Pancreas Flashcards
(107 cards)
1
Q
Pancreatic Islet Cells (Islets of Langerhans)
A
90% Exocrine 10% Endocrine
2
Q
Insulin is produced by _______and facilitates
A
Produced by beta cells. Facilitates transport of glucose & K+ into cell.
3
Q
Normal adult production of insulin is
A
40 – 50 units / Day.
4
Q
Insulin is metabolized by
A
Liver and Kidney.
5
Q
Normal fasting glucose
A
70 – 100 mg/dL
6
Q
Diabetes
A
↓insulin production
↑ insulin resistance
7
Q
Hyperglycemia results in abnormal
A
metabolic effects and tissue/organ damage
8
Q
Why does Hyponatremia occurs with hyperglycemia ? It occurs as each
A
100 mg/dL increase in glucose = 1.6 mEq/L decrease in sodium (dilutional)
9
Q
What are Some tissues can transport glucose without insulin:
A
Neurons, Kidney, Retina, RBCs, Vascular endothelium
Damaged results from prolonged hyperglycemia.
10
Q
Diabetes Type 1a
A
T-cell mediated autoimmune destruction of beta cells.
11
Q
Diabetes Type 1b
A
Not immune mediated.
12
Q
10% of all cases.
IDDM
A
Type 1
13
Q
Acute onset in children and adolescents.
A
Type 1
14
Q
Previously “Juvenile Diabetes”.
A
Type 1
15
Q
Etiology unknown, genetic factors may play a role.
A
Type 1
16
Q
**Trick to remember short acting
A
Onset 30, peak 3, Duration 6
17
Q
***Trick to remember Intermediate acting (2x)
A
Onset 1 peak 6 duration 12
18
Q
***Trick to remember long acting (2x interm)
A
ONset 2, peak 12, Duration 24
19
Q
_____________ before hyperglycemia
occurs.
A
80-90% beta cell function lost before hyperglycemia
occurs.
20
Q
Type 1 Presentation is often
A
severe and sudden: Hyperglycemia occurs over days to weeks.
21
Q
Type I with Signs/Symptoms:
A
Fatigue Weight loss Polyuria Polydipsia Blurred vision Volume depletion Random Glucose >200 HbA1c >7%
22
Q
Type 1 DM 2 most important signs and symptos
A
Random Glucose >200
HbA1c >7%
23
Q
Type 2 DM Immune?
A
Not immune mediated.
24
Q
Type 2 DM results form
A
Results from insulin deficiency with receptor defect
25
90% of all cases.
Type II DM
26
Affects older age group.
Type II DM
27
Subtle presentation (4 – 7 yrs. before dx)
Type II DM
28
What are the 3 defects with NIDDM
3 defects:
↓ insulin
↑ hepatic glucose release
↑ insulin resistance
29
Non–insulin-dependent
Type 2
30
Oral hypoglycemic medications may be used.
Type 2
31
Type 2 DM caused by
Caused by decreased production of insulin
and/or increased resistance by body cells to
insulin
32
Commonly associated with obesity
Type 2
33
In type 2 “Beta cell burnout” –
compensatory hyperinsulinemia to maintain normoglycemia. Increasing incidence in teens and young
adults
34
Type 2 Component of Metabolic Syndrome
(aka insulin-resistance syndrome):
35
Metabolic syndrome At least 3 of the following:
```
Fasting glucose >110 mg/dL
Abdominal obesity (waist >40 m / 35 f)
Trigycerides => 150 mg/dL
HDL < 40 (m) / 50 (f)
BP => 130/85
```
36
***DM diagnostic Criteria
DM Diagnostic Criteria
• Fasting glucose > 100 mg/dL
∞ 101 – 125 = “impaired fasting glucose”
∞ 126+ = “clinical diabetes”
OR
∞ 2 hr. glucose >200 during glucose tolerance test
OR
∞ Random glucose >200 with symptoms of polyuria,
polydispsia, unexplained weight loss
∞ HbA1c > 6.5%
∞ Urine glucose poor indicator since renal glucose
threshold not reached until conc. >180 mg/dL
37
****Oral Hypoglycemics classes
Sulfonyureas
Biguaides
Thiazolidinediones
Alpha-Glucosidase inhibitors
38
***Sulfonyureas
Sulfonyureas (glimepiride)
| ↑ insulin secretion
39
****Biguanides
Biguanides (metformin)
| ↓ hepatic glucose release (& ↑ insulin sensitivity
40
***Thiazolidinediones (
rosiglitazone, pioglitazone)
| ↑ insulin sensitivity
41
***α-glucosidase inhibitors
(acarbose, miglitol)
| ↓ GI glucose absorption
42
Insulin and Hypoglycemia
Hypoglycemia: most frequent and dangerous complication of insulin therapy.
43
Adrenergic Warning Symptoms:
```
HTN
tachycardia
diaphoresis
palpitations,
restlessness,
pallor,
lacrimation
```
44
Neuroglycopenic Warning Symptoms:
Fatigue, confusion, HA, somnolence, convulsions, coma
45
Repetitive episodes result in Hypoglycemia
Unawareness (secondary to autonomic sympathectomy)
46
***Acute Complications of DM
* HYPOGLYCEMIA
| * DKA (Diabetic Ketoacidosis) •HHS (Hyperglycemic Hyperosmotic Syndrome)
47
Hypoglycemia glucose level
Glucose < 60
48
3 causes of hypoglycemia
Caused by medication, alcohol, exercise
49
***Hypoglycemia symptoms
```
Tachycardia
Palpitations
Diaphoresis
Tremors
Pallor
```
50
If hypoglycemia not corrected
If uncorrected, Neuroglycopenia occurs
51
***Signs and symptoms of Hypoglycemia Neuroglycopenia
```
HA
Dizziness
Irritability
Fatigue
Poor judgment
Confusion
Visual changes
Hunger
Seizures
Coma
```
52
****Hypoglycemia Treatment:
* Conscious pt. – 20g glucose (tablets or gel)
| * Unconscious pt. – 0.5 g/kg IV or glucagon 0.5 to 1 mg IV, IM, or SC
53
DKA Occurs more commonly in
Type 1
54
***DKA is associated with
Profound insulin deficiency = ↑ lipolysis and
| gluconeogenesis
55
***Pathophysiology : In DKA, Gluconeogenesis =>
↑ production of production of ketones ketones, permits strong organic acids to circulate freely. Bicarbonate buffering does not correct it. Metabolic acidosis develops.
56
***DKA Precipitated by
by infection or acute illness:(CVA, MI, acute pancreatitis)
57
***Symptoms: VADANK
```
Vomiting
Abdominal pain
Dehydration
Acetone odor on breath
Neurologic changes/stupor
Kussmaul respirations
```
58
***DKA Labs:
```
glucose > 250 mg/dL
pH < 7.3
Bicarb < 18
Osmolarity < 320
Hyponatremia
Presence of anion gap
Presence of serum & urine ketones
```
59
Electrolyte deficits of K+ and Phos. can
| lead to
diaphragmatic dysfunction and impaired myocardial contractility
60
DKA Treatment:
Large amounts of saline
Effective doses of insulin
Electrolytes
61
During DKA treatment Fluid and Na+ levels should be
monitored closely to avoid development of cerebral edema during correction
62
***HHS
Hyperglycemic Hyperosmolar Syndrome
63
“HHNKS”
hyperosmolar hyperglycemic nonketotic syndrome
64
HHS Characterized by:
↑ ↑ hyperglycemia
↑ ↑ hyperosmolarity
↑ ↑ Dehydration (more severe than in DKA)
65
In HHS , it Occurs more commonly in
Type 2 (60+ yrs) evolves over days-wks with ↑↑↑ glucosuric diuresis
66
In HHS No ketosis why?
ketosis - insulin levels are still high enough to
preclude lipolysis/ketosis.
Precipitated by dehydration and acute illness
67
***HHS Symptoms/Presentation:
```
Polyuria
Polydipsia
Hypovolemia
Hypotension
Tachycardia
Organ hypoperfusion
Neurologic changes/stupor/coma
```
68
***HHS Labs:
```
Glucose >600
Near-normal pH & Bicarb.
Osmolarity >320
Vascular occlusions may occur
(secondary to mesenteric artery thrombosis)
```
69
HHS Treatment:
Large amounts of saline
Effective doses of insulin
Electrolytes
70
In HHS treatment, If renal blood flow and GFR are not restored,
hyperglycemia will persist. (Normally perfused kidney will not permit extreme hyperglycemia)
71
***Chronic Complications of DM
```
Vascular Disease (CAD, PAD, PVD)
Nephropathy
Retinopathy
Neuropathy
Immune suppression
Glycosylated Hb & Collagen
```
72
Chronic Complications: Vascular Macrovascular
Cardiovascular
Cerebrovascular
Peripheral vascular disease
73
****Chronic Complications: Vascular Microvascular
Nephropathy
| Retinopathy
74
Macrovascular Complications
Poorly controlled pts develop Dyslipidemia:
↑ Triglycerides
↑ LDL
↓ HDL
75
Macrovascular complications Leads to
```
Atherosclerosis with increased tendency for thrombosis resulting in:
Cardiovascular (CAD)
HTN
Angina
MI
CHF
```
Cerebrovascular (PAD)
CVA
76
Oxidative Stress from
↑ ROS (reactive oxygen Species) also plays a
| roll in vessel damag
77
Macrovascular Complications PVD (arterial & venous)
```
May result in ulcers on lower extremities with:
Slow healing
Frequent infections
Gangrene
Amputation
```
78
Microvascular Complications
* Nephropathy
* Glomerulosclerosis develops with thickening of basement membrane over several years.
* Proteinuria (albuminuria) is earliest lab manifestation; w/ HTN and peripheral edema.
* Pt.s progress to renal failure within 3 – 5 yrs
79
Microvascular Complications Diabetic Retinopathy Caused by:
```
Occlusions
Microaneurysms
Hemorrhages
Exudates
Abnormal vessels
Fibrous tissue
```
80
Cotton wool spots
Diabetic retinopathy
81
Cataracts and hyperglycemia
Hyperglycemia also accelerates lens
degeneration leading to formation of
cataracts
82
****Neuropathy
↓ Sensory and motor) nerve conduction
| Distal symmetrical polyneuropathy most common
83
****In Neurpopathy Polyol Pathway (Sorbitol Pathway) causes
neuroedema
84
Neuropathy Deficits appear in
toes and feet, then progress proximally
85
***Neuropathy Results in loss of:
```
Light touch
Pain
proprioception
Temperature
Muscle weakness
Paresthesias
Neuropathic pain
```
86
Neuropathy
| Ulcers develop secondary to________results in
loss of sensation
•Impaired circulation (PVD)
•Autonomic dysfunction
• Charcot’s joint
87
Neuropathy Signs of autonomic neuropathy:
| LELIG
```
Lack of orthostatic changes in HR
Early satiety
Lack of sweating
Impotence
Gastroparesis (carries ↑ risk of aspiration
perioperatively)
```
88
Immune Suppression ; Infections
Common and often more severe in diabetics
| Infections in feet and legs caused by vascular and neurological impairment
89
Fungal infections common
| • Caused by
```
Candida
• In vagina and/or oral cavity
Urinary tract infections
Dental caries
Gingivitis and periodontitis
```
90
****Glycosylation
A process that normally involves reversible
| attachment of glucose to proteins, lipids and nucleic acids
91
****Glycosylation With persistent
hyperglycemia, glucose becomes irreversibly bound to collagen, decreasing elasticity.
92
***Glycosulation Can cause
“Stiff Joint Syndrome” which may affect cervical mobility leading to difficult intubation.
93
****Insulinoma is a
Insulin-secreting tumor of beta cells.
94
Insulinoma Manifest as
fasting hypoglycemia.
| 10% are malignant.
95
****Insulinoma associated
Profound hypoglycemia can occur with manipulation of tumor during surgical excision.
96
Insulinoma: Signs of hypoglycemia
* (HTN, tachycardia, diaphoresis) may be masked during anesthesia.
* Preop mgmt. is w/ Diazoxide, inhibits insulin release.
* Glucose should be included in IV fluids administered intra-op.
97
Anesthesia Considerations – pre-op
| Evaluation
Pre-op evaluation should emphasize cardiovascular, renal, neurologic and musculoskeletal joint mobility.
98
Anesthetic consideration: Labs should include
full electrolyte, urea and creatinine screen, CBC w/ diff, CXR, ECG.
99
Beta Blockers and ACEI
Beta blockers recommended if CAD present.
| ACE inhibitors for HTN if renal disease present.
100
Autonomic neuropathy predisposes pt. to peri-op.
dysrhythmias and intra-op. hypotension, gastroparesis with possible aspiration.
101
Anesthetics considerations
Morning dose of insulin should be held.
| IV with D5 ½ NS @100ml/hr. should be started pre-op
102
When to delay surgery
If glucose >270, delay surgery until corrected
| If glucose >400, postpone nonemergent surgery
103
Anesthesia Considerations – intra-op
| Aggressive
glycemic control necessary to minimize
| hyperglycemia and avoid hypoglycemia.
104
Anesthesia Considerations – intra-op glucose
Intra-op serum glucose s/b 120 – 180 mg/dL.
105
Typically, one Unit of insulin lowers glucose
25 mg/dL
106
Post-op hypoglycemia may be masked by
anesthetics, sedatives, analgesics, Beta-blockers, sympatholytics and autonomic neuropathy
107
Hypoglycemia Treatment:
50 mL of 50% dextrose (D50).
| Increases glucose 100 mg/dL.
