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NUR 228 > NUR 228 Exam 2 > Flashcards

NUR 228 Exam 2 Flashcards

1
Q

Name 2 esophageal disorders?

A

GERD, Hiatal hernia

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2
Q

3 Inflammatory disorders of the stomach?

A

gastritis, PUD, acute gastroenteritis

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3
Q

What means difficulty difficulty swallowing?

A

Dysphagia

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4
Q

Examples of mechanical obstruction of swallowing?

A

stenosis, diverticula, tumor

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5
Q

What can dysphagia lead to?

A

Aspiration

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6
Q

What is it called when the LES can’t open properly?

A

Achalasia

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7
Q

What does GERD stand for?

A

Gastroesophageal Reflux Disease

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8
Q

GERD is ? from the ? to the ? ……

A

Backflow, stomach, esophagus

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9
Q

GERD occurs via the lower __ ____?

A

esophageal sphincter

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10
Q

what is the PH of the material with GERD ?

A

Highly acidic

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11
Q

List some irritants of GERD?

A

Caffeine, fatty foods, alcohol, cigarette smoking, sleep, and spicy foods.

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12
Q

List the clinical manifestations of GERD?

A

Heartburn (pyrosis), dyspepsia, regurgitation, chest pain, dysphagia.

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13
Q

What are other causes of esophagitis?

A

Infection, chemical ingestion, drugs, emesis.

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14
Q

Worst sleeping position for GERD?

A

flat on the back

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15
Q

What is a defect in the diaphragm that allows part of the stomach to pass into the thorax?

A

Hiatal hernia

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16
Q

What are the 2 main types of hiatal hernias?

A

Sliding hernia, Paraesophageal hernia

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17
Q

Name risk factors of hiatal hernia?

A

Age, anything that loosens the muscular band around the gastroesophageal junction

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18
Q

Clinical manifestations of hiatal hernia?

A

Asymptomatic OR same as GERD

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19
Q

What is the temporary inflammation of the stomach lining?

A

acute gastritis

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20
Q

What can cause acute gastritis?

A

alcohol, NSAIDS, infection

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21
Q

What is a progressive disorder with chronic inflammation in the stomach?

A

Chronic gastritis

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22
Q

Two main etiologies of chronic gastritis?

A

autoimmune, H. pylori

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23
Q

What does H. pylori stand for?

A

Heliobacter pylori

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24
Q

What environment does H. pylori prefer?

A

Acidic

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25
Q

What does H. pylori cause?

A

destructive pattern of persistent inflammation

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26
Q

How is H. pylori transmitted?

A

Oral

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27
Q

Symptoms of gastritis?

A

anorexia, N/V, postprandial discomfort, hematemesis, anemia

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28
Q

What is acute gastroenteritis?

A

inflammation of stomach & small intestine

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29
Q

What are the clinical manifestations of acute gastroenteritis?

A

diarrhea, abdominal pain, N/V, fever/malaise.

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30
Q

Complication of acute gastroenteritis?

A

Fluid volume deficit

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31
Q

Peptic ulcer disease is any kind of ulcer in the ?

A

Upper GI tract (esophagus, stomach, duodenum)

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32
Q

Peptic ulcer disease develops when GI tract is exposed to acid & ____?

A

Pepsin

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33
Q

Defensive factors in Upper GI?

A

mucus, bicarbonate, blood flow, prostaglandins.

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34
Q

Aggressive factors of Upper GI Health?

A

H. pylori, NSAIDs, Acid, Pepsin, Smoking

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35
Q

What are some common causes of Peptic ulcer disease?

A

H. pylori, NSAIDs, Alcohol, Excess acid secretion, stress, smoking, and family history.

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36
Q

How does H pylori cause PUD?

A

They can imbed themselves into the stomach lining and grow there.

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37
Q

What 2 enzymes do NSAIDs inhibit?

A

COX-1 and COX-2

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38
Q

where are COX-1 enzymes found?

A

In all tissues

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39
Q

Where are COX-2 enzymes found?

A

at site of injury

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40
Q

What do COX-2 enzymes do?

A

Mediates inflammation and pain

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41
Q

What is the job of COX-1 enzymes?

A

to protect gastric mucosa by secreting prostaglandin E

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42
Q

What is the pathogenesis of PUD?

A

1.) Mucosa is damaged
2.) histamine is secreted which results in :
- Increase in acid and pepsin secretion
- Vasodilation
3.) Ulcer formed

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43
Q

PUD clinical manifestations:

A

N/V, anorexia, weight loss, bleeding, pain

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44
Q

Characteristics of gastric ulcer?

A

Burning, cramping, gas like

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45
Q

Characteristics of duodenal ulcer?

A

Burning, cramping, gas like

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46
Q

Location of both gastric and duodenal ulcer?

A

epigastrium, back

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47
Q

When does gastric ulcer pain develop>

A

1-2 hours after eating

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48
Q

When does Duodenal ulcer pain occur?

A

2-4 hours after eating

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49
Q

PUD “HOP” complications ?

A

H: Hemorrhage
O: Obstruction
P: Perforation and Peritonitis

50
Q

MOA of large doses of Antacids?

A

Neutralizes acid- 50%

51
Q

MOA of small dose antacids?

A

increased secretion of mucous, PGE, HC03

52
Q

Indication of antacids?

A

PUD healing, GERD symptoms, Stress ulcers

53
Q

Side effect of aluminum based antacids?

A

constipation

54
Q

Side effect of calcium based antacids?

A

Constipation

55
Q

Side effect of magnesium based antacids?

A

Diarrhea

56
Q

Adverse effects of Antacids?

A

Diarrhea or constipation, Acid rebound

57
Q

Interactions of antacids?

A

Chelation(cause other meds to not be absorbed), altered gastric absorption

58
Q

Sucralafate is composed of?

A

Sucrose and aluminum hydroxide

59
Q

MOA fo sucralafte?

A

alters when exposed to gastric acid. Sticky, thick gel–> protective barrier

60
Q

Indication of sucralafate ?

A

Duodenal uclers, gastric ulcers

61
Q

Should sucralfate be take with antacids?

A

NO

62
Q

Sucralafate route?

A

PO- tablet or suspension

63
Q

Interaction of sucralfate?

A

decreased drug absorption, take 2 hours apart

64
Q

How to treat H. pylori?

A

several antibiotics + gastric acid inhibitor
- metrinidazole, tetracycline, bismuth

65
Q

Why combination therapy to treat H. pylori?

A

minimize resistance

66
Q

What is the prototype of Histamine Type 2 receptor antagonists (H2RA)?

A

Cimetidine and famotodine

67
Q

MOA of histamine type 2 receptor antagonists?

A

Block H2 receptor, reduces gastric acid secretion

68
Q

Indications og H2RA

A

GERD, PUD

69
Q

Adverse effects of H2RA?

A

CNS in elderly, slight pneumonia risk in elderly

70
Q

Interactions of H2RA?

A

inhibits CYP 450 enzymes

71
Q

Proton pump inhibitors prototype?

A

Omeprazole, pantoprazole

72
Q

MOA of PPIs?

A

Binds to proton pump, irreversibly inhibits secretion of HCL?

73
Q

Indication of PPIs?

A

Short term treatment of PUD and GERD

74
Q

Adverse effects of PPIs?

A

Long term: pneumonia, hip fx, stomach CA

75
Q

Nursing implications of PPIs?

A

short term use only
other PPIs given IV
Monitor VB12

76
Q

What does the intrinsic factor do?

A

Binds to B12 in stomach and travels to terminal ileum where b12 is then absorbed

77
Q

Metoclopramide class?

A

pro kinetic, antiemetic

78
Q

MOA of metoclopramide?

A

Increases Upper GI motility, suppresses emesis

79
Q

Indications fo metoclopramide?

A

GERD, chemo induced N/v

80
Q

AE of metocloprmaide ?

A

Sedation, restlessness, extrapyramidal reactions

81
Q

NC for metoclopramide?

A

Short term therapy, check pt drug regimen

82
Q

What is the extrapyramidal system?

A

network of neurons in the brain that coordinate movement

83
Q

Symptoms of extrapyramidal reactions?

A

Akinesia, akasthesia

84
Q

Total body water %?

A

60% of body weight

85
Q

Functions of body fluid?

A

lubricant, metabolism, transport of O2, nutrients, chemical, regulate body temp

86
Q

What perfect of total body water is extracellular fluid?

A

33%

87
Q

What percent of total body water is blood plasma?

A

8%

88
Q

What is osmolality?

A

solute concentration in the the blood

89
Q

What is water movement across a semi-permeable membrane from low to high concentration?

A

osmosis

90
Q

What is the movement of particles down a concentration gradient?

A

diffusion

91
Q

what is movement of particles against a concentration gradient and requires energy?

A

active transport

92
Q

Water Pushing pressure?

A

Hydrostatic

93
Q

water pulling pressure?

A

Osmotic

94
Q

What particle has a large impact on pressure?

A

protein

95
Q

Colloidal osmotic pressure has to do with what molecule?

A

protein

96
Q

What protein is the main colloid?

A

Albumon

97
Q

Artery pressure is ?

A

High

98
Q

Venous pressure is ?

A

low

99
Q

What secretes aldosterone?

A

adrenal cortex

100
Q

Renal tubes reabsorb ___ & ____ and excrete ____?

A

Na, Water, K

101
Q

Where is Antidiuretic hormone synthesized?

A

hypothalamus

102
Q

Where is ADH stored and released from?

A

posterior pituitary

103
Q

Where is atrial natriuretic peptide released from?

A

Right atrium when heart is stretched

104
Q

What is increased production of urine by the kidneys?

A

Diuresis

105
Q

Where is the most sodium and water reabsorption

A

Loop Of Henle

106
Q

Diuretic types with class?

A

Furosemide: Loop
Hydrochlorothiazide: Thiazide
Spironolactone: Potassium sparing
Mannitol: Osmotic

107
Q

What is related to the osmotic pressure of a solution and how much it influences the movement of water?

A

Tonicity

108
Q

Tonicity equation?

A

2(Na+) + Gluc/18

109
Q

When concentration of stuff is equal to intravascular plasma?

A

Isotonic

110
Q

When concentration of stuff is less than plasma?

A

hypotonic

111
Q

When concentration of stuff is more than plasma?

A

Hypertonic

112
Q

Hypertonic causes the cell to?

A

shrink

113
Q

Hypotonic causes the cell to?

A

Enlarge

114
Q

Imbalance of volume is?

A

too much or too little

115
Q

Imbalance of concentration is?

A

too many or too few

116
Q

What is equal decreased water & Na+?

A

isotonic hypovalemia

117
Q

What can cause isotonic hypovalemia?

A

emesis , diarrhea, burns, hemorrhage, excessive perspiration.

118
Q

Clinical manifestations of hypovalemia?

A

Increased HR, weight loss, oliguria, decreased skin tumor, Dry mucous membranes, hard stools, absence of sweat, dizziness.

119
Q

Causes of hypervalemia?

A

excessive infusion of fluids, CHF, Cirrhosis

120
Q

Clinical manifestations of hypervalemia?

A

Weight gain, edema, bounding pulses, DJV, crackles, orthopnea.

NUR 228 (2 decks)

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