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SRNA3AdvancedPatho2 > GI Disorders > Flashcards

GI Disorders Flashcards

1
Q

Initial phase of mechanical breakdown of food, happens in the

A

Oral Cavity

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2
Q

Mastication by teeth

A

Initial phase of the mechanical breakdown of food

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3
Q

– Initial chemical digestion (enzyme)

A

• Salivary amylase

– starts chemical breakdown of carbohydrates

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4
Q

Pharynx is involved in

A

Swallowing (deglutition)

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5
Q

Esophagus

A

Closed except during swallowing, skeletal muscle

at superior end – followed by smooth muscle

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6
Q

Can effect airway mgmt

A

Disorders of oral cavity, pharynx or esophagus

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7
Q

Stomach

A

Expansible muscular sac – acts as reservoir for food and

fluid

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8
Q

The stomach and layers

A

Three smooth muscle layers

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9
Q

What do the parietal cells secrete?

A

HCL

IF

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10
Q

What do the CHIEF cells secrete?

A

PEPSIN

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11
Q

What do the G Cells cells secrete?

A

GASTRIN

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12
Q

Role of the Production of intrinsic factor –

A

Essential for the absorption of vitamin B12 in ileum

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13
Q

Initial digestion of proteins is accomplished by?

A

By pepsin (formed by pepsinogen + HCl)

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14
Q

What is the role of the liver?

A

“Metabolic factory” of the body

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15
Q

The liver receives blood from the

A

Receives blood from hepatic portal vein –

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16
Q

Transport of nutrients form intestine to liver

A

Hepatic portal vein

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17
Q

Hepatocytes store nutrients and what is other role

A

play role in carbohydrate, protein, fat metabolism

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18
Q

Other roles of the liver

A

• Production of plasma proteins and clotting
factors
• Breakdown of old/damaged erythrocytes
• Bile production

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19
Q

Pancreas: Exocrine

A

• Exocrine pancreas arranged in lobules

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20
Q

Pancreas Secretes digestive enzymes, electrolytes –

TCC RPB

A 
Trypsin
Chymotrypsin
Carobodxypeptidase
Ribonuclease
Pancreatic amylase
Bicarbonate ions
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21
Q

Pancreatic duct joins

A

bile duct to enter duodenum.

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22
Q

Lower Gastrointestinal Tract: Small intestine (DJI)

A

Duodenum, jejunum, ileum

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23
Q

Villi and microvill role in the small intestine:

A

Villi (folds of the mucosa) and

microvilli (folds of cell membranes)

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24
Q

2 substance that increase surface area for absorption

A

Villi and microvilli

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25
Q

Major site for absorption of nutrients

A

Small intestines

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26
Q

Lacteal –What are they?

A

lymphatic vessels of the small intestine which absorb digested fats.

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27
Q

Immune surveillance of materials within your digestive system

A

Peyer’s patches

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28
Q

Small intestine production of

A

• Mucus
• Enterokinase, peptidases, nucleosidases, lipase, sucrase,
maltase, lactase; cholecystokinin (hormone)

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29
Q

Lower Gastrointestinal Tract: Large intestine

A
  • Resident normal flora

* Vitamin K synthesis by bacteria

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30
Q

Large intestine responsible for

A

Fluid and electrolyte reabsorption

Formation and elimination of solid waste

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31
Q

Neural and Hormonal Controls

Parasympathetic nervous system: Stimulatory or inhibitory

A

Stimulatory

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32
Q

Parasympathetic nervous system: Stimulatory -> Primarily through

A

vagus cranial nerve

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33
Q

Role of Parasympathetic nervous system: Stimulatory through vagus CN

A

Increase motility

Increase secretions

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34
Q

Sympathetic nervous system Stimulatory or inhibitory

A

Inhibitory

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35
Q

Sympathetic nervous system stimulated by

A

Fear and anger

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36
Q

SNS on GI

A

Inhibits gastrointestinal activity

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37
Q

SNS on GI Vasoconstriction/Vasodilation

A

Causes vasoconstriction

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38
Q

SNS on cells

A

Reduced secretions & regeneration epithelial cells

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39
Q

Neural Controls 2 CN –

A

• C.N. VII & IX

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40
Q

Role of CN VII and IX

A

Maintain continuous flow of saliva in mouth

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41
Q

Distention and stretching of stomach: What happens?

A

PNS activation – ↑ Peristalsis and gastric secretions

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42
Q

When does the stomach empties after a meal?

A

Stomach empties within 2 to 6 hours after meal.

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43
Q

Food in intestine stimulates?

A

Stimulates intestinal activity

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44
Q

What is the role of the Enterogastric reflex ?

A

Inhibits gastric emptying

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45
Q

Hormonal controls: Gastrin

When is it secreted and what does it increase and promote?

A
  • Secreted by stomach in response to distention
  • Increases gastric secretions & motility, relaxes pyloric and ileocecal sphincters –
  • Promotes stomach emptying
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46
Q

Hormonal controls: Histamine(H2 receptor) role

A

Increased secretion of hydrochloric acid

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47
Q

What is the role of Secretin?

A

Decreases gastric secretions

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48
Q

What is the role of Cholecystokinin (CCK)?

A

Inhibits gastric emptying; stimulates contraction of gallbladder

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49
Q

Digestion and Absorption: Carbohydrates

A

– Digestion starts in mouth.

– Followed by digestion in the small intestine

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50
Q

Digestion and Absorption: Proteins

A

Digestion starts in stomach; continues in small intestine

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51
Q

Digestion and Absorption: Lipids

FEA

A

– Formation of chylomicrons
– Emulsified by bile prior to chemical breakdown
– Action of enzymes forms monoglycerides and free
fatty acids

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52
Q

Digestion and Absorption: Fat-soluble vitamins are? Meaning

A

– Vitamins A, D, E, K ; Absorbed with fats

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53
Q

What are the Water-soluble vitamins?

Meaning

A

– Vitamins B and C – diffuse into blood

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54
Q

Digestion and Absorption: Electrolytes

A

Absorbed by active transport or diffusion

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55
Q

Digestion and Absorption: Drugs are primarily absorbed where? and how about transport mechanism

A

In the intestine.
– Various transport mechanisms
– Some (i.e., aspirin) absorbed in the stomach

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56
Q

Digestion and Absorption
• Water Absorbed primarily by

– Severe vomiting or diarrhea interrupts recycling
mechanism.
• Affects fluid and electrolyte balance of body

A

osmosis

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57
Q

How much water is secreted into the digestive

tract each day?

A

700 mL

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58
Q

Amount of water ingested in food and fluids?

A

2300 mL

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59
Q

Amount of water leaves the body in feces.

A

Only 50 to 200 mL

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60
Q

What can interrupt recycling mechanism?

A

Severe vomiting or diarrhea

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61
Q

Affects fluid and electrolyte balance of body

A

Severe vomiting or diarrhea

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62
Q

Neuroendocrine cells of G.I. tract type of cells

A

Enterochromaffin Cells

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63
Q

What does the enterochromaffin cells do?

A

Use tryptophan hydroxylase-1 to synthesize Serotonin (5-HT)

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64
Q

Serotonin does what?

A

Stimulates secretory, peristaltic and vagal reflexes

via 5-HT3 receptor

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65
Q

Role of 5HT3 receptor ?

A

Important in generating nausea/vomiting

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66
Q

What is the mechanism of Ondansetron (Zofran) ? What other herbal is considered like zofran

A

5-HT 3 receptor antagonist

• (Ginger)

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67
Q

Neuroendocrine cells of G.I. tract

Just like the Enterochromaffin cells

A

Enterochromaffin-like cells (ECL)

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68
Q

Where are the ECL found?

A

Only in the stomach wall

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69
Q

Does ECL contain 5-HT?

A

NO

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70
Q

ECL responds to

A

Respond to Gastrin from G-cells
• Release Histamine –> stimulates parietal cells–>
via H2 receptors –> Increase HCl production

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71
Q

Action of H2 blockers?

A

H2 blockers inhibit HCl pathway leading to decrease gastric secretions

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72
Q

May be signs of digestive disorders or other

conditions elsewhere in the body (PUSMEPO)

A 
– Pain
– Uremia
– Systemic infection
– Motion sickness
– Emotional responses
– Pressure in the brain
– Overindulgence of food, drugs
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73
Q

Common manifestations of Digestive System Disorders

A

Anorexia, Nausea, Vomiting

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74
Q

Anorexia and vomiting

– Can cause serious complications such as (MAD)

A

• Dehydration, acidosis, malnutrition

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75
Q

Anorexia

– Often precedes

A

nausea and vomiting

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76
Q

– Unpleasant subjective feeling
– Also stimulated by smells, visual images, pain, and
chemical toxins and/or drug

A

Nausea

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77
Q

Nausea is Stimulated by IDI

A

irritation,distention, inflammation of digestive tract

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78
Q

Vomiting :Vomiting center located in the______

A

medulla

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79
Q

Role of vomiting center in the medulla?

A
  • Coordinates activities involved in vomiting

* Protects airway during vomiting

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80
Q

Vomiting Forceful expulsion from stomach

• Sometimes includes ____

A

bile from intestine

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81
Q

Vomiting Center Activation DSRPV

A

Distention or irritation in digestive tract
Stimuli from various parts of the brain
Response to unpleasant sights or smells, ischemia
Pain or stress
Vestibular apparatus of inner ear (motion)

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82
Q

Vomiting Center activation and Increased ICP

A

Increased intracranial pressure

– Sudden projectile vomiting without previous nausea

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83
Q

Stimulation of chemoreceptor trigger zone By

A

drugs, toxins, chemicals

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84
Q

Vomiting Reflex Activities : Deep inspiration

A
  • Deep inspiration
  • Closing glottis, raising the soft palate
  • Ceasing respiration: Minimizes risk of aspiration of vomitus into lungs
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85
Q

Vomiting Reflex Activities : Relaxes

A

• Relaxing the gastroesophageal sphincter
• Contracting the abdominal muscles
– Forces gastric contents upward
• Reverse peristaltic waves
– Promotes expulsion of stomach contents

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86
Q

Characteristics of Vomitus

• Hematemesis

A

“Coffee grounds” – brown granular material indicates action of HCl on hemoglobin

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87
Q

Characteristics of Vomitus– Frank blood –

A

acute esophageal or gastric Hemorrhage

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88
Q

Characteristics of Vomitus– Yellow or green vomitus

A

– Bile from the duodenum

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89
Q

Characteristics of Vomitus: Deeper brown color

– May indicate

A

content from lower intestine

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90
Q

Recurrent vomiting of undigested food

A

– Problem with gastric emptying or infection

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91
Q

Diarrhea

A

Excessive frequency of stools – loose or watery consistency

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92
Q

Diarrhea May be accompanied by

A

cramping pain

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93
Q

• Prolonged diarrhea may lead to DEMAW

A

dehydration, electrolyte imbalance,malnutrition, acidosis, weight loss

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94
Q

Common Types of Diarrhea
• Large-volume diarrhea (secretory or osmotic)
LOW

A

– Limited reabsorption due to reversal of normal carriers for sodium and/or glucose
– Often related to infection
– Watery stool resulting from increased secretions into
intestine from the plasma

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95
Q

Small-volume diarrhea (DSM)

A

– Due to inflammatory bowel disease
– Stool may contain blood, mucus, pus
– May be accompanied by abdominal cramps and tenesmus (recurrent inclination to evacuate the bowel)

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96
Q

Common Types of Diarrhea: Steatorrhea

A

“fatty diarrhea”Frequent bulky, greasy, loose stools

Foul odor

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97
Q

Steatorrhea, Characteristic of malabsorption syndromes

A

• i.e., celiac disease or cystic fibrosis

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98
Q

Cystic and celiac first affected

A

Fat usually the first dietary component affected
• Presence interferes with digestion of other
nutrients. Abdomen often distended

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99
Q

GI bleeding – Upper GI bleeding

A

• Esophagus, stomach, or duodenum

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100
Q

Lower GI bleeding is______ and involves bleeding from the

A

Below the ligament of Treitz: bleeding from the

jejunum, ileum, colon, or rectum

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101
Q

4 signs of UPPER/LOWER GIB

A

– Hematemesis
– Hematochezia
– Occult bleeding
– Melena

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102
Q

Hematochezia; What is it?

A

• Red blood – usually from lesions in rectum or anal canal

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103
Q

Occult blood

A
  • Small hidden amounts, detectable with stool test

* May be caused by small bleeding ulcers

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104
Q

Melena

A
  • Dark-colored, tarry stool

* from significant bleeding in upper GI tract

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105
Q

Constipation may be due to

A

May be due to decreased peristalsis – Increases time for reabsorption of fluids

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106
Q

Effects of Chronic constipation (HAD)

A

may cause hemorrhoids, anal fissures, or diverticulitis.

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107
Q

Main Cause of Constipation

A

• Weakness of smooth muscle due to age or

illness

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108
Q

Other Causes of constipation

FINDOS

A
  • ↓ dietary fiber
  • ↓ fluid intake
  • Failure to respond to defecation reflex
  • Immobility
  • Neurologic disorders
  • Drugs (i.e., opiates)
  • Some antacids, iron supplements
  • Obstructions caused by tumors or strictures
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109
Q

Constipation Fiber and water

A
  • ↓ dietary fiber

* ↓ fluid intake

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110
Q

Common complications of GI tract disorders.

A

Dehydration and hypovolemia

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111
Q

• Electrolytes and N/V/D

A

Lost in vomiting and diarrhea

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112
Q

Acid-base imbalances

– Metabolic alkalosis

A

loss of HCl w/ vomiting

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113
Q

Severe vomiting causes a change to_____

A

Metabolic acidosis

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114
Q

Why do you have metabolic acidosis?

A

Severe vomiting causes a change to metabolic acidosis due to the loss of bicarbonate of duodenal secretions.
• Diarrhea causes loss of bicarbonate.

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115
Q

3 types of Abdominal Pain

A
  • Visceral
  • Somatic
  • Referred
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116
Q

Visceral Pain are

A

Burning Sensation
Dull, aching pain
Cramping or diffuse pain
Colicky often severe pain

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117
Q

Visceral Pain : Burning sensation associated with

A

Inflammation and ulceration in upper GI tract

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118
Q

Visceral Pain: Dull, aching pain is

A

Typical result of stretching of liver capsule

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119
Q

Visceral Pain: Cramping or diffuse pain

A

– Inflammation, distention, stretching of intestines

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120
Q

Visceral Pain: Colicky, often severe pain –

A

Recurrent sooth muscle spasms or contraction

• Response to severe inflammation or obstruction

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121
Q

Somatic pain receptors directly linked to

A

spinal nerves

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122
Q

Somatic pain may cause

A

May cause reflex spasm of overlying abdominal

muscles

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123
Q

Somatic pain characteristics

A

Steady, intense, often well-localized pain

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124
Q

What is rebound tenderness?

A

“Rebound tenderness” – over area of involvement / inflammation of peritoneum

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125
Q

What is referred pain?

A

• Pain perceived at a site different from origin.

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126
Q

Referred pain results when

A

when visceral and somatic nerves converge at one spinal cord level.

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127
Q

Types of Malnutrition

A

Malnutrition

• May be limited to a specific nutrient or general limited

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128
Q

Limited malnutrition

A

Vitamin B12 deficiency = pernicious anemia

– Iron deficiency = iron deficient anemia

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129
Q

Generalized malnutrition

A

Chronic anorexia, vomiting, diarrhea

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130
Q

Malnutrition: Other systemic causes

A
  • IBS
  • Cancer tx
  • Cachexia
  • Limited availability of food
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131
Q

Basic Diagnostic Tests

•

A

Radiographs: With or w/o Contrast
• Ultrasound: May show unusual masses
• CT scans
• MRI
• CT and MRI may use radioactive tracers.
– Can be used for liver and pancreatic abnormalities

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132
Q

Use for liver and pancreatic abnormalities

A

CT and MRI

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133
Q

Diagnostic tests using

A

Radioactive tracers

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134
Q

Basic Diagnostic Tests UPPER GI

A

• Endoscopy for upper GI

– Biopsy may be done

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135
Q

Sigmoid & colonoscopy can do

A

– Biopsy and removal removal of polyps

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136
Q

Laboratory analysis of stool specimens

A

Check for infection, parasites / ova, bleeding, tumors,

malabsorption

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137
Q

Blood tests for GI

A

– LFT, pancreatic function, cancer markers

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138
Q

Common Therapies

• Dietary modifications (GFR)

A

– e.g., gluten-free diet (celiac disease)
– Reduced intake of alcohol and coffee
– ↑ fiber and fluid intake

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139
Q

GI disorders; Stress reduction why?

A

– Stress impairs immune function and tissue healing

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140
Q

Drugs For GI disorders

A 
Antacids
Antiemetics
Laxatives or enemas
Antidiarrheals
Sulfasalazine
ABX
Sulcrafate
Anticholinergics
H2 Blockers
PPIs
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141
Q

Role of antacids?

A

– To relieve pyrosis

142
Q

Role of Antiemetics

A

– To relieve vomiting

143
Q

Role of Laxatives or enemas

A

– Treatment of acute constipation

144
Q

Role of Antidiarrheals

A

– Reduction of peristalsis

– Relieve cramps

145
Q

Sulfasalazine action

A

– Anti-inflammatory and antibacterial

– For acute episodes of inflammatory bowel disease

146
Q

ABX action

- Clarithromycin or azithromycin

A

– Effective against Heliobacter pylori infection

• Usually combined with a proton pump inhibitor

147
Q

Sucralfate action

A

– Coating agent
– Enhance gastric mucosal barrier against irritants
such as NSAIDs

148
Q

Anticholinergic drugs action

A

– Reduce secretions &motility

149
Q

H-2 blockers action

A

– Useful in gastric reflux

150
Q

PPIs action

A

– Reduce gastric secretion

151
Q

Congenital abnormalities: Cleft lip and cleft palate

A

High risk of aspirating fluid into respiratory passages

152
Q

Cleft lip and palate implications

A

May require intubation with RAE endotracheal tube for

surgical repair

153
Q

Disorders of the Oral Cavity Inflammatory lesions: aphthous ulcers USS

A

– Streptococcus sanguies may be involved
– Small, painful lesions
– Usually heal spontaneously

154
Q

Candidiasis
– May appear as red, swollen areas
– May be irregular patches of a white curdlike material

A

– Oral candidiasis (thrush)

155
Q

People at risk of developing oral candidiasis (3)

PID

A
  • People receiving broad-spectrum antibiotics
  • Immunocompromised individuals or persons with diabetes
  • During and after cancer therapy
156
Q

May appears as red, swollen areas

A

Oral Candidiasis

157
Q

– May be irregular patches of a white curdlike material

A

Oral Candidiasis

158
Q

Herpes simplex type 1 infection
– Herpes simplex virus type 1 (HSV-1)
– Transmitted by

A

close contact

159
Q

HSV-1 Virus

A

remains dormant in sensory ganglion

160
Q

HSV-1 Virus

A

– Activated by stress, trauma, other infection

161
Q

HSV-1 virus results in the Formation of

A

blister, ulcers, clear fluid release – contains virus. Acute stage may be alleviated by antiviral medication.

162
Q

When HSV-1 may spread to

A

– May spread to eyes

• Conjunctivitis and keratitis

163
Q

Syphilis: when is it contagious

A

– Highly contagious during first and second

stages

164
Q

Syphillis; Primary stage

A
  • Chancre, a painless ulcer on tongue, lip, palate

* Heals spontaneously (1 or 2 weeks)

165
Q

Syphillis: Secondary stage

A

Red macules or papules on palate – highly infectious
• Heals spontaneously
– Both stages treated with long-acting penicillin

166
Q

Syphillis: Tertiary stage

A

• Infects CNS

167
Q

Caries : what is the initiating microbe? and what follows

A

– Streptococcus mutans – – Lactobacillus follows in large numbers

168
Q

With CARIES

A

– Bacteria break down sugars and produce large

quantities of lactic acid –>Lactic acid dissolves mineral in tooth enamel–> Tooth erosion and caries formation

169
Q

What is Caries promoted by?

A

frequent intake of sugars and acids

170
Q

Anti-caries treatment

A

– Fluoride –

171
Q

Gingivitis: Changes in the gingivae may be a______and what is it ?
• Creates extensive grooving on tooth surface
• Increase plaque retention and damage to gingivae

A

local or systemic problem

– Inflammation of the gingiva

172
Q

In gingivitis, Tissue becomes becomes

A

red, soft, swollen, bleeds easily

173
Q

Gingivitis, May be a result from

A

– accumulated plaque
– Toothbrush trauma
– Inadequate oral hygiene

174
Q

• Results from improper or excessive brushing

A

Gingivitis

175
Q

Periodontal disease is a

A

– Infection and damage to the periodontal ligament

and bone

176
Q

Peridontal disease Predisposing condition is

A

gingivitis.

177
Q

Peridontal disease caused by _________as a result of __________causing ________

A

– Caused by microorganisms as a result of poor
dental hygiene
– Subsequent loss of teeth possible

178
Q

Peridontal have several________ what is it aggravated by?

A

– Several categories depending on degree of disease
– May be aggravated by systemic disease and
medications that reduce salivary secretions

179
Q

Periodontitis occurs when_________and as a result

•

A

organisms enter the gingival blood vessels and travel to the connective tissues and bone of the dental
arch.• Resorption of bone and loss of ligament fibers
result in weakened attachment of teeth.

180
Q

May result in total loss of tooth from socket

A

Peridontitis

181
Q

Treatment of Peridontitis (ALI)

A

• Treated by
Antimicrobials
local surgery of gingiva, and
Improved dental hygiene

182
Q

Disorders of the Oral Cavity: Hyperkeratosis – ex. Leukoplakia – What is it?

A

Whitish plaque or epidermal thickening of mucosa

183
Q

Hyperkeratosis : is related to :

A

– related to smoking /chronic irritation
– Epithelial dysplasia beneath plaque may develop
into squamous cell carcinoma.

184
Q

Can also occur on vocal cords

A

Hyperkeratosis

185
Q

Squamous cell carcinoma

• Often develops when (age)

A

after 40

186
Q

Squamous cell carcinoma causes

A

– Smokers, preexisting leukoplakia, alcohol abuse

– Multiple lesions possible

187
Q

Squamous cell carcinoma affect the

A

– Floor of the mouth, lateral lateral borders of the borders of the tongue

188
Q

• Kaposi sarcoma in patients with

A

AIDS

189
Q

Has better prognosis.

A

• Lip cancer

190
Q

Lip cancer is common

A

– Common in smokers, particularly pipe smokers

191
Q

Sialadenitis

•

A

– Inflammation of the salivary glands
– May be infectious or noninfectious
– Most commonly affected is parotid gland

192
Q

What is Mumps? It is a ______infection

A

infectious parotitis; – Viral infection

193
Q

Noninfectious parotitis, occurs in

A

– Often in older adults who lack adequate fluid

intake and mouth care

194
Q

DysphaSia

A

Inability to speak

195
Q

DysphaGIA

A

Difficulty swallowing

196
Q

Causes of DysphaGIA

A

Causes:
– Neurologic deficit
– Muscular disorder
– Mechanical obstruction

197
Q

Presentation of DYSPHAGIA

A

Results/presentation
– Pain with swallowing
– Inability to swallow larger pieces of solid material
– Difficulty swallowing liquids

198
Q

Dysphagia –>Neurologic deficit from: – SIBA

A

– Stroke
– Infection
– Brain damage
– Achalasia

199
Q

DysphaGIA is a failure of the

A

Failure of the lower esophageal sphincter to relax

due to lack of innervation

200
Q

DYSPHAGIA- Muscular disorder –

A

Impairment from muscular dystrophy

201
Q

Dysphagia

• Mechanical obstruction: Congenital Atresia

A

Congenital atresia
• Developmental anomaly
• Upper and lower esophageal segments are separated –

202
Q

What is Stenosis?
May be ____or _____
May be secondary to CUFR

A

• Narrowing of the esophagus
• May be developmental or acquired
• May be secondary to chronic inflammation,
ulceration, radiation therapy, fibrosis,

203
Q

• Stenosis or stricture may also result from ? and may requ9ired

A
  • from scar tissue.
    • May require treatment with repeated mechanical
    dilation
204
Q

Dysphagia
• Mechanical obstruction (Cont’d) – Esophageal diverticula
What is it?
It is ______or _________ following ______
What does it cause?

A
  • Outpouchings of the esophageal wall
  • Congenital or acquired following inflammation
  • Causes irritation, inflammation, scar tissue
205
Q

Dysphagia ESOPHAGEAL DIVERTICULA Signs include

DFCCH

A

dysphagia, foul breath, chronic cough, hoarseness –

206
Q

Dysphagia: Mechanical Obstruction : Tumors

A

• May be internal or external

207
Q

Scar tissue contract associated with

A

Fibrosis

208
Q

Tumor associated with

A

Compression

209
Q

What happens with Diverticulum?

A

Undigested food in pouch obstructs esophagus

210
Q

Fistula can

A

complicates airway

211
Q

Fistula is a developmental

A

Defect connection between esophagus and trachea

212
Q

Congenigal Tracheoesophagus FISTULA

A

Dilation may cause airway impingement

213
Q

What happens in TEF

A

Loss of peristalsis in lower esophagus

Food collection in lower esophagus

214
Q

Esophageal Cancer: What is it? and where does it commonly occur?

A
  • Primarily squamous cell carcinoma

* Most commonly in distal esophagus

215
Q

• Significant dysphagia in later stages in this cancer

A

Esophageal CA

216
Q

Esophageal CA prognosis

A

• Poor prognosis due to late manifestations

217
Q

Esophageal CA: Associated with chronic irritation due to

CAHA

A

– Chronic esophagitis
– Achalasia
– Hiatal hernia
– Alcohol abuse, smoking

218
Q

Hiatal Hernia: What is it?

A

Part of the stomach protrudes into the thoracic cavity.

219
Q

What is a Sliding hernia?

A

– More common type
– Portion and part of stomach and gastroesophageal
junction slide up above the diaphragm

220
Q

• Rolling or paraesophageal hernia –

A

Part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm and may become trapped.

221
Q

Which hernia is the most common type

A

Sliding hernia

222
Q

Paraesophageal hernia is associated with

A

Sac and peritoneum in mediastinum

223
Q

Sliding hiatal hernia

A

Part of the fundus above diaphragm

224
Q

Hiatal Hernia- Food may_________ causes __________

reflux of ___________may cause ?

A

may lodge in pouch of the hernia – Causes inflammation of the mucosa – Reflux of food up the esophagus from hernia – May cause chronic esophagitis

225
Q

What are the Signs of Hiatal hernia?

SIFH

A

– Substernal pain that may radiate to shoulder and jaw
– Increased discomfort when laying down
– Frequent belching
– Heartburn or pyrosis

226
Q

GERD: What occurs with GERD?

A

• reflux of gastric contents into esophagus causing erosion and inflammation

227
Q

Where is GERD Seen and what does the severity depends on?

A
  • Often seen in conjunction with hiatal hernia

* Severity depends on competence of the LES

228
Q

Causes of GERD : What may be a factor and how does medication help?

A
  • Delayed gastric emptying may be a factor.

* Use of medication may reduce reflux and inflammation.

229
Q

GERD

• Anesthesia concerns:

A

Aspiration

230
Q

Possible related respiratory concerns with GERD:

A

• Laryngitis
• Asthma (50% of pt.s have endoscopic evidence of
esophagitis)
• Recurrent pneumonia

231
Q

Gastritis – Acute

A
  • Gastric mucosa is inflamed.

* May be ulcerated and bleeding

232
Q

Gastritis is Caused by:

ISIA RIE

A 
– Infection by microorganisms
– Spicy or irritating foods
– Ingestion of corrosive or toxic substances 
– Allergies to foods 
– Radiation or chemotherapy
– Ingestion of aspirin or other NSAIDs 
– Excessive alcohol intake
233
Q

Gastritis – Acute

• Basic signs (AIHE)

A

–Anorexia, nausea, vomiting may develop
– Infection, diarrhea may develop.
– Hematemesis due to bleeding
– Epigastric pain, cramps or general discomfort

234
Q

Gastritis is usually UCS

A

Usually self-limiting:
– Complete regeneration of gastric mucosa 1-2 days
– Supportive treatment with prolonged vomiting – (May require treatment with antimicrobial drugs)

235
Q 
Gastritis – Chronic
Characterized by \_\_\_\_\_
loss of \_\_\_\_\_\_\_
Reduced production of \_\_\_\_\_\_\_\_
Often present is
A

• Characterized by atrophy of stomach mucosa
– Loss of secretory glands
– Reduced production of intrinsic factor
– H. pylori infection is often present.

236
Q

Gastritis – Chronic signs

A

Signs may be vague.
– Mild epigastric discomfort, anorexia, intolerance
for certain foods

237
Q

Risk associated with Gastritis - Chronic

A

Increased risk of peptic ulcers and gastric
carcinoma
• (Certain autoimmune disorders are associated
with one type of chronic gastric atrophy.)

238
Q

Gastroenteritis MIU

A

• Inflammation of stomach and intestine
• Usually caused by infection
• May also be caused by allergic reactions to food or
drugs

239
Q

Gastroenteritis microbes

A

• Microbes can be transmitted by fecally contaminated

food, soil, and/or water

240
Q

Gastroenteritis most infections are

A

Self limiting

241
Q

Essential for prevention of gastroenteritis

A

– Safe sanitation essential for prevention.

242
Q

Peptic Ulcers – Gastric & Duodenal

Most are due to

A

• Most are due to H. pylori infection.

243
Q

Peptic ulcers - Occur most commonly

Found in

A

Occur most commonly in the proximal duodenum

• Also found in the antrum of the stomach

244
Q

Peptic Ulcers- GASTRIC and DUODENAL: development

A

Development begins with breakdown of mucosal barrier. –

245
Q

What is the predominant factor in duodenal ulcers?

A

Increased acid secretion

246
Q

What is More common in gastric ulcer development?

A

Decreased mucosal defense

247
Q

Peptic Ulcers – Gastric & Duodenal PATHO
Damage to __________Predisposes to___________ and is associated with
IEUA

A

• Damage to mucosal barrier predisposes to
development of ulcers and is associated with – Inadequate blood supply
Excessive Glucocorticoids(secretion or medication)
Ulcerogenic substances break down mucus layer (ASA, NSAIDS, alcohol)
Atrophy of gastric mucosa (chronic gastritis)

248
Q

Damage to mucosal barrier predisposes to development of ulcers is associated with Inadequate blood supply, how?

A

Caused by vasoconstriction (by stress, smoking, shock;

circulatory impairment in older adults; scar tissue; anemia)

249
Q

Peptic Ulcers – Gastric & Duodenal

• Also caused by increases in: VAG - SIR

A

– *acid-pepsin secretion (alcohol, caffeine)
– *gastrin secretion
– *vagal stimulation
– sensitivity to vagal stimuli
– Increased number of acid-pepsin secretory
cells in the stomach (genetic anomaly)
– Rapid gastric emptying

250
Q

Peptic Ulcers – Gastric & Duodenal

• Complications: Hemorrhage (MCD)

A
  • Due to erosion of blood vessels
  • Common complication
  • May be the first sign of a peptic ulcer
251
Q

Peptic Ulcers – Gastric & Duodenal

• Complications: Perforation (CUR)

A
  • Chyme can enter the peritoneal cavity
  • Ulcer erodes completely through the wall.
  • Results in chemical peritonitis
252
Q

Peptic Ulcers – Gastric & Duodenal

• Complications: Obstruction

A

• May result later due to the formation of scar tissue

253
Q

Peptic Ulcers – Gastric & Duodenal

Signs and symptoms:

A

Epigastric burning or localized pain usually following

stomach emptying

254
Q

Peptic Ulcers – Gastric & Duodenal-> Diagnostic tests:

A

– Fiberoptic endoscopy
– Barium x-ray
– biopsy

255
Q

Peptic Ulcers – Gastric & Duodenal; TREATMENT

A

– Combination of antimicrobial & PPI to eliminate H. pylori

256
Q

Stress Ulcers

• Associated with (SBH)

A

– Severe trauma or systemic problems
– Burns, head injury
– Hemorrhage or sepsis

257
Q

Stress ulcer associated with (RMF)

A

– Rapid onset
– Multiple ulcers (usually gastric) may form within hours of precipitating event
– First indicator – hemorrhage and severe pain

258
Q

Gastric Cancer: Arises primarily in________

• Mostly in_________

A

mucous glands

antrum or pyloric area

259
Q

Gastric Cancer: Early carcinoma –

A

Confined to mucosa & submucosa

260
Q

Gastric Cancer• Later stages –

A

Involves muscularis – Eventually invades serosa and spreads to lymph nodes

261
Q

Gastric Cancer : Early stages and prognosis

A

Asymptomatic in the early stages – prognosis often poor

262
Q

Gastric Cancer Key contributing factors

A

• Diet seems to be a key factor particularly
smoked foods, nitrites, and nitrates.
• Genetic influences play a role, too.

263
Q

Gastric Cancer : Symptoms

A

Symptoms vague until cancer is cancer is advanced which IS THE REASON for late diagnosis

264
Q

GASTRIC cancer Tx or therapy and survival

A

Surgery together with chemotherapy and

radiation may relieve symptoms. – Survival rate < 20%

265
Q

What is Dumping syndrome and when does it develop?

A
  • Can develop after gastric surgery.

* Control of emptying lost and gastric contents are “dumped” into the duodenum without complete digestion.

266
Q

Pathophysiology of Dumping Syndrome

A

Hyperosmolar chyme draws fluid from vascular compartment into intestine.
– Intestinal distention
– Increased intestinal motility

267
Q

Signs and symptoms of Dumping Syndrome

A

– Hypotension, Tachycardia, Diaphoresis, Pallor

268
Q

Dumping Syndrome when does it occur? Other symptoms

A

• Occurs during or shortly after meals

– Abdominal cramps, nausea, diarrhea

269
Q

Dumping and glucose and how it may be resolved

A

• Hypoglycemia 2 to 3 hours after meal:
– High glucose levels in chyme stimulate
increased insulin secretion → hypoglycemia
• May be resolved by dietary changes

270
Q

How to prevent Dumping syndrome? and when does it resolve.?

A

– Frequent small meals – high in protein, low in simple carbohydrates
• Often resolves over time

271
Q

Pyloric Stenosis: what is it?
•
• Surgery often required.
• May be acquired later in life – Persistent feeling of fullness – Increased incidence of vomiting

A

Narrowing and obstruction of pyloric sphincter

• developmental anomaly

272
Q

Pyloric Stenosis Signs appear within –

A

several weeks after birth.

273
Q

Primary signs of Pyloric Stenosis (PIF)

A

– Projectile vomiting immediately after feeding
– Infant fails to gain weight ,dehydration, persistent hunger
– Firm mass can be palpated at pylorus.

274
Q

Acute Pancreatitis

A

• Inflammation of the pancreas
– Results in auto-digestion of the tissue
• May be acute or chronic

275
Q

Pancreatitis emergent?

A

Acute form is considered a medical emergency

276
Q

Pancreatitis Pathophysiology

A

– Pancreas lacks a fibrous capsule
– Destruction may progress into tissue surrounding the
pancreas
– Substances released by necrotic tissue lead to
widespread inflammation

277
Q

Acute Pancreatitis untreated can lead to

A

– Hypovolemia and circulatory collapse may follow

278
Q

Acute Pancreatitis complications

CAGS

A

• Chemical peritonitis results in bacterial peritonitis
– Septicemia may result
**– Adult respiratory distress syndrome and acute renal
failure occur in 25% of patients
**– GI hemorrhage & DIC may also occur

279
Q

Etiology of Pancreatitis is (GAS)

A

– Gallstones
– Alcohol abuse
– Sudden onset may follow intake of a large meal or a
large amount of alcohol

280
Q

Acute Pancreatitis – PRIMARY Signs and Symptoms

A
  • Severe epigastric or abdominal pain radiating to the back – primary symptoms
  • Signs of shock due to hypovolemia
281
Q

Acute pancreatitis and fever

A

• Low-grade fever until infection develops

– Then body temperature may rise significantly

282
Q

Abdominal assessment with Acute pancreatitis

A

• Abdominal distention and decreased bowel sounds

– Decreased peristalsis and paralytic ileus

283
Q

Acute Pancreatitis SSHL

• Diagnostic tests

A

– Serum amylase: first rise, then fall after 48 hours
– Serum lipid levels elevated
– Hypocalcemia (pancreatic lipase chelates Ca++)
– Leukocytosis

284
Q

Treatment of Acute Pancreatitis (OTA)

A

– Oral intake is stopped.
– Treatment of shock and electrolyte imbalances
– Analgesics for pain relief

285
Q

Pancreatic Cancer

• Risk factors

A

– Smoking

– Pancreatitis and dietary factors

286
Q

Pancreatic CA: Adenocarcinoma

A

– most common form

– Arises from the epithelial cells in the ducts

287
Q

Pancreatic Cancer : Signs and symptoms
Early manifestations?
What occur early?

A
  • Weight loss and jaundice early manifestations
  • Frequently asymptomatic until well advanced
  • Metastases occur early.
288
Q

Pancreatic Cancer mortality

A

– Mortality is close to 95%.

289
Q

Gastrinoma: What it it and what does it cause?

A
  • Gastrin secreting tumor in Pancreas or Duodenum

* Causes gastric hypersecretion.

290
Q

Gastrinoma and Anesthesia considerations.

A

– Large volumes of gastric fluid usually present at
time of anesthesia induction = ↑risk of reflux /aspiration.
– Profuse watery diarrhea = hypokalemia & metabolic
alkalosis.

291
Q

Useful medication for preventing acid hypersecretion

A 
IV ranitidine (H2 blocker) useful for preventing acid
hypersecretion intra-op.
292
Q

Celiac Disease: what is it? What is it primarily?

A

Malabsorption syndrome
• Primarily a childhood disorder
– May occur in middle age adults

293
Q

Celiac disease Pathophysiology DPCM

A 
• genetic link
• Defect in intestinal enzyme
– Prevents digestion of gluten
– Causes atrophy of villi
• Malabsorption and malnutrition result.
294
Q

Celiac Disease

• First signs appear

A

about 4 - 6 months of age (with

addition of cereals to newborn’s diet)

295
Q

Celiac disease: Manifestation –

A

Steatorrhea , muscle wasting wasting, failure to gain weight

– Irritability and malaise common

296
Q

Celiac disease:

Dx and Tx

A
  • Diagnosed by a series of blood tests

* Treatment: Gluten-free diet – Intestinal mucosa returns to normal after a few weeks without gluten intake.

297
Q

IBD - Inflammatory Bowel Disease: what are they ? what is the _________.

A

• Crohn disease & Ulcerative Colitis

Exact cause unknown.• Genetic factors involved

298
Q

• Crohn disease vs UC age of manifestation

A

often during adolescence

• Ulcerative colitis – 20s to 30s

299
Q

Crohn Disease area affected

•

A

• May affect any area of the digestive tract – Most frequently the small intestine

300
Q

Cronh’s disease Inflammation occurs in

A

in characteristic distribution. – “Skip lesions lesions” – affected areas separated by areas of normal tissue

301
Q

Croh’s disease with progressive PDI

A

– Progressive inflammation and fibrosis may cause obstructed areas.
– Damaged walls impair processing and absorption of food.
– Inflammation stimulates intestinal motility

302
Q

Crohn Disease there is interference with: HAMP

A 
Digestion and absorption leading to 
Hypoproteinemia,
Avitaminosis
Malnutrition
Possibly steatorrhea
303
Q

Crohn’ s: Other complications, Children and treatment

A

Adhesions between loops may form and fistulas may develop.
• Children – Delayed growth
• Treatment: Glucocorticoids

304
Q

Ulcerative Colitis: inflammation

A

• Inflammation starts in the rectum
• Progresses through the colon
• Mucosa and submucosa are inflamed.
– Tissue destruction destruction interferes interferes with absorption of fluid and electrolytes in the colon.

305
Q

UC and diarrhea

A

Severe acute episodes – toxic megacolon may develop
• Diarrhea marked with up to 12 stools per day.
– Contains blood and mucus
– Accompanied by cramping pain

306
Q

Treatment of IBD

A

Anti-inflammatory medications
– Sulfasalazine or glucocorticoids
• Antimotility agents: Nutritional supplements
• Antimicrobials: Immunotherapeutic agents

307
Q

IBD surgical resection

A

Surgical resection

– Usually ileostomy or colostomy

308
Q

What is appendicitis? Pathophysiology OFIA

A

Obstruction by fecalith, gallstone, or foreign material
Fluid builds up inside the appendix – Microorganisms proliferate
Ischemia and necrosis of the wall – Results in increased permeability
Appendix wall becomes inflamed – Purulent exudate forms – Appendix is swollen.

309
Q

Appendicitis and peritonitis

A

Bacteria and toxins escape into surroundings. – Leads to abscess formation or localized bacterial peritonitis

310
Q

Appendicitis when does it Abscess develop?

A

may develop when inflamed area is walled off. – Inflammation and pain may temporarily subside.
• Localized infection or peritonitis develops
around the appendix. – May spread along the peritoneal membranes

311
Q

Appendicitis

Pathophysiology

A
  • Increased necrosis and gangrene in the wall – Due to increasing pressure within the appendix
  • Appendix ruptures or perforates – Release of contents into peritoneal cavity – Generalized peritonitis
  • May be life-threatening
312
Q

Treatment of Appendicits

A

Treatment – Surgical removal of appendix and

antimicrobial drugs

313
Q

Appendicitis – Signs and Symptoms

A

• General periumbilical pain
• Nausea and vomiting common
• Pain becomes severe and localized in LRQ.
• LRQ rebound tenderness develops.
– Involvement of parietal peritoneum over
appendix

314
Q

Appendicitis – Signs and Symptoms

• After rupture

A

– Pain subsides temporarily.
• Pain recurs – severe generalized abdominal pain and guarding
• Low grade fever and leukocytosis
– Development of inflammation

315
Q

Appendicitis: Peritonitis “______”

A

Boardlike; abdomen, tachycardia, hypotension
– As peritonitis develops, abdominal wall muscles
spasm.
– Toxins lead to reduced blood pressure.

316
Q

Diverticulum

A

– Outpouching (herniation) of the mucosa

through the muscular layer of the colon

317
Q

• Diverticulosis

A

– Asymptomatic

318
Q

• Diverticulitis

A

– Inflammation

319
Q

Diverticular Disease
Form
Congenital
weaker areas

A

• Form at gaps between muscle layers
• Congenital weakness of wall may be a factor.
Weaker areas bulge when pressure increases.
• Many cases are asymptomatic.

320
Q

Diverticula disease symptoms

A

– Cramping, tenderness, nausea, vomiting

– Slight fever and elevated white blood cell count

321
Q

In diverticula stasis

A

• stasis of material in diverticula leads to inflammation and
infection.

322
Q

• Treatment of diverticulitis

A

– ABX

– Dietary modifications to prevent stasis

323
Q

Initial signs of Colorectal Cancer depend

A

largely on the location of the growth.

324
Q

Colorectal Cancer Treatment

A

– Surgical removal with radiation and/or chemotherapy

325
Q

General signs of Colorectal Cancer

A

– Fatigue, weight loss, anemia
– Change in bowel habits
• Alternating diarrhea and constipation
– Bleeding

326
Q

What is intestinal Obstruction? Where is more common?

A

• Lack of movement of intestinal contents

– More common in small intestine

327
Q

What are the Mechanical obstructions?

A

– tumors, adhesions, hernias, other tangible obstructions

328
Q

Functional obstructions

A

– impaired peristalsis

329
Q

Disease associated with Functional obstructions

A
  • Spinal cord injury

* Paralytic ileus due to toxins or electrolyte imbalance

330
Q

Intestinal Obstruction

•

A

• Gases and fluids accumulate proximal to blockage, distending the intestine.
• Increasingly strong contractions of proximal
intestine – Effort to move contents along

331
Q

When Pressure increases in lumen.

A

– More secretions enter the intestine.
– Compression of veins in wall
• Intestinal wall becomes edematous.
• Prevention of absorption

332
Q

Intestinal Obstruction leads to

A

• Intestinal distention leads to persistent vomiting.
– Additional loss of fluid and electrolytes
– Hypovolemia can result.

333
Q

During intestinal Obstruction, Intestinal wall becomes

A

ischemic wall becomes ischemic and necrotic

334
Q

During intestinal Obstruction If obstruction is not removed,

A

gangrene follows.
• Ischemia and necrosis → decreased innervation
and cessation of peristalsis
• Paralytic ileus occurs if it is not a cause to begin
with

335
Q

Intestinal Obstruction promotes

A

• Obstruction promotes rapid reproduction of
intestinal bacteria.
– Some produce endotoxins.
– Affected wall becomes necrotic and more
permeable.

336
Q

During intestinal obstruction– Bacteria and toxins

A

leak into peritoneal cavity (peritonitis) or into blood (bacteremia and septicemia).
• Perforation of the necrotic segment may occur.
– Generalized peritonitis and septic shock

337
Q

Intestinal Obstruction
• Functional obstructions (paralytic ileus) from:
MAS PITSH

A

– ***Mesenteric thrombosis (Dehydration in HHS)
– abdominal surgery
– Pancreatitis, peritonitis, infection in the abdominal
cavity
– Inflammation related to severe ischemia
– Toxemia
– spinal cord injury
– Hypokalemia

338
Q

Mechanical obstruction from:

MAH SIV HP

A 
– Masses – tumors or foreign bodies
– Adhesions that twist or constrict intestine
– Hernias
– Strictures from scar tissue
– Intussusception
– Volvulus
– Hirschsprung disease
– persimmons
339
Q

• Mechanical obstruction - small intestine signs and symptoms.

A

– Severe colicky abdominal pain

– Intermittent bowel sounds can be heard.

340
Q

Paralytic ileus Signs and symptoms

A

– Pain is steady.

– Bowel sounds decreased or absent

341
Q

Intestinal obstruction: Vomiting and abdominal distention

A

– Occurs quickly with obstruction of S.I.
– Vomiting is recurrent – eventually with bile-stained
content

342
Q

• Obstruction of the small intestine is

A

a medical emergency!

343
Q

Large Intestine Obstruction

– Develops slowly with mild signs such as:

A

– Constipation
– Mild abdominal pain, followed by abdominal distention
– Anorexia, vomiting, more severe pain

344
Q

• Treatment of Large Intestinal Obstruction

A

– Treatment of underlying cause
– Fluid and electrolyte replacement
– Surgery and antimicrobial therapy

345
Q

What is Peritonitis?

A

• Inflammation of the peritoneal membranes

346
Q

Chemical peritonitis may result from (CUBBE)

A 
– Chyme spilled from perforated ulcer 
– Urine leaking from ruptured bladder 
– Bile from ruptured gallbladder
– Blood – Any other foreign material in cavity
– Enzymes released with pancreatitis
347
Q

Peritonitis

• Bacterial peritonitis Develop by

A

– By direct trauma to intestine
– Ruptured appendix
– Intestinal obstruction and gangrene
– Any abdominal surgery – If foreign material is left or infection develops

348
Q

Peritonitis and women

A

Pelvic inflammatory disease in women

– When infection reaches the cavity through fallopian tubes

349
Q

Peritonitis Signs and symptoms

A

– Sudden, severe, generalized abdominal pain
– Localized tenderness at site of underlying problem
– Vomiting is common; abdominal distention
– Dehydration, hypovolemia, hypotension – Tachycardia, fever, and leukocytosis

350
Q

Treatment of Peritonitis (DAS)

A

– Depends on primary cause
– Aggressive ABX treatment – specific to causative organism
– Surgery may be required

SRNA3AdvancedPatho2 (15 decks)

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