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NURS 316A > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Where is insulin created?

A

beta cells of the islets of Langerhans in the pancreas

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2
Q

When is insulin released?

A

when levels of blood glucose rise

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3
Q

What are the 3 functions of insulin?

A
  1. stimulation of glycogen synthesis
  2. conversion of lipids into fats to be stored as adipose tissue
  3. synthesis of proteins from amino acids
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4
Q

What is the range of normal fasting blood glucose?

A

70 - 100 mg/dL

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5
Q

What is hypoglycemia?

A
  • blood glucose < 70 mg/dL
  • affects brain function
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6
Q

What is hyperglycemia?

A

blood glucose > 200 mg/dL

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7
Q

What is prediabetes?

A
  • fasting blood glucose = 100 - 125 mg/dL
  • impaired glucose tolerance (IGT)
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8
Q

What is the fasting blood glucose range for diabetes? What is the postprandial blood glucose for diabetes?

A
  • fasting = 126+ mg/dL
  • postprandial = 200+ mg/dL
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9
Q

What is postprandial blood glucose?

A

blood glucose after eating

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10
Q

What is an oral glucose tolerance test (OGTT)?

A

measurement of blood glucose after about 1 hour of ingestion of 75 g of glucose; usually done for pregnant women to test for gestational diabetes

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11
Q

What is A1c? How can A1c be used to determine diabetes?

A

– A1c = glycated hemoglobin

  • diagnoses diabetes by assessing blood glucose levels over the past 3 months
  • < 5.7% = normal
  • 5.7 - 6.4% = pre-diabetes
  • > 6.5% = diabetes

– when paired with a fasting blood glucose test on the same day, can determine diabetes diagnosis:

  • if values for both are in diabetic range, confirmed DM diagnosis
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12
Q

What is DKA?

A

– diabetic ketoacidosis

  • critical condition requiring immediate treatment
  • develops in pts with no insulin reserves
  • results in ketone production from the breakdown of fats for energy in the place of glucose
  • results from hyperglycemia (lack of insulin) and ketosis
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13
Q

What are signs and symptoms of DKA?

A
  • BG > 250 mg/dL
  • pH < 7.3
  • rapid onset
  • low mortality rate
  • occurs commonly in DM1 pts
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14
Q

How common is DKA in DM children?

A

1/3 of DM1 children first present with DKA

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15
Q

What is the pathology of DM1?

A

T-cells attack beta cells of the pancreas (autoimmune disorder)

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16
Q

What are the common symptoms of DM1?

A
  • DKA – usually presenting sign
  • polyuria
  • polydipsia
  • polyphagia
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17
Q

What is hyperosmolar-hyperglycemic syndrome (HHS)?

A

– caused by hyperglycemia (lack of insulin) and dehydration

  • hyperglycemia
    • lack of insulin
    • gluconeogenesis in response to lack of insulin
    • glycogenolysis in response to lack of insulin
  • hyperosmolarity
    • osmotic diuresis from high blood glucose
    • polyuria
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18
Q

How quickly does HHS develop when compared with DKA?

A

HHS develops over days to weeks; DKA develops within hours

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19
Q

What are the symptoms of HHS?

A
  • weakness
  • poor tissue turgor
  • tachycardia
  • rapid, thready pulse
  • confusion
  • polyuria
  • polydipsia
  • coma – 25% of pts present with this
  • gradual onset
  • BG > 600 mg/dL
  • pH > 7.3
  • high mortality rate
  • occurs rarely in DM2 pts
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20
Q

What are some causes of HHS?

A
  • infection (pneumonia, sepsis)
  • noncompliance with DM medication
  • substance abuse
  • coexisiting diseases
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21
Q

Who typically gets HHS?

A

DM2 pts

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22
Q

What are some treatments of HHS?

A
  • FIE
    • fluids
    • insulin
      • if insulin is replaced before fluids, ECF water will move into ICF
      • will worsen hypotension and could lead to shock
    • electrolyte replacement
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23
Q

What is the Somogyi effect?

A

– morning hyperglycemia due to:

  • excessive insulin therapy or insulin peak during sleep causing hypoglycemia
  • compensatory mechanisms raise blood glucose by morning (rebound hyperglycemia)
    • epinephrine, norepinephrine, cortisol, glucagon, etc. increase blood glucose levels

– it is essentially hyperglycemia in response to hypoglycemia

– occurs more commonly in DM1 pts

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24
Q

What should DM pts do to prevent the Somogyi effect?

A
  • adjust insulin amounts as needed
    • decrease dose
    • take earlier
  • take snack with evening dose
  • avoid eating carbohydrates at night
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25
Q

What can cause hypoglycemia in DM pts?

A
  • excessice exogenous insulin
  • inadequate food intake
  • excessive physical activity
  • infection
  • illness
  • drug interaction
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26
Q

What are the compensatory mechanisms that counteract hypoglycemia?

A
  • epinephrine
  • glucagon
  • activation of SNS
    • epinephrine
    • norepinephrine
    • cortisol
    • ^these all work to raise BG levels
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27
Q

What are some signs and symptoms of hypoglycemia?

A
  • sweating
  • hunger
  • dizziness
  • headache
  • heart palpitations
  • confusion
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28
Q

How do DM pts address hypoglycemia?

A
  • eat fast-acting carbohydrates
  • avoid fats – delay glucose absorption
  • transient response – providing a meal or snack if blood glucose is greater than 70 mg/dL to prevent hypoglycemia
  • avoid foods and drugs that cause hypoglycemia:
    • alcohol
    • beta-blockers
    • aspirin
    • herbs
    • ACE-inhibitors
    • sulfonylureas
  • 50% dextrose IV
  • glucagon subq
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29
Q

What are 4 conventional insulin medications? What are their effects?

A
  1. regular – rapid acting, short duration
  2. NPH – intermediate acting, longer duration
  3. Lente – intermediate acting, longer duration
  4. Ultra Lente – long acting, long duration
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30
Q

What are 4 analogue insulin drugs? What are their effects?

A
  1. Lispro (Humalog) – rapid acting
  2. Aspart (Novalog) – rapid acting
  3. Glargine (Lantus) – long acting
  4. Detemir (Levemir) – long acting
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31
Q

What are 3 types of pain?

A
  1. acute: lasts hours or days and resolves with healing; serves biological purpose or protective function
  2. chronic: lasts beyond expected time; does not serve biological purpose or protective function
    • may be due to persistent inflammation
    • may become pt’s focus
    • affects QOL
  3. neuropathic: caused by injury or malfunction of nervous tissue
    • burning, tingling, paresthesia (pins and needles)
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32
Q

What are 5 sources of pain?

A
  1. cutaneous: stemming from superficial tissue
    • minor cuts and bruises
  2. deep somatic: stemming from ligaments or tendons
    • dull and poorly localized
  3. visceral: stemming from deep organs
  4. referred: pain that occurs at a distance from the actual pathology
  5. phantom: stemming from an amputated part of the body
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33
Q

What are the 3 types of pain medications? What is the general rule for taking pain medications?

A
  • opioids
  • nonopioids
  • adjuvant medications

– 2 products belonging to the same category should not be used simultaneously

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34
Q

What are the 3 steps to the WHO analgesic pain relief ladder?

A
  1. step 1: mild to moderate pain
    • use nonopioids – aspirin, acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs)
  2. step 2: moderate to severe pain
    • use mild opioids (like codeine)
    • with or without adjuvants
  3. step 3: severe pain
    • use strong opioids (like morphine)
    • with or without adjuvants
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35
Q

What are opioids?

A
  • considered controlled substances
  • produce analgesia, euphoria, and sedation
  • most effective when given before pain onset
  • side effects:
    • respiratory depression
    • constipation
    • nausea
    • dizziness
    • physical dependence
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36
Q

What are narcotic antagonists?

A

they reverse the effect or assist in the management of narcotic or alcohol abuse

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37
Q

What are 2 examples of narcotic antagonists, and what are their indications?

A
  1. naloxone (Narcan, Evzio)
    • reverses adverse effect of narcotics
    • used to diagnose suspected narcotic overdose
  2. naltrexone (ReVia)
    • PO medication for management of alcohol or narcotic dependence
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38
Q

What is GERD?

A

gastroesophageal reflux disease

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39
Q

What are signs and symptoms of GERD?

A
  • dysphagia
  • heartburn
  • epigastric pain
  • regurgitation
  • dyspepsia (acid indigestion)
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40
Q

How is GERD diagnosed?

A
  • endoscopy – view of the esophagus to analyze for damage to the esophagus
  • manometry – measures the pressure in the GI tract; determines contractile muscle strength, peristalsis, and sphincter strength
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41
Q

What are treatments for GERD?

A
  • lifestyle changes
  • dietary changes
  • PPIs
    • block the proton pumps on parietal cells, preventing the secretion of HCl
  • antacids
    • neutralize HCl in the stomach
  • laproscopic antireflux (fundoplication)
    • fundus wrapped around esophagus to block the parietal cells of the stomach, preventing them from releasing excess acid
  • endoscopic radiofrequency delivery
    • using radio frequency to destroy parietal cells on stomach lining
  • LINX reflux management system – magnets
    • a ring of magnets places at the base of the esophagus to narrow the esophageal sphincter and prevent reflux
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42
Q

What is dumping syndrome?

A

rapid gastric emptying

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43
Q

What is a common reason pts experience dumping syndrome?

A

post-bariatric surgery

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44
Q

What can result from dumping syndrome?

A

dehydration – hypertonic fluid in the intestines causes fluid to shift into intestines and be excreted

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45
Q

What are the 2 phases of dumping syndrome?

A
  1. early – occurs 30 minutes after eating
  2. late – occurs 2 - 3 hours after eating
46
Q

What is the treatment for dumping syndrome?

A

dietary management

47
Q

What is UGIB?

A

upper gastrointestinal bleeding

48
Q

What are the signs and symptoms of UGIB?

A
  • melena – black stools due to partially digested blood
  • occult blood
  • hematemesis
    • bright red blood in vomit
    • “coffee ground” emesis
    • indicates that blood has mixed with acid of the stomach
49
Q

How is UGIB diagnosed?

A
  • CBC – reduced H+H
  • FOBT (fecal occult blood test) – test for blood in stools; 3 tests on 3 different days
  • endoscopy
50
Q

What is the treatment for UGIB?

A
  • acute UGIB
    • hemodynamic stabilization – helping blood and fluids restabilize
    • endoscopic techniques to stop bleeds
  • chronic UGIB
    • PPIs – decreases the amount of HCl secreted, preventing the deterioration of the gastric lining
51
Q

What are esophageal varices? How do they result?

A

– esophageal varices: engorged veins at distal end of the esophagus; these veins are at risk for rupture

– result from portal vein hypertension – blood backs up in the main portal vein, causing blood to back up into smaller vessels in the esophagus

  • may be caused by liver damage (hepatitis or cirrhosis for example)
  • may result in UGIB
52
Q

What are the signs and symptoms of esophageal varices?

A
  • signs of liver dysfunction
    • jaundice
    • nausea
53
Q

How are esophageal varices diagnosed?

A
  • imaging
    • ultrasound
    • MRI
    • CT scan
54
Q

How are esophageal varices treated?

A
  • prevention of rupture
    • eating soft foods decreases pressure on esophagus and varices
  • immediate surgery required if the varices rupture
  • esophageal tamponade – balloon inserted into the stomach and esophagus and inflated in order to stop the bleeding
55
Q

What is Celiac disease?

A
  • AKA sprue or gluten-sensitive enteropathy
  • hypersensitivity reaction to gluten
    • gliadin – gluten-derived protein
  • autoimmune disease
  • unknown cause
56
Q

What are some signs and symptoms of Celiac disease?

A
  • ingestion of gluten causes:
    • bloating
    • gas
    • steatorrhea (loss of fat in stool)
57
Q

What is a primary concern for pts with Celiac disease?

A

malnutrition

58
Q

How is Celiac disease diagnosed?

A
  • Celiac panel – tests sensitivity and antibody reaction to gluten
  • antibody titer of IgA antitissue transglutaminase (IgA TTG)
  • intestinal biopsy
59
Q

How is Celiac disease treated?

A

dietary modification

60
Q

What is Crohn’s disease?

A
  • chronic, transmural (entire GI wall) inflammatory process
  • can affect GI tract from mouth to anus
    • most common are terminal ileum and ascending colon
  • can be autoimmune disease if attacking the cells of the GI tract; not autoimmune if attacking the natural gut flora which then causes inflammation
61
Q

What are the major characteristics of Crohn’s disease?

A
  • skip lesions: areas of disease separated by healthy areas
  • cobblestone: granulomas form in intestine resulting in a cobblestone appearance
  • toxic megacolon: extreme dilation of diseased colon
    • this can cause complete obstruction or life-threatening perforation
62
Q

How is Crohn’s disease diagnosed?

A
  • colonoscopy
    • helps differentiate between Crohn’s and UC
  • biopsy
  • Crohn’s Disease Activity Index (CDAI)
    • grades pt’s symptoms
    • pt will be in 1 of 4 disease states:
      • clinical remission
      • mild
      • moderate
      • severe
  • could also do blood and stool tests
    • blood in stool
    • decreased H+H
    • WBCs in stool
63
Q

What is ulcerative colitis?

A

chronic inflammatory disease that causes ulcers in the lining of the colon

64
Q

What are the signs and symptoms of UC?

A
  • presents similarly to Crohn’s
  • diarrhea
  • abdominal pain
  • abdominal distention
  • fever
  • leukocytosis
  • uveitis – inflammation of the eye
  • erythema nodosum – tender, red bumps found symmetrically on shins
  • arthritis
65
Q

How is UC diagnosed?

A

colonoscopy – distinguishes UC from Crohn’s

66
Q

What are treatments for UC?

A
  • corticosteroids
  • anti-inflammatories
  • antidiarrheals
  • topical or suppository 5-aminosalicylic acid (5-ASA)
  • mesalamine enema (5-ASA enema)
  • surgery
67
Q

What is volvulus?

A
  • twisting of the large intestine
    • most common in sigmoid
  • results in obstruction and ischemia
68
Q

What are the signs and symptoms of volvulus?

A
  • bilious vomiting
  • abdominal pain (colicky [contractile pain around partial or complete blockage of organs], then steady)
  • abdominal tenderness
69
Q

How is volvulus diagnosed?

A

upper and lower barium GI studies

70
Q

How is volvulus treated?

A

surgery to correct twisting of colon

71
Q

What is nonalcoholic fatty liver disease (NAFLD)?

A
  • accumulation of triglycerides in hepatocytes
    • steatosis: 5%+ of liver contains fat
  • most common cause of chronic liver disease in the US
  • unclear etiology
    • associated with metabolic syndrome, insulin resistance, and obesity
72
Q

What is nonalcoholic steatohepatitis (NASH)?

A

an extreme form of NAFLD in which the liver becomes inflammed and scars

73
Q

Why is the common bile duct important in GI considerations?

A
  • obstructions in the common bile duct can occur
    • gallstones (accumulation of fats which block outflow of bile)
    • tumors in pancreas
  • obstructions may result in jaundice
74
Q

What is acute pancreatitis?

A
  • serious disorder
  • potentially lethal
  • dysfunctional pancreas results in the leakage of pancreatic digestive enzymes into glandular parenchyma (the interstitial spaces)
  • this results in the inflammation of the pancreas and damage to pancreatic tissues (autodigestion)
  • could lead to hemorrhagic pancreatitis and accumulation of retroperitoneal blood
75
Q

What are some risk factors for acute pancreatitis?

A
  • biliary disease (cholelithiasis or gallstones)
  • alcohol ingestion
  • hypertriglyceridemia
  • infection
76
Q

What are some signs and symptoms of acute pancreatitis?

A
  • severe abdominal pain
    • sudden onset of pain that gradually intensifies
    • pain in epigastric region
    • pain can radiate to the back
  • nausea
  • vomiting
  • diarrhea
  • decreased bowel sounds
  • abdominal tenderness
  • guarding
  • abdominal distention
77
Q

What is chronic pancreatitis?

A

chronic inflammation of the pancreas due to autodigestion (from leakage of pancreatic enzymes); chronic inflammation of the pancreas because the pancreas is unable to heal, causing permanent damage to pancreas beta cells

often develops after several instances of acute pancreatitis

78
Q

What is a major risk factor of chronic pancreatitis?

A

chronic, heavy alcohol consumption

79
Q

What could result from chronic pancreatitis?

A

since the pancreas is damaged, the alpha and beta cells of the pancreas may become permanently damaged, compromising the pt’s ability to maintain glucose homeostasis

80
Q

What are histamine-2 (H2) antagonists?

A

drugs that block the release of HCl in response to gastrin

81
Q

What is the mechanism of action for H2 antagonists?

A
  • selectively blocks H2 receptor sites
  • results in reduction of gastric acid secretion
  • reduces amount of pepsin produced
82
Q

What are the indications for H2 antagonists?

A
  • short-term treatment of
    • active duodenal ulcers
    • benign gastric ulcers
  • treats pathological hypersecretory conditions
    • Zollinger-Ellison syndrome – production of too much gastric acid disorder
  • prevents
    • stress-induced ulcers
    • acute UGIB
83
Q

What are some examples of H2 antagonists?

A
  • cimetidine (Tagamet HB)
  • ranitidine (Zantac)
  • famotidine (Pepcid)
  • nizatidine (Axid)
84
Q

What are proton pump inhibitors (PPIs)?

A

drugs that suppress the secretion of HCl into the stomach

85
Q

What is the mechanism of action for PPIs?

A

prevent final step of HCl production in order to decrease amount of stomach acid

86
Q

What are the indications for PPIs?

A
  • short-term treatment of
    • active duodenal ulcers
    • GERD
    • erosive esophagitis
    • benign active gastric disease
  • long-term treatment of pathological hypersecretory conditions
87
Q

What are the pharmacokinetics of PPIs?

A
  • dissolves in acid
  • rapidly absorbed in GI tract
  • metabolized in liver
  • excreted in the urine
88
Q

What are some examples of PPIs?

A
  • omeprazole (Prilosec)
  • esomeprazole (Nexium)
  • lansoprazole (Prevacid)
  • dexlansoprazole (Kapidex)
  • pantoprazole (Protonix)
  • rabeprazole (Aciphex)
89
Q

What are GI protectants?

A

used to protect the GI tract against acids and salts and prevent ulcers

90
Q

What is the mechanism of action for GI protectants?

A

forms ulcer-adherent complex at duodenal ulcer sites

91
Q

What is the indication for GI protectants?

A

promote ulcer healing

92
Q

What are the pharmacokinetics for GI protectants?

A
  • rapidly absorbed
  • metabolized in the liver
  • excreted in the feces
93
Q

What are some contraindications for GI protectants?

A
  • allergy
  • renal failure
94
Q

What population should be caution when taking GI protectants?

A

pregnant or lactating women

95
Q

What are some adverse effects of GI protectants?

A
  • GI effects
    • constipation
    • diarrhea
    • nausea
    • indigestioin
    • gastric discomfort
    • dry mouth
  • dizziness
  • sleepiness
  • vertigo
  • skin rash
  • back pain
96
Q

What is an example of a GI protectant?

A

sucralfate

97
Q

What are birthmarks?

A

pigments on skin present at birth or that develop during infancy

98
Q

What are hemangiomas?

A

benign tumors of blood vessels

affects 30% of newborns

99
Q

What are port wine stains?

A

permanent blood vessel abnormalities

affects 0.5% of the population

100
Q

What is psoriasis?

A
  • AKA papulosquamous dermatoses
  • chronic thickening of epidermis with silver-white scales covering red plaques
  • lesions are frequently on extensor surface of knee and elbows
  • lesions bleed when scales are removed
  • autoimmune disease – T cells attack epidermis
101
Q

What are some risk factors of psoriasis?

A
  • skin trauma
  • stress
  • infection
  • some medications
102
Q

What are some treatments for psoriasis?

A

topical and systemic treatments

103
Q

What other disease is psoriasis linked to?

A

psoriasis arthritis

104
Q

What are some medications for fungal infections? Try to remember dosages for each.

A
  • fluconazole – 3 - 6 mg/kg PO daily
  • itraconazole – 2.5 mg/kg PO BID
  • ketoconazole – 5 - 10 mg/kd PO daily in two doses
  • amphotericin – oral suspension or IV
105
Q

What is bulimia nervosa?

A

binge eating followed by purging of food by vomiting, laxatives, or excessive exercise; binges occur 2+ times per week for 3 months

thought to be significantly underreported

106
Q

What are some signs and symptoms of bulimia nervosa?

A
  • BMI in normal range
  • electrolyte imbalance
  • tooth decay
  • severe dehydration
107
Q

What is binge eating?

A

food bingeing is not followed by compensatory mechanisms to prevent weight gain; can result in severe obesity

108
Q

What are purging disorders?

A

use of vomiting, laxatives, or diuretics to control weight; pt is often of normal weight

109
Q

What is night eating syndrome (NES)?

A

late-night binge eating; may be associated with low nocturnal levels of melatonin or leptin

110
Q

What are some complications of bariatric surgery?

A
  • vitamin and mineral deficiencies
    • B12
    • calcium
    • iron
  • herniation
  • dumping syndrome
    • undigested contents of stomach are dumped into small intestine too rapidly
    • diarrhea
    • abdominal cramps
    • hypotension
    • need to modify diet

NURS 316A (3 decks)

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