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Nur 210 > Unit One Part 2 > Flashcards

Unit One Part 2 Flashcards

1
Q

What glands first begins food breakdown? Enzyme released here? How much is secreted?

A 
Salivary glands:
Parotid 
Sublingual
Submandibular 
Enzymes: ptalyin and amylase
1.5 L saliva/day
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2
Q

Where does nervous stimulation begin for GI and the following processes?
What vessels supply the GI system?

A

Medulla-CNS then
Enteric nervous system-PNS takes over

Mesenteric A (sup/inf)

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3
Q

What are the 4 major functions of the GI system?

A

Secretions: mucous production (mouth, duodenum/jejunum, colon).
Movement: peristalsis (rhythmic contractions) and segmental (push)/propulsive (mix)
Digestion: bolus breakdown into absorbable chemicals.
Absorption: nutrient uptake.

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4
Q

What are the actions of the stomach? How long can food store? What is the acidity level? How much gastric fluid secreted/day?

A

Break up bolus into chyme by means of HCL, pepsin, and intrinsic factor (B12 absorp, w/o causes pern. Anemia).
30 min-6hrs.
1-under 5.5ph
2.4L/day

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5
Q

Separate the parts of the small intestines and identify what is absorbed in each area.

A

All-Mg, Phosphate, potassium.
Duodenum-iron, calcium.
Jejunum-fat, protein, carb, Na, Cl.
Illeum-Vit b12, bile salts.

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6
Q

What enzymes do the pancreas, liver, and GB and function in GI.

A 
Pancreas:carb and protein digestion. (1 L)
Trypsin-Protein
Amylase-carb
Lipase-fat
Liver:fat digestion, secrete bile (0.5L)
GB:bile storage, ADEK absorption.
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7
Q

What does the large intestine primarily secrete and absorb?

A

Mucous (micro flora present here)

Water/electrolytes

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8
Q

Explain the nutrition for Mexican Americans.

A

Low fat, high fiber/carb and veg protein.
Lactose intolerant.
Cold/hot food for healing.
Overweight, alcohol, t2d, cavity/gingivitis.

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9
Q

Explain the nutrition for Chinese Americans.

A

Little meat, high sodium.
Lactose intol.
Yin/yang.
Cancer/diabetes.

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10
Q

In order to receive enteral nutrition, what must be partially functional? What are the indications for enteral nut?

A 
Accessible, safe, and functional GI tract.
Decompression (rem. Gas/fluid)
Lavage (flush, rem. Toxins)
Compression (bleeding)
Admin food, fluid, meds
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11
Q

What types of enteral nutrition are avail?

A

Routine: 1-1.2 cal/ml
Hi cal:1.5-2 cal/ml
1,000-2,000 ml/day
Water: 30-40 ml/kg/day

Hypertonic sol:diarrhea
Hi fiber: Thick, need large bore tubing

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12
Q

What types of administration are there for enteral feeding?

A

Intermittent or continuous over period of 8-24 hrs (HOB 30-45)
Intermit: resid over 200 ml in 2 times=poor tolerance.
Bolus:large vol quick-dumping syndrome-30ml syringe
Cont:rate 16-24 HR-interrupted q 4hr-cyclic

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13
Q

What skills must the nurse follow when initiating enteral feedings?

A

Tube placement-X-ray, pos BS. Initial feed 25-50ml/HR advancing 10-25ml/HR q 8-12hr. Max flow:125ml/HR
Flush 15-30ml water pre/post drug, DC while meds admin.

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14
Q

What are s/s of dumping syndrome?

A

Early: diar/cramps/epigastric pain
Later: tachy, ortho hypo, flush, diaphoresis, dizzy (dec blood vol)

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15
Q

What intervention skills are essential for PN?

A

Vs q 4hr
Sterile tech dressing change w/ mask.
Asses insertion site, signs of infection. Hypo/hyperglycemia, labs.
Taper end of cycle, by 1/2 in last HR to prevent.

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16
Q

What is achalasia? Clinical manifestations? Treatment?

A

Ineffective peristalsis (dilation) distal esophagus and failure of LES to relax in swallow response.
Difficult swallow
Food sticking sensating w/ regurgitate action
Chest pain/pyrsosis
Pneumonia (w/ aspiration)
CCB and nitrates dec. esoph pressure and inc swallow. Pneumatic dilation stretches narrowed LES area.botox.

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17
Q

What occurs in hiatal hernia? Diff the two types.

A

Opening in diaphragm, esophagus, and part of upper stomach passes through and enlarges. (More often in women)
Sliding (type 1)-most common, upper stomach and gastroesophogeal junction displaced upward through diaphragm and slides in and out.
Paraesophageal-all/part of stomach pushes through diaphragm beside esophagus.

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18
Q

What are the s/s and tx for hiatal hernia?

A

50% asymptomatic.
Sliding-pyrsosis, regurgitation, dysphagia.
Paraesoph-fullness/chest pain after eating.

Hemmorhage, obstruction, and strangulation.
Tx:small meal, no spicy/hot/gassy/smoking, fowlers 1 HR s/p eat, elevate 4-8”
Meds:antacids, h2 antag (Zantac/Tagamet), PPI (omeprazole)
Surg: Nissen fundoplication

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19
Q

What happens w/ esophageal diverticulum?

S/s?

A

Out-pouching of mucosa and submucosa protruding through weak portion of muscle. Many types. Becomes filled w/ food/fluid.when laying down, food regurgitated and cough.halitosis/sour taste.
Difficult swallow, fullness in neck, belching, regurgitate, gurgling.

*egd/NG contraindicated (until preop), withhold food post op until X-ray confirm no leak.

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20
Q

What is the tx’s for esophageal perforation? What is the common syndrome associated?

A

Antibiotics (if contents spill into mediastinum-cause sepsis)
Enteral/parenteral nutrition
Surg-no food 6 months

Boerhaave syndrome-spontaneous rupture s/p forceful vomiting.

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21
Q

What are the two types of esophageal cancer?

A

Adenocarcinoma and squamous cell carcinoma neoplasms

22
Q

What are the clinical manifestations to esophageal carcinoma?

A

(Complications:metastatis into lymphatics, esophageal obstruction, esophageal perforation)
Dysphagia, painful swallowing, throat fullness
Later:regurgitate, halitosis, hiccups, hemorrhage, resp diff.
(Weight and strength loss)

23
Q

What are the nursing interventions w/ esophageal carcinoma?

A

Preop care
Enteral/parenteral, hi cal, hi prot, upright x2hrs s/p eat
Vs-infection-drainage
Closed chest tube, NG, gastric tube, Trach/resp tx
Meds:antacids, metoclopramide, antibiotics

24
Q

Explain the patho for gastritis and types.

A

Inflammation of stomach mucosa. Mucus membranes edematous and hyperemic (blood/fluid congestion), superficial erosion, secreting mucous and little gastric juice, superficial ulceration, hemorrhage.
Acute/chronic, erosive/nonerosive.

25
What are some cuases of gastritis?
``` Systemic inflammation Ingestion of acid or alkali (acute) Autoimmune (chronic) Nonerosive (H. Pylori) Erosive (NSAIDs, alcohol, radiation) ```
26
What are the clinical manifestations of gastritis, acute vs. chronic.
Acute: abdominal discomfort, n/v, anorexia, ha, hi coughing, blood in vomit/stool. Chronic:pyrosis, anorexia, n/v, belching, sour taste, intolerance to spicy/fatty food, pain relieved by eating, unable to absorb b12 (lead to pern anemia).
27
What are the tx's for gastritis?
Acute-self repair Avoid alcohol/food until symptoms subside, IV therapy. NG tube. Meds:antacids, h2 receptors, PPIs. Gastric resection, gastrojunostomy (bypass pylorus) Chronic:diet mod, no alcohol/NSAIDs, same meds, rest/stress reduction.
28
What can the nurse do for gastritis?
PO until symptoms subside. IV therapy-I&O, electrolytes, ice chips to clear diet. No carb bev, alcohol, smoking, spicy, irritating, high seasoned food, caffeine. Mon for hemorrhage, b12 injections.
29
What is a peptic ulcer? Cause? Types?
Gastric, duodenal, or esophageal excavation (hollowing) formed in the mucosal wall. H. Pylori, stress, anxiety, p to p transmission, emesis exposure, NSAIDs use. (Gastrin/HCL damage) Stress, gastric, and duodenal.
30
What are the signs for perforation/peritonitis?
Sudden abd pain, vomiting, fainting, tender, hard/rigid abd, hypotension, tachycardia. (Monitor in peptic ulcer pts)
31
What are the signs for gastric outlet obstruction? When can this occur, why?
N/v, epigastric fullness, constipation, weight loss, NG resid greater than 400ml Peptic ulcer (acute inflammation/scarring/muscle spasm)
32
What nutrition is important for post op care in morbid obesity surgery?
6 small meals 600-800 cal/day Sip 30ml q 15 min Stop eating when full Sugar free/low fat
33
What are some common obstacles to adequate nutrition with gastric surgery?
``` Dysphagia Gastric retention Bile reflux Dumping syndrome Vitamin/mineral def Weight loss ```
34
What are the post op care treatments to keep in mind for gastric surgery?
Liquids and solids taken separately Inc. fat and protein intake Dec carbs Dietary supps (vitamins, iron, b12 injections)
35
What are some common medications used for IBS?
Bulk forming laxatives Anticholinergics (Bentyl) Anti diar (Imodium, lomotil) Antidepressant
36
What are some dietary measures to keep in mind with IBS relief?
Inc dietary fiber Limit lactose dairy Limit carbonated bevs Avoid gassy foods, smoking, chewing gum, drinking fast.
37
What are some complications of peritonitis?
Abscess Fibrous adhesions Septicemia, septic shock and hypovolemia due to fluid shift into third space-can lead to hypovolemia shock.
38
Where is chrons most common? What are defining characteristics? These cause?
Can occur mouth to anus-but more common in terminal ileum and ascending colon. Ulcerations effect all layers of bowel wall. Absorption issues-anemia, protein def. diarrhea, abd pain, RLQ pain relieved by elimination. Fever malaise fissures
39
What manifestations are seen in ulcerative colitis that differ it from chrons?
Bloody stool Rebound tenderness after elimination in RLQ Only effects lining, only in colon and continuous . Systemic complications.
40
What are two types of bowel obstruction? What occurs with each?
1. Mechanical: outside intestines, inside intestine, and luminal:intussusception (telescoping), volvulus:twisted bowel, foreign bodies, strictures. 2. Functional: peristalsis failure(neuro, muscle, meds, surg, injury, anoxia)
41
What innervates and stimulates the pancreas?
Vagal nerve PNS-stims secretion SNS-inhib secretion (anticholin)
42
What are the endocrine and exocrine functions of the pancreas? What cells are responsible?
ENDO-hormonal: islet of langerhans beta cell-insulin. Cell uptake of sugar, protein, fat. Alpha cell-glucagon.inc blood sugar by stim liver release. Delta-somatostatin. Inhib both (and motility/gastric acid) EXO-enzyme: 1500-2500ml/day Acinar-amylase, trypsin, lipase, trypsin inhib. Duct cells-(Hormones)secretin-bicarb CCK-enzyme secretion
43
What do both CCK and Secretin do from the pancreas?
CCK-initiates GB contraction and stimulates enzyme release. | Secretion-tells duct cells to make bicarb (ph of 8 needed in duodenum for enzyme to function)
44
what activates enzymes in duodenum?
Bile and trypsin
45
What does the cells in the pancreas do in acute pancreatitis?
Acinar cells premature activation of enzymes-leading to auto digestion of pancreas by enzymes
46
In acute pancreatitis, when the enzymes are prematurely released and auto digestion occurs, what downfall of occurrences begins? This ultimately leads to?
Activation of other enzymes. Duct obstruction. Inflam response. Cell damage. Spreading edema to other organs/systemic. Fluid shifts. HYPOVOLEMIA(Dec prot leads to dec osmotic press, inc vas permeab.) Fatty necrotic tissue draws in calcium-leading to hypocalcemia (tentany and cardiac d/o).
47
What are s/s and tx for acute pancreatitis?
No tx-self limiting. Nutritional therapy:NPO (inhib panc secretion), small freq feeds once resolved, hi carb, low fat/prot, Sudden onset Pain (luq, epigastric), inc WBC, hypo tension/tachy, hypovolemia, n/v, cold/clammy, abd distention/rigid. Resp dist/renal fail/jaundice
48
What changes occur in chronic pancreatitis?
Progressive destruction of exocrine functions. Cells become fibrous. Endocrine function ceases. Irreversible.
49
What is a pseudo cyst? And when is it classified that?
Collection of amylase rich, lipase rich, and trypsin rich fluid. Present for atleast 4 weeks.
50
What arises from pancreatic tumors? What syndrome is associated? And the 3 factors present?
Ulcerogenic tumors Zollinger-Ellison syndrome: gastric acid hyper secretion, gastric ulcers, pancreatic tumors

Nur 210 (4 decks)

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