hypoglycemia is liver ______ breakdown. The ________ response is less important early and becomes increasingly important progressively
glycogen / glucagon
132
Late response to hypolglycemia is sympathetic stimulation with _______ release
epi
133
Very late response to hypoglycemia is ____ and ______ are secreted
GH and cortisol
134
An insulinoma is a _____ cell adenoma. This can result in insulin shock (coma under 20 mg/dL). This is treated with ______
beta / glucose, glucagon, epi
135
Hypoglycemic chock develops in range of __ to ___. It is characterized by progressive nervous irritiability that leads to fainting, seizures and coma. Brain uses only glucose available but can use fats/ketones with difficulty in times of stress. Treat hypoglycemic shock with _____.
20-50 / D50 + infusion of D5
136
Prolonged hypoglycemia leads to brain cell ___ and ____
death and apoptosis
