1
Q
Where is insulin created?
A
beta cells of the islets of Langerhans in the pancreas
2
Q
When is insulin released?
A
when levels of blood glucose rise
3
Q
What are the 3 functions of insulin?
A
- stimulation of glycogen synthesis
- conversion of lipids into fats to be stored as adipose tissue
- synthesis of proteins from amino acids
4
Q
What is the range of normal fasting blood glucose?
A
70 - 100 mg/dL
5
Q
What is hypoglycemia?
A
- blood glucose < 70 mg/dL
- affects brain function
6
Q
What is hyperglycemia?
A
blood glucose > 200 mg/dL
7
Q
What is prediabetes?
A
- fasting blood glucose = 100 - 125 mg/dL
- impaired glucose tolerance (IGT)
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
9
Q
What is postprandial blood glucose?
A
blood glucose after eating
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
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
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
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
14
Q
How common is DKA in DM children?
A
1/3 of DM1 children first present with DKA
15
Q
What is the pathology of DM1?
A
T-cells attack beta cells of the pancreas (autoimmune disorder)
16
Q
What are the common symptoms of DM1?
A
- DKA – usually presenting sign
- polyuria
- polydipsia
- polyphagia
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
18
Q
How quickly does HHS develop when compared with DKA?
A
HHS develops over days to weeks; DKA develops within hours
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
20
Q
What are some causes of HHS?
A
- infection (pneumonia, sepsis)
- noncompliance with DM medication
- substance abuse
- coexisiting diseases
21
Q
Who typically gets HHS?
A
DM2 pts
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
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
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
25
What can cause hypoglycemia in DM pts?
* excessice exogenous insulin
* inadequate food intake
* excessive physical activity
* infection
* illness
* drug interaction
26
What are the compensatory mechanisms that counteract hypoglycemia?
* epinephrine
* glucagon
* activation of SNS
* epinephrine
* norepinephrine
* cortisol
* ^these all work to raise BG levels
27
What are some signs and symptoms of hypoglycemia?
* sweating
* hunger
* dizziness
* headache
* heart palpitations
* confusion
28
How do DM pts address hypoglycemia?
* 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
29
What are 4 conventional insulin medications? What are their effects?
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
30
What are 4 analogue insulin drugs? What are their effects?
1. Lispro (Humalog) -- rapid acting
2. Aspart (Novalog) -- rapid acting
3. Glargine (Lantus) -- long acting
4. Detemir (Levemir) -- long acting
31
What are 3 types of pain?
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)
32
What are 5 sources of pain?
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
33
What are the 3 types of pain medications? What is the general rule for taking pain medications?
* opioids
* nonopioids
* adjuvant medications
-- 2 products belonging to the same category should not be used simultaneously
34
What are the 3 steps to the WHO analgesic pain relief ladder?
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
35
What are opioids?
* considered controlled substances
* produce analgesia, euphoria, and sedation
* most effective when given before pain onset
* side effects:
* respiratory depression
* constipation
* nausea
* dizziness
* physical dependence
36
What are narcotic antagonists?
they reverse the effect or assist in the management of narcotic or alcohol abuse
37
What are 2 examples of narcotic antagonists, and what are their indications?
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
38
What is GERD?
gastroesophageal reflux disease
39
What are signs and symptoms of GERD?
* dysphagia
* heartburn
* epigastric pain
* regurgitation
* dyspepsia (acid indigestion)
40
How is GERD diagnosed?
* 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
41
What are treatments for GERD?
* 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
42
What is dumping syndrome?
rapid gastric emptying
43
What is a common reason pts experience dumping syndrome?
post-bariatric surgery
44
What can result from dumping syndrome?
dehydration -- hypertonic fluid in the intestines causes fluid to shift into intestines and be excreted
45
What are the 2 phases of dumping syndrome?
1. early -- occurs 30 minutes after eating
2. late -- occurs 2 - 3 hours after eating
46
What is the treatment for dumping syndrome?
dietary management
47
What is UGIB?
upper gastrointestinal bleeding
48
What are the signs and symptoms of UGIB?
* 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
How is UGIB diagnosed?
* CBC -- reduced H+H
* FOBT (fecal occult blood test) -- test for blood in stools; 3 tests on 3 different days
* endoscopy
50
What is the treatment for UGIB?
* 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
What are esophageal varices? How do they result?
-- **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
What are the signs and symptoms of esophageal varices?
* signs of liver dysfunction
* jaundice
* nausea
53
How are esophageal varices diagnosed?
* imaging
* ultrasound
* MRI
* CT scan
54
How are esophageal varices treated?
* 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
What is Celiac disease?
* AKA sprue or gluten-sensitive enteropathy
* hypersensitivity reaction to gluten
* gliadin -- gluten-derived protein
* autoimmune disease
* unknown cause
56
What are some signs and symptoms of Celiac disease?
* ingestion of gluten causes:
* bloating
* gas
* steatorrhea (loss of fat in stool)
57
What is a primary concern for pts with Celiac disease?
malnutrition
58
How is Celiac disease diagnosed?
* Celiac panel -- tests sensitivity and antibody reaction to gluten
* antibody titer of IgA antitissue transglutaminase (IgA TTG)
* intestinal biopsy
59
How is Celiac disease treated?
dietary modification
60
What is Crohn's disease?
* 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
What are the major characteristics of Crohn's disease?
* **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
How is Crohn's disease diagnosed?
* 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
What is ulcerative colitis?
chronic inflammatory disease that causes ulcers in the lining of the colon
64
What are the signs and symptoms of UC?
* 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
How is UC diagnosed?
colonoscopy -- distinguishes UC from Crohn's
66
What are treatments for UC?
* corticosteroids
* anti-inflammatories
* antidiarrheals
* topical or suppository 5-aminosalicylic acid (5-ASA)
* mesalamine enema (5-ASA enema)
* surgery
67
What is volvulus?
* twisting of the large intestine
* most common in sigmoid
* results in obstruction and ischemia
68
What are the signs and symptoms of volvulus?
* bilious vomiting
* abdominal pain (colicky [contractile pain around partial or complete blockage of organs], then steady)
* abdominal tenderness
69
How is volvulus diagnosed?
upper and lower barium GI studies
70
How is volvulus treated?
surgery to correct twisting of colon
71
What is nonalcoholic fatty liver disease (NAFLD)?
* 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
What is nonalcoholic steatohepatitis (NASH)?
an extreme form of NAFLD in which the liver becomes inflammed and scars
73
Why is the common bile duct important in GI considerations?
* 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
What is acute pancreatitis?
* 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
What are some risk factors for acute pancreatitis?
* biliary disease (cholelithiasis or gallstones)
* alcohol ingestion
* hypertriglyceridemia
* infection
76
What are some signs and symptoms of acute pancreatitis?
* 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
What is chronic pancreatitis?
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
What is a major risk factor of chronic pancreatitis?
chronic, heavy alcohol consumption
79
What could result from chronic pancreatitis?
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
What are histamine-2 (H2) antagonists?
drugs that block the release of HCl in response to gastrin
81
What is the mechanism of action for H2 antagonists?
* selectively blocks H2 receptor sites
* results in reduction of gastric acid secretion
* reduces amount of pepsin produced
82
What are the indications for H2 antagonists?
* 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
What are some examples of H2 antagonists?
* cimetidine (Tagamet HB)
* ranitidine (Zantac)
* famotidine (Pepcid)
* nizatidine (Axid)
84
What are proton pump inhibitors (PPIs)?
drugs that suppress the secretion of HCl into the stomach
85
What is the mechanism of action for PPIs?
prevent final step of HCl production in order to decrease amount of stomach acid
86
What are the indications for PPIs?
* short-term treatment of
* active duodenal ulcers
* GERD
* erosive esophagitis
* benign active gastric disease
* long-term treatment of pathological hypersecretory conditions
87
What are the pharmacokinetics of PPIs?
* dissolves in acid
* rapidly absorbed in GI tract
* metabolized in liver
* excreted in the urine
88
What are some examples of PPIs?
* omeprazole (Prilosec)
* esomeprazole (Nexium)
* lansoprazole (Prevacid)
* dexlansoprazole (Kapidex)
* pantoprazole (Protonix)
* rabeprazole (Aciphex)
89
What are GI protectants?
used to protect the GI tract against acids and salts and prevent ulcers
90
What is the mechanism of action for GI protectants?
forms ulcer-adherent complex at duodenal ulcer sites
91
What is the indication for GI protectants?
promote ulcer healing
92
What are the pharmacokinetics for GI protectants?
* rapidly absorbed
* metabolized in the liver
* excreted in the feces
93
What are some contraindications for GI protectants?
* allergy
* renal failure
94
What population should be caution when taking GI protectants?
pregnant or lactating women
95
What are some adverse effects of GI protectants?
* GI effects
* constipation
* diarrhea
* nausea
* indigestioin
* gastric discomfort
* dry mouth
* dizziness
* sleepiness
* vertigo
* skin rash
* back pain
96
What is an example of a GI protectant?
sucralfate
97
What are birthmarks?
pigments on skin present at birth or that develop during infancy
98
What are hemangiomas?
benign tumors of blood vessels
affects 30% of newborns
99
What are port wine stains?
permanent blood vessel abnormalities
affects 0.5% of the population
100
What is psoriasis?
* 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
What are some risk factors of psoriasis?
* skin trauma
* stress
* infection
* some medications
102
What are some treatments for psoriasis?
topical and systemic treatments
103
What other disease is psoriasis linked to?
psoriasis arthritis
104
What are some medications for fungal infections? Try to remember dosages for each.
* 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
What is bulimia nervosa?
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
What are some signs and symptoms of bulimia nervosa?
* BMI in normal range
* electrolyte imbalance
* tooth decay
* severe dehydration
107
What is binge eating?
food bingeing is not followed by compensatory mechanisms to prevent weight gain; can result in severe obesity
108
What are purging disorders?
use of vomiting, laxatives, or diuretics to control weight; pt is often of normal weight
109
What is night eating syndrome (NES)?
late-night binge eating; may be associated with low nocturnal levels of melatonin or leptin
110
What are some complications of bariatric surgery?
* 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
flashcards
Decks in class (3)
# Cards
