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SRNA3AdvancedPatho2 > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Pancreatic Islet Cells (Islets of Langerhans)

A

90% Exocrine 10% Endocrine

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2
Q

Insulin is produced by _______and facilitates

A

Produced by beta cells. Facilitates transport of glucose & K+ into cell.

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3
Q

Normal adult production of insulin is

A

40 – 50 units / Day.

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4
Q

Insulin is metabolized by

A

Liver and Kidney.

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5
Q

Normal fasting glucose

A

70 – 100 mg/dL

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6
Q

Diabetes

A

↓insulin production

↑ insulin resistance

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7
Q

Hyperglycemia results in abnormal

A

metabolic effects and tissue/organ damage

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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)

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9
Q

What are Some tissues can transport glucose without insulin:

A

Neurons, Kidney, Retina, RBCs, Vascular endothelium

Damaged results from prolonged hyperglycemia.

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10
Q

Diabetes Type 1a

A

T-cell mediated autoimmune destruction of beta cells.

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11
Q

Diabetes Type 1b

A

Not immune mediated.

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12
Q

10% of all cases.

IDDM

A

Type 1

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13
Q

Acute onset in children and adolescents.

A

Type 1

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14
Q

Previously “Juvenile Diabetes”.

A

Type 1

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15
Q

Etiology unknown, genetic factors may play a role.

A

Type 1

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16
Q

**Trick to remember short acting

A

Onset 30, peak 3, Duration 6

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17
Q

***Trick to remember Intermediate acting (2x)

A

Onset 1 peak 6 duration 12

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18
Q

***Trick to remember long acting (2x interm)

A

ONset 2, peak 12, Duration 24

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19
Q

_____________ before hyperglycemia

occurs.

A

80-90% beta cell function lost before hyperglycemia

occurs.

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20
Q

Type 1 Presentation is often

A

severe and sudden: Hyperglycemia occurs over days to weeks.

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21
Q

Type I with Signs/Symptoms:

A 
Fatigue
Weight loss
Polyuria
Polydipsia
Blurred vision
Volume depletion
Random Glucose >200
HbA1c >7%
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22
Q

Type 1 DM 2 most important signs and symptos

A

Random Glucose >200

HbA1c >7%

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23
Q

Type 2 DM Immune?

A

Not immune mediated.

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24
Q

Type 2 DM results form

A

Results from insulin deficiency with receptor defect

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25
Q

90% of all cases.

A

Type II DM

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26
Q

Affects older age group.

A

Type II DM

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27
Q

Subtle presentation (4 – 7 yrs. before dx)

A

Type II DM

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28
Q

What are the 3 defects with NIDDM

A

3 defects:
↓ insulin
↑ hepatic glucose release
↑ insulin resistance

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29
Q

Non–insulin-dependent

A

Type 2

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30
Q

Oral hypoglycemic medications may be used.

A

Type 2

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31
Q

Type 2 DM caused by

A

Caused by decreased production of insulin
and/or increased resistance by body cells to
insulin

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32
Q

Commonly associated with obesity

A

Type 2

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33
Q

In type 2 “Beta cell burnout” –

A

compensatory hyperinsulinemia to maintain normoglycemia. Increasing incidence in teens and young
adults

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34
Q

Type 2 Component of Metabolic Syndrome

A

(aka insulin-resistance syndrome):

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35
Q

Metabolic syndrome At least 3 of the following:

A 
Fasting glucose >110 mg/dL
 Abdominal obesity (waist >40 m / 35 f)
 Trigycerides => 150 mg/dL
 HDL < 40 (m) / 50 (f)
 BP => 130/85
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36
Q

***DM diagnostic Criteria

A

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

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37
Q

**Oral Hypoglycemics classes

A

Sulfonyureas
Biguaides
Thiazolidinediones
Alpha-Glucosidase inhibitors

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38
Q

***Sulfonyureas

A

Sulfonyureas (glimepiride)

↑ insulin secretion

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39
Q

**Biguanides

A

Biguanides (metformin)

↓ hepatic glucose release (& ↑ insulin sensitivity

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40
Q

***Thiazolidinediones (

A

rosiglitazone, pioglitazone)

↑ insulin sensitivity

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41
Q

***α-glucosidase inhibitors

A

(acarbose, miglitol)

↓ GI glucose absorption

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42
Q

Insulin and Hypoglycemia

A

Hypoglycemia: most frequent and dangerous complication of insulin therapy.

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43
Q

Adrenergic Warning Symptoms:

A 
HTN
tachycardia
diaphoresis
palpitations, 
restlessness,
pallor, 
lacrimation
44
Q

Neuroglycopenic Warning Symptoms:

A

Fatigue, confusion, HA, somnolence, convulsions, coma

45
Q

Repetitive episodes result in Hypoglycemia

A

Unawareness (secondary to autonomic sympathectomy)

46
Q

***Acute Complications of DM

A
  • HYPOGLYCEMIA

* DKA (Diabetic Ketoacidosis) •HHS (Hyperglycemic Hyperosmotic Syndrome)

47
Q

Hypoglycemia glucose level

A

Glucose < 60

48
Q

3 causes of hypoglycemia

A

Caused by medication, alcohol, exercise

49
Q

***Hypoglycemia symptoms

A 
Tachycardia
Palpitations
Diaphoresis
Tremors
Pallor
50
Q

If hypoglycemia not corrected

A

If uncorrected, Neuroglycopenia occurs

51
Q

***Signs and symptoms of Hypoglycemia Neuroglycopenia

A 
HA
Dizziness
Irritability
Fatigue
Poor judgment
Confusion
Visual changes
Hunger
Seizures
Coma
52
Q

**Hypoglycemia Treatment:

A
  • 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
Q

DKA Occurs more commonly in

A

Type 1

54
Q

***DKA is associated with

A

Profound insulin deficiency = ↑ lipolysis and

gluconeogenesis

55
Q

***Pathophysiology : In DKA, Gluconeogenesis =>

A

↑ production of production of ketones ketones, permits strong organic acids to circulate freely. Bicarbonate buffering does not correct it. Metabolic acidosis develops.

56
Q

***DKA Precipitated by

A

by infection or acute illness:(CVA, MI, acute pancreatitis)

57
Q

***Symptoms: VADANK

A 
Vomiting
Abdominal pain
Dehydration
Acetone odor on breath
Neurologic changes/stupor
Kussmaul respirations
58
Q

***DKA Labs:

A 
glucose > 250 mg/dL
pH < 7.3
Bicarb < 18
Osmolarity < 320
Hyponatremia
Presence of anion gap
Presence of serum &amp; urine ketones
59
Q

Electrolyte deficits of K+ and Phos. can

lead to

A

diaphragmatic dysfunction and impaired myocardial contractility

60
Q

DKA Treatment:

A

Large amounts of saline
Effective doses of insulin
Electrolytes

61
Q

During DKA treatment Fluid and Na+ levels should be

A

monitored closely to avoid development of cerebral edema during correction

62
Q

***HHS

A

Hyperglycemic Hyperosmolar Syndrome

63
Q

“HHNKS”

A

hyperosmolar hyperglycemic nonketotic syndrome

64
Q

HHS Characterized by:

A

↑ ↑ hyperglycemia
↑ ↑ hyperosmolarity
↑ ↑ Dehydration (more severe than in DKA)

65
Q

In HHS , it Occurs more commonly in

A

Type 2 (60+ yrs) evolves over days-wks with ↑↑↑ glucosuric diuresis

66
Q

In HHS No ketosis why?

A

ketosis - insulin levels are still high enough to
preclude lipolysis/ketosis.
Precipitated by dehydration and acute illness

67
Q

***HHS Symptoms/Presentation:

A 
Polyuria
Polydipsia
Hypovolemia
Hypotension
Tachycardia
Organ hypoperfusion
Neurologic changes/stupor/coma
68
Q

***HHS Labs:

A 
Glucose >600
Near-normal pH &amp; Bicarb.
Osmolarity >320
Vascular occlusions may occur
(secondary to mesenteric artery thrombosis)
69
Q

HHS Treatment:

A

Large amounts of saline
Effective doses of insulin
Electrolytes

70
Q

In HHS treatment, If renal blood flow and GFR are not restored,

A

hyperglycemia will persist. (Normally perfused kidney will not permit extreme hyperglycemia)

71
Q

***Chronic Complications of DM

A 
Vascular Disease (CAD, PAD, PVD)
 Nephropathy
 Retinopathy
 Neuropathy
 Immune suppression
 Glycosylated Hb &amp; Collagen
72
Q

Chronic Complications: Vascular Macrovascular

A

Cardiovascular
Cerebrovascular
Peripheral vascular disease

73
Q

**Chronic Complications: Vascular Microvascular

A

Nephropathy

Retinopathy

74
Q

Macrovascular Complications

A

Poorly controlled pts develop Dyslipidemia:
↑ Triglycerides
↑ LDL
↓ HDL

75
Q

Macrovascular complications Leads to

A 
Atherosclerosis with increased tendency for thrombosis resulting in:
Cardiovascular (CAD)
 HTN
 Angina
 MI
 CHF

Cerebrovascular (PAD)
CVA

76
Q

Oxidative Stress from

A

↑ ROS (reactive oxygen Species) also plays a

roll in vessel damag

77
Q

Macrovascular Complications PVD (arterial & venous)

A 
May result in ulcers on lower extremities with:
 Slow healing
 Frequent infections
 Gangrene
 Amputation
78
Q

Microvascular Complications

A
  • 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
Q

Microvascular Complications Diabetic Retinopathy Caused by:

A 
Occlusions
 Microaneurysms
 Hemorrhages
 Exudates
 Abnormal vessels
 Fibrous tissue
80
Q

Cotton wool spots

A

Diabetic retinopathy

81
Q

Cataracts and hyperglycemia

A

Hyperglycemia also accelerates lens
degeneration leading to formation of
cataracts

82
Q

**Neuropathy

A

↓ Sensory and motor) nerve conduction

Distal symmetrical polyneuropathy most common

83
Q

**In Neurpopathy Polyol Pathway (Sorbitol Pathway) causes

A

neuroedema

84
Q

Neuropathy Deficits appear in

A

toes and feet, then progress proximally

85
Q

***Neuropathy Results in loss of:

A 
Light touch
Pain
proprioception
Temperature
Muscle weakness
Paresthesias
Neuropathic pain
86
Q

Neuropathy

Ulcers develop secondary to________results in

A

loss of sensation
•Impaired circulation (PVD)
•Autonomic dysfunction
• Charcot’s joint

87
Q

Neuropathy Signs of autonomic neuropathy:

LELIG

A 
Lack of orthostatic changes in HR
Early satiety
Lack of sweating
Impotence
Gastroparesis (carries ↑ risk of aspiration
perioperatively)
88
Q

Immune Suppression ; Infections

A

Common and often more severe in diabetics

Infections in feet and legs caused by vascular and neurological impairment

89
Q

Fungal infections common

• Caused by

A 
Candida
• In vagina and/or oral cavity
 Urinary tract infections
 Dental caries
 Gingivitis and periodontitis
90
Q

**Glycosylation

A

A process that normally involves reversible

attachment of glucose to proteins, lipids and nucleic acids

91
Q

**Glycosylation With persistent

A

hyperglycemia, glucose becomes irreversibly bound to collagen, decreasing elasticity.

92
Q

***Glycosulation Can cause

A

“Stiff Joint Syndrome” which may affect cervical mobility leading to difficult intubation.

93
Q

**Insulinoma is a

A

Insulin-secreting tumor of beta cells.

94
Q

Insulinoma Manifest as

A

fasting hypoglycemia.

10% are malignant.

95
Q

**Insulinoma associated

A

Profound hypoglycemia can occur with manipulation of tumor during surgical excision.

96
Q

Insulinoma: Signs of hypoglycemia

A
  • (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
Q

Anesthesia Considerations – pre-op

Evaluation

A

Pre-op evaluation should emphasize cardiovascular, renal, neurologic and musculoskeletal joint mobility.

98
Q

Anesthetic consideration: Labs should include

A

full electrolyte, urea and creatinine screen, CBC w/ diff, CXR, ECG.

99
Q

Beta Blockers and ACEI

A

Beta blockers recommended if CAD present.

ACE inhibitors for HTN if renal disease present.

100
Q

Autonomic neuropathy predisposes pt. to peri-op.

A

dysrhythmias and intra-op. hypotension, gastroparesis with possible aspiration.

101
Q

Anesthetics considerations

A

Morning dose of insulin should be held.

IV with D5 ½ NS @100ml/hr. should be started pre-op

102
Q

When to delay surgery

A

If glucose >270, delay surgery until corrected

If glucose >400, postpone nonemergent surgery

103
Q

Anesthesia Considerations – intra-op

Aggressive

A

glycemic control necessary to minimize

hyperglycemia and avoid hypoglycemia.

104
Q

Anesthesia Considerations – intra-op glucose

A

Intra-op serum glucose s/b 120 – 180 mg/dL.

105
Q

Typically, one Unit of insulin lowers glucose

A

25 mg/dL

106
Q

Post-op hypoglycemia may be masked by

A

anesthetics, sedatives, analgesics, Beta-blockers, sympatholytics and autonomic neuropathy

107
Q

Hypoglycemia Treatment:

A

50 mL of 50% dextrose (D50).

Increases glucose 100 mg/dL.

SRNA3AdvancedPatho2 (15 decks)

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