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CV487 > Class 8: Endocrine > Flashcards

Class 8: Endocrine Flashcards

1
Q

Pancreas endocrine functions

A

Secretes insulin, glucagon, somatostatin & pancreatic polypeptides

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2
Q

Pancreas exocrine functions

A

Acinar cells secrete enzymes and alkaline fluids; important for digestive functions

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3
Q

Aqueous secretions + exocrine functions of the pancreas

A

Contain K+, Na+, bicarb & Cl-

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4
Q

Alkaline pancreation juice + pancreas exocrine functions

A

-Neutralizes acid in duodenum and provides the medium for actions of digestive enzymes and intestinal absorption of fat
-Secretion of pancreatic juice is controlled by hormonal and vagal stimuli

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5
Q

Pancreatic enzymes + pancreas exocrine functions

A

Hydrolyze proteins, carbohydrates (amylases) and fats

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6
Q

After pancreatic juice is released…

A

Cholecystokinin and acetylcholin stimulates enzymatic secretion

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7
Q

Risk factors of acute pancreatitis

A

Alcoholism , obstructive biliary tract disease (cholelithiasis), obesity, peptic ulcers, trauma, hyperlipidemia, hypercalcemia, smoking, certain drugs & genetic factors

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8
Q

Pathophysiology of acute pancreatitis + obstruction

A

-Mild but can lead to necrosis or hemorrhaging
-Outflow of pancreatic digestive enzymes is obstructed in the bile and pancreatic duct which…
-Leads to autodigestion of pancreatic cells resulting in vascular damage, coagulation & fat necrosis and edema

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9
Q

Pathophysiology of acute pancreatitis + ETOH

A

ETOH; acinar cell metabolizes ethanol with toxic metabolites which injures them resulting in the release of activated enzymes

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10
Q

Pathophysiology of acute pancreatitis + chronic ETOH

A

Causes formation of protein plugs in the pancreatic ducts and spasms of the sphincter of Oddi which leads to an obstruction. Activated enzymes are released causing inflammation & pancreatitis

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11
Q

Severe acute pancreatitis pathophysiology

A

-Inflammation injures vessel walls and causes abnormal coagulation in the lungs & kidneys; paralytic ileus and GIB can occur; bacteria in the bloodstream may cause peritonitis or sepsis; vasoactive peptides are released; ARDS, renal failure and systemic inflammatory response syndrome (SIRS); EMERGENCY!

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12
Q

Clinical manifestations of acute pancreatitis

A

Mid-epigastric or LUQ pain, N/V (paralytic ileus), distention, jaundice, fever, leukocytosis, hypovolemia (hypotension), tachycardia, myocardial insufficiency & shock

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13
Q

Clinical manifestations of severe acute pancreatitis

A

Tachypnea and hypoxemia d/t pulmonary edema, atelectasis or pleural effusions, hypovolemia, renal failure (ATN), tetany due to hypocalemia, transient hyperglycemia, multi-system organ failure

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14
Q

Nursing assessment of acute pancreatitis

A

-GI: Distention, N/V & guarding
-Hyperlipidemia, hyperglycemia & hypocalcemia

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15
Q

Acute pancreatitis pertinent lab values

A

-Lipase & amylase (may be 3x normal)
-WBC, bilirubin, trops & ABG
-Na+, K+, Cr, Ca+ BUN, & lipids (TC, TG, HDL, LDL)

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16
Q

Diagnosing diabetes & prediabetes

A

Prediabetes is the presence of an impaired fasting glucose and/or impaired glucose tolerance on two separate testing occasions

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17
Q

Types of DM

A

-Type 1&2, gestational & other

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18
Q

Classification of type 1 diabetes

A

-Primarily a result of pancreatic beta cell destruction resulting in vulnerability to DKA
-Includes the result of autoimmune processes (ie. LADA) and those for which the etiology of beta cell destruction is unknown

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19
Q

Latent autoimmune diabetes in adults (LADA)

A

People with apparent type 2 diabetes who appear to have immune-mediated loss of pancreatic beta cells

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20
Q

Type 2 diabetes

A

-May range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance
-Ketosis is not as common

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21
Q

Gestational diabetes

A

-Glucose intolerance associated w pregnancy

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22
Q

Other diabetes

A

Specific types include uncommon conditions, primarily specific genetically defined forms of diabetes or diabetes associated with other diseases or drug use

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23
Q

About type 1 diabetes

A

-Pancreas does not produce any insulin
-Complete loss of beta cell function
-Unknown etiology but may be autoimmune or idiopathic
-Requires exogenous insulin
-Occurs in 10% of population

24
Q

About type 2 diabetes

A

-Pancreas does not produce enough insulin or is insulin resistant
-Usually diagnosed as an adult but more children are being diagnosed
-Progressive loss of beta cell function as the patient gets older
-Occurs in 90% of population

25
Q

About other specific types of diabetes

A

-Genetic defects of beta-cell function or of insulin action
-Diseases of exocrine pancreas
-Endocrinopathies
-Drug-or-chemical-induced beta cell dysfunction
-Infections
-Uncommon forms of immune-mediated DM
-Other genetic syndromes associated with DM

26
Q

About gestational diabetes

A

-Insulin resistance combined with inadequate insulin secretion in relation to hyperglycemia
-Metabolic stress of pregnancy may uncover tendency for T2DM

27
Q

Those at risk for gestational diabetes

A

Women who are obese, older than 25 yrs old, family hx of DM, history of previous GDM, or of certain ethnic groups (Hispanic, Indigenous, Asian, or African American) increased risk of developing GDM

28
Q

About type 1 diabetes

A

-10% of patients with diabetes
-Diagnosed in childhood, adolescence & early adulthood
-Absolute lack of insulin

29
Q

Autoimmune etiology of diabetes type 1

A

-Genetic (HLA) plus environmental trigger; autoimmune response; destruction of beta cells
-Years/seasonal

30
Q

Idiopathic etiology of diabetes type 1

A

Beta cell destruction without markers

31
Q

About type 2 diabetes

A

-Accounts for 90% of people with DM

32
Q

Etiology of type 2 diabetes

A

-Genetic
-Metabolic syndrome
-Insulin receptor substrate proteins - young adults
-Sedentary lifestyle, visceral obesity

33
Q

Type 2 diabetes is…

A

Preventable

34
Q

About gestational diabetes

A

-Affects 1-2% of pregnancies
-At 24-28 wks gestation placental hormones cause insulin resistance
-50g oral glucose screen
-C-section
-Disappears in 97% postpartum
-20-50% develop type 2 diabetes
-Offspring are at an ↑risk for DM & obesity

35
Q

Gestational diabetes + neonate

A

-Macrosomia, hypoglycemia & hypocalcemia lead to
-…polycythemia & hyperbilirubinemia

36
Q

Macrovascular complications of diabetes

A

-Cardiac ischemia: CAD/ACS, angina & MI
-PAD
-Cerebrovascular/carotid disease: TIA & stroke

37
Q

Microvascular compications of diabetes

A

-Retinopathy, neuropathy & nephropathy (CKD)

38
Q

Definition of hypoglycemia

A

-Development of autonomic or neuroglycopenic symptoms
-< 4.0 mmol/L for patients treated with insulin or an insulin secretagogue
-Symptoms responding to the administration of carbohydrate

39
Q

Complications of hypoglycemia

A

-Prolonged coma associated with paresis, convulsions & encephalopathy
-Intellectual impairment
-Recurrent hypoglycemia impairs the individuals ability to sense hypoglycemia

40
Q

Neurogenic symptoms of hypoglycemia

A

-Trembling, palpitations, tingling, sweating & anxiety
-Hunger & nausea

41
Q

Neuroglycopenic symptoms of hypoglycemia

A

-Difficulty concentrating, confusion, weakness, drowsiness, dizziness & headache
-Brain related
-aVision & speech

42
Q

Mild severity of hypoglycemia

A

-Autonomic symptoms are present
-The individual is able to self-treat

43
Q

Moderate symptoms of hypoglycemia

A

-Autonomic and neuroglycopenic symptoms are present
-The individual is still able to self-treat

44
Q

Severe symptoms of hypoglycemia

A

-Individual requires assistance of another person
-Loss of consciousness
-BG < 2.8 mmol/L

45
Q

DKA

A

-Hyperglycemia: Gluconeogenesis, glycogenolysis & use of glucose by the liver, muscle & fat
-BG may range from 27.8-44mmol/L
-Anion gap with metabolic acidosis
-Ketonemia
-Develops within 24-48 hours

46
Q

Contributing factors to DKA

A

-Insulin deficiency, dehydration, fasting/starvation & excess cortisol

47
Q

Clinical manifestations of DKA

A

-Dehydration, hypotension (systolic < 90 mmHg), tachycardia (HR > 125)
-Kussmaul respiration / tachypnea, fruity breath
-aMental status, weakness & N/V

48
Q

S&S of hyperglycemia in DKA

A

-Polyuria, polydipsia, weakness & ECF volume contraction

49
Q

S&S of acidosis in DKA

A

-Air hunger, N/V, abdominal pain, aSensorium & precipitating condition

50
Q

S&S of precipitating condition in DKA

A

List on link in slide 31

51
Q

What to monitor for in DKA

A

-Glucose, CBC differential, Cr, venous (NOT ARTERIAL) blood gas for pH
-Electrolytes to calculate anion gap
-Urinalysis for glucose and ketone bodies

52
Q

Nursing considerations for DKA

A

-Airway management, cerebral edema
-Increase incidence of thrombotic events
-Anticoagulation, phosphate & magnesium

53
Q

Hyperglycemia hyperosmolar state (HHS)

A

-Hyperglycemia (>56mmol/L), endogenous insulin is present but not effective
-Severe dehydration
-Hyperosmolarity leads to aLOC
-Decreased/absent ketones
-More common in elderly with type 2 DM
-Develops over days

54
Q

Slide 35

A
55
Q

Hyperglycemia causes…

A

Gluconeogenesis & glycogenolysis

56
Q

DKA is more common in…

A

Type I diabetes

CV487 (15 decks)

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