endocrine Flashcards

1
Q

pancreas structure and function

A

Has both endocrine and exocrine functions
Endocrine: secretes hormones such as insulin, glucagon, somatostatin and pancreatic polypeptide
Exocrine: acinar cells secret enzymes and networks of ducts that secret alkaline fluids important for digestive functions

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2
Q

exocrine digestive functions

A

Aqueous secretions contain potassium, sodium, bicarbonate and chloride
Alkaline pancreatic juice neutralizes the acidic chime that enters the duodenum from the stomach and provides the medium for actions of digestive enzymes and intestinal absorption of fat.
Pancreatic enzymes hydrolyze proteins (proteases), carbohydrates (amylases), and fats (lipases)
Secretion of pancreatic juice is controlled by hormonal and vagal stimuli
Secretin stimulates the acinar and duct cells to secrete the bicarbonate rich fluid that neutralizes chime and prepares for digestion
Enzymatic secretion follows and stimulated by cholecystokinin and acetylcholine

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3
Q

acute pancreatitis risk factors

A

Risk factors include: obstructive biliary tract disease (particularly cholelithiasis), alcoholism, obesity, peptic ulcers, trauma, hyperlipidemia, hypercalcemia, smoking, certain drugs and genetic factors

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4
Q

acute pancreatitis patho

A

Usually mild but can lead to necrotizing or hemorrhagic
Develops due to an obstruction of the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction (i.e.: gallstones)
Leads to autodigestion of pancreatic cells  vascular damage, coagulation necrosis, fat necrosis and edema
ETOH  acinar cell metabolizes ethanol with toxic metabolites which in turn injure pancreatic acinar cells, causing a release of activated enzymes
Chronic ETOH use causes formation of protein plugs in pancreatic ducts and spasm of the sphincter of Oddi, resulting in obstruction release of activated enzymes, inflammation and pancreatitis
Severe acute pancreatitis, proinflammatory cytokines activate leukocytes, cause injury the vessel walls and abnormal coagulation in the lungs and kidneys paralytic ileus and GIB can occur bacteria in the bloodstream may cause peritonitis or sepsis vasoactive peptides cause vasodilation, hypotension, and shock ARDS, renal failure and Systemic inflammatory Response syndrome (SIRS) EMERGENCY!

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5
Q

acute pancreatitis clinical manifestations

A

Mid-epigastric or LUQ pain, nausea and vomiting (paralytic ileus), jaundice, fever and leukocytosis, abdominal distention, hypovolemia, hypotension, tachycardia, myocardial insufficiency and shock.
Severe acute pancreatitis tachypnea and hypoxemia due to pulmonary edema, atelectasis or pleural effusions, hypovolemia, renal failure (ATN), tetany due to hypocalemia, transient hyperglycemia, multi-system organ failure

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6
Q

nursing assessment of acute pancreatitis

A

I-PAP
GI Assessment: bowel sounds, distention, nausea and vomiting, guarding
Respiratory
Cardiovascular
Renal
Hyperlipidemia, hyperglycemia, hypocalcemia
Lab Values: Lipase and Amylase (may be 3x normal), WBC, Bilirubin, Sodium, Potassium, Creatinine, BUN, Lipids (TC, TG, HDL, LDL), Calcium, Troponin, ABG’s

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7
Q

diagnosing 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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8
Q

types of diabetes

A

Type 1
Type 2
Other
Gestational

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9
Q

type 1 diabetes

A

encompasses diabetes that is primarily a result of pancreatic beta cell destruction with consequent insulin deficiency, which is prone to ketoacidosis. This form includes cases due to an autoimmune process and those for which the etiology of beta cell destruction is unknown.
∗ Includes latent autoimmune diabetes in adults (LADA); the term used to describe the small number of people with apparent type 2 diabetes who appear to have immune-mediated loss of pancreatic beta cells

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10
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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11
Q

gestational diabetes

A

refers to glucose intolerance with onset or first recognition during pregnancy.

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12
Q

other diabetes

A

specific types include a wide variety of relatively uncommon conditions, primarily specific genetically defined forms of diabetes or diabetes associated with other diseases or drug use (see Appendix 2. Etiologic Classification of Diabetes Mellitus).

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13
Q

type 1 vs type 2 diabetes

A

type 1
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
type 2
Pancreas does not produce enough insulin or insulin resistance
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

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14
Q

other types of diabetes vs gestational

A

other
Genetic defects of beta-cell function
Genetic defects in 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
gestational
Insulin resistance combined with inadequate insulin secretion in relation to hyperglycemia
Women who are obese, older than 25 yrs old, family hx of DM, history of previous GDM, or of certain ethnic groups (Hispanic, First Nations, Asian, or African American) increased risk of developing GDM
Metabolic stress of pregnancy may uncover tendency for T2DM

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15
Q

etiology of type 1 diabetes

A
10% of patients with diabetes
Diagnosed in childhood, adolescence, early adulthood
absolute lack of insulin
Autoimmune
genetic(HLA) plus environmental trigger  autoimmune response - destruction of  cells
years / seasonal
Idiopathic
 cell destruction without markers
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16
Q

etiology of type 2 diabetes

A
Accounts for 90% DM
 2004: 1:4 Canadians >45 yrs
genetic
metabolic syndrome
Insulin Receptor Substrate proteins -  young adults
Sedentary lifestyle, visceral obesity

Preventable

17
Q

etiology of gestational diabetes

A
Affects 1-2%
24-28 wks gestation placental hormones cause insulin resistance
50g oral glucose screen
C-section
disappears in 97% postpartum
20-50% develop type 2
Offspring ↑risk DM & obesity
Neonate:
macrosomia,  hypoglycemia, hypocalcemia, 
...polycythemia, hyperbilirubinemia
18
Q

macrovascular complications of diabetes

A
Cardiac ischemia
CAD/ACS
Angina
MI
Peripheral Arterial Disease
Cerebrovascular/Carotid Disease
TIA
Stroke
19
Q

microvascular complications of diabetes

A

Retinopathy
Neuropathy
Nephropathy
CKD

20
Q

hypoglycemia

A

Development of autonomic or neuroglycopenic symptoms
Low plasma glucose level (< 4.0 mmol/L for patients treated with insulin or an insulin secretagogue)
Symptoms responding to the administration of carbohydrate

21
Q

complications of hypoglycemia

A

Prolonged coma associated with paresis, convulsions and encephalopathy
Mild intellectual impairment
Recurrent hypoglycemia impairs the individuals ability to sense hypoglycemia

22
Q

neurogenic (autonomic) symptoms of hypoglycemia

A
Trembling
Palpitations
Sweating
Anxiety
Hunger
Nausea
Tingling
23
Q

neuroglycopenic symptoms of hypoglycemia

A
Difficulty concentrating
Confusion
Weakness
Drowsiness
Vision changes
Difficulty speaking
Headache
Dizziness
24
Q

mild severity of hypoglycemia

A

Autonomic symptoms are present

The individual is able to self-treat

25
Q

moderate severity of hypoglycemia

A

Autonomic and neuroglycopenic symptoms are present

The individual is able to self-treat

26
Q

severe severity of hypoglycemia

A

Individual requires assistance of another person
Unconsciousness may occur
Plasma Glucose is typically < 2.8 mmol/L

27
Q

diabetic ketoacidosis

A

Hyperglycemia
Gluconeogenesis
Glycogenolysis
use of Glucose by the Liver, Muscle and Fat
Serum Glucose Concentration may be > 27.8 mmol/L to 44 mmol/L
Anion Gap with Metabolic Acidosis
Ketonemia

Develops within 1-24 hours

28
Q

clinical presentation of DKA

A
Dehydration
Hypotension or shock (systolic < 90 mmHg)
Tachycardia (HR > 125 b/min)
Kussmaul respiration / tachypnea
Fruity breath
Altered level of mental status
Signs of precipitating cause
Dry mouth and thirst
Weakness, dehydration, nausea or vomiting
29
Q

everything else to look at for DKA

A
Glucose
CBC with differential
Electrolytes to calculate anion gap
Serum creatinine
Venous (NOT arterial) blood gas for pH
Urine for glucose and ketone bodies
30
Q

other considerations for DKA

A
Airway Management
Cerebral Edema
Increase incidence of thrombotic events
Anticoagulation
Phosphate
Magnesium
31
Q

hyperglycemia hyperosmolar state

A
Hyperglycemia
Serum glucose concentration > 56 mmol/L
Endogenous insulin present but not effective
Severe dehydration
Hyperosmolarity
Leads to neurologic abnormalities coma

Little to no ketosis present
More common in elderly
Develops over Days*

32
Q

metabolic priorities to be addressed in the management of adults presenting with hyperglycemic emergencies

A

ECFV contraction
Potassium deficit and abnormal concentration
Metabolic acidosis
Hyperosmolality (water deficit leading to increased corrected sodium concentration plus hyperglycemia)

33
Q

precipitating cause of DKA and HHS

A
New diagnosis of diabetes
Insulin omission
Infection
Myocardial infarction
Stroke
ECG changes may reflect hyperkalemia
A small increase in troponin may occur without overt ischemia
Thyrotoxicosis
Trauma
Drugs
34
Q

other complications of DKA and HHS

A
Hyper/hypokalemia
ECFV overexpansion
Cerebral edema
Hypoglycemia
Pulmonary emboli
Aspiration
Hypocalcemia (if phosphate used)
Stroke
Acute renal failure
Deep vein thrombosis