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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
Q

What are some cuases of gastritis?

A 
Systemic inflammation
Ingestion of acid or alkali (acute)
Autoimmune (chronic)
Nonerosive (H. Pylori)
Erosive (NSAIDs, alcohol, radiation)
26
Q

What are the clinical manifestations of gastritis, acute vs. chronic.

A

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
Q

What are the tx’s for gastritis?

A

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
Q

What can the nurse do for gastritis?

A

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
Q

What is a peptic ulcer? Cause? Types?

A

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
Q

What are the signs for perforation/peritonitis?

A

Sudden abd pain, vomiting, fainting, tender, hard/rigid abd, hypotension, tachycardia.

(Monitor in peptic ulcer pts)

31
Q

What are the signs for gastric outlet obstruction? When can this occur, why?

A

N/v, epigastric fullness, constipation, weight loss, NG resid greater than 400ml

Peptic ulcer (acute inflammation/scarring/muscle spasm)

32
Q

What nutrition is important for post op care in morbid obesity surgery?

A

6 small meals 600-800 cal/day
Sip 30ml q 15 min
Stop eating when full
Sugar free/low fat

33
Q

What are some common obstacles to adequate nutrition with gastric surgery?

A 
Dysphagia
Gastric retention
Bile reflux
Dumping syndrome
Vitamin/mineral def
Weight loss
34
Q

What are the post op care treatments to keep in mind for gastric surgery?

A

Liquids and solids taken separately
Inc. fat and protein intake
Dec carbs
Dietary supps (vitamins, iron, b12 injections)

35
Q

What are some common medications used for IBS?

A

Bulk forming laxatives
Anticholinergics (Bentyl)
Anti diar (Imodium, lomotil)
Antidepressant

36
Q

What are some dietary measures to keep in mind with IBS relief?

A

Inc dietary fiber
Limit lactose dairy
Limit carbonated bevs
Avoid gassy foods, smoking, chewing gum, drinking fast.

37
Q

What are some complications of peritonitis?

A

Abscess
Fibrous adhesions
Septicemia, septic shock and hypovolemia due to fluid shift into third space-can lead to hypovolemia shock.

38
Q

Where is chrons most common? What are defining characteristics? These cause?

A

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
Q

What manifestations are seen in ulcerative colitis that differ it from chrons?

A

Bloody stool
Rebound tenderness after elimination in RLQ
Only effects lining, only in colon and continuous . Systemic complications.

40
Q

What are two types of bowel obstruction? What occurs with each?

A
  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
Q

What innervates and stimulates the pancreas?

A

Vagal nerve
PNS-stims secretion
SNS-inhib secretion (anticholin)

42
Q

What are the endocrine and exocrine functions of the pancreas? What cells are responsible?

A

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
Q

What do both CCK and Secretin do from the pancreas?

A

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
Q

what activates enzymes in duodenum?

A

Bile and trypsin

45
Q

What does the cells in the pancreas do in acute pancreatitis?

A

Acinar cells premature activation of enzymes-leading to auto digestion of pancreas by enzymes

46
Q

In acute pancreatitis, when the enzymes are prematurely released and auto digestion occurs, what downfall of occurrences begins? This ultimately leads to?

A

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
Q

What are s/s and tx for acute pancreatitis?

A

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
Q

What changes occur in chronic pancreatitis?

A

Progressive destruction of exocrine functions.
Cells become fibrous.
Endocrine function ceases.
Irreversible.

49
Q

What is a pseudo cyst? And when is it classified that?

A

Collection of amylase rich, lipase rich, and trypsin rich fluid.
Present for atleast 4 weeks.

50
Q

What arises from pancreatic tumors? What syndrome is associated? And the 3 factors present?

A

Ulcerogenic tumors

Zollinger-Ellison syndrome: gastric acid hyper secretion, gastric ulcers, pancreatic tumors

Nur 210 (4 decks)

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