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CV487 > Class 9: GI > Flashcards

Class 9: GI Flashcards

1
Q

Slide 6

A
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2
Q

Gastritis

A

-Acute or chronic inflammation of the stomach

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3
Q

Acute gastritis

A

-d/t local irritants
-Symptomatic or asymptomatic

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4
Q

Etiology of chronic gastritis

A

-H. pylori is most common
-Autoimmune & multifocal is least common but increases the risk of carcinoma
-Chemical from reflux of duodenal contents, pancreatic secretions, bile

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5
Q

Chronic gastritis can lead to…

A

Atrophy of the epithelium of the stomach

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6
Q

Pathophysiology of gastritis

A

-Occurs as a result of the breakdown of the normal gastric mucosal barrier
-Hydrochloric acid backflows into the mucosa
-Edema & disruption of capillary walls with loss of plasma into the gastric lumen… possible hemorrhage

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7
Q

Clinical manifestations of gastritis

A

-Anorexia, N/V, epigastric pain, feeling of fullness
-Hemorrhage with ETOH
-Self limiting, lasting from a few hours to days with complete healing

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8
Q

Clinical manifestations of chronic gastritis

A

-Patients lose intrinsic factor leading to cobalamin deficiency; changes in RBC production; anemia and neurological complications

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9
Q

Intrinsic factor

A

A substance secreted by gastric mucosa that is essential for absorption of cobalamin (vitamin B12)

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10
Q

Etiology of gastritis + drugs

A

-ASA, corticosteroids & NSAIDS

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11
Q

Etiology of gastritis + diet

A

Alcohol & spicy/irritating foods

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12
Q

Etiology of gastritis + microorganisms

A

-H. pylori, salmonella & staphylococcus organisms

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13
Q

Etiology of gastritis + environmental factors

A

-Radiation & smoking

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14
Q

Etiology of gastritis + pathophysiological conditions

A

-Burns, hiatal hernia, physiological stress, reflux, renal failure (uraemia), sepsis & shock

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15
Q

Etiology of gastritis + other factors

A

-Endoscopic procedures, nasogastric suction & psychological stress

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16
Q

Gastritis is that…

A

Gut feeling you get when you stay up all night & do not eat

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17
Q

Diet considerations in gastritis

A

Stomach lining needs to be coated, if they cannot eat then TF is initiated

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18
Q

GERD pathophysiology

A

Backflow regulated by the stomach sphincter; transient relaxation is common after meals (especially with fatty foods)

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19
Q

Most common clinical manifestation of GERD

A

Epigastric pain or heartburn, belching & chest pain

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20
Q

Other manifestations of GERD

A

-Respiratory symptoms: Wheezing, coughing, and dyspnea
-Otolaryngologic symptoms: Hoarseness, sore/lump in throat and choking

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21
Q

Differentiating between GERD & MI

A

-Give a pink lady (antacid)
-Trops

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22
Q

GERD assessment + neuro

A

Dysphagia & pain

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23
Q

GERD assessment + CV

A

Chest pain, tachycardia & aBP

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24
Q

GERD assessment + resp

A

Sore/lump in throat, hoarseness of cords, wheezing, coughing, dyspnea, crackles if aspiration pneumonia has occurred

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25
Q

GERD assessment + GI

A

Nutritional status, odynophagia (painful swallowing), heartburn, N/V & weight loss

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26
Q

Food..

A

Makes GERD feel better if pt is sitting up

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27
Q

Complication of GERD

A

Barret esophagus-scarring, edema & spasms (strictures)

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28
Q

PUD

A

-Group of disorders resulting from exposure of upper GI acid-pepsin secretions. Mostly duodenal and gastric; (duodenal much more common)
-Men 55-70 most commonly affected

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29
Q

Etiology of PUD

A

H. Pylori & NSAIDs

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30
Q

Pathophysiology of PUD

A

-Only develops in the presence of an acidity
-Mucosa barrier becomes impaired, and backflow of acid lead to PUD
-Affects all layers of mucosa and eventually penetrates through

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31
Q

Manifestations of PUD

A

-Pain usually on empty stomach; relieved by food or antacids
-Burning or cramping

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32
Q

Complications of PUD

A

Hemorrhage, gastric outlet obstruction (from edema, spasm or contraction of scar tissue), and perforation (which can lead to peritonitis)

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33
Q

In a true ulcer…`

A

A GI bleed develops

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34
Q

Gastric ulcers often leads to…

A

Duodenal ulcers

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35
Q

GERD leads to…

A

Duodenal ulcers

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36
Q

Ulcers can…

A

Develop into shock

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37
Q

Slide 18

A
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38
Q

GI bleed indications

A

Site of bleeding is indicated by colour and texture: bright red to tarry black (melena)

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39
Q

Upper GI bleeds..

A

Often coffee-ground material (partially digested) or bright red

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40
Q

Bright red vs dark red blood

A

Brighter red means bleeding closer to the source; darker means further from source (e.g. source is duodenum, which is high up, blood in stools will be dark; hemorrhoids often produce bright red blood)

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41
Q

Considerations when determining if it is an upper or lower GI bleed

A

May be hard to pinpoint source such as with hypermotility. Blood may be bright red even if source is high in GI tract

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42
Q

GI bleeds are…

A

An emergency

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43
Q

Slide 21

A
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44
Q

Slide 22

A
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45
Q

Urine output

A

-0.5-1cc/kg/hr
-If pt is not voiding it will lead to ketoacidosis

46
Q

Obstruction/ileus

A

-Any condition that prevents normal flow of chime through intestine
-Loss of intestinal motility in the absence of an ileus

47
Q

Classification of an obstruction/ileus

A

Simple or functional

48
Q

Primary causes of small bowel obstructions

A

-Adhesions * (most common for adults)
-Hernia
-Tumors

49
Q

Primary causes of large bowel obstructions

A

-Malignancy
-Volvulus (twisting, torsion)
-Strictures related to diverticulitis

50
Q

Paralytic ileus is caused by…

A

-Narcotics, sedation, anesthetics, & giving a lot of food or liquids too quickly

51
Q

Functional obstructions

A

Paralytic ileus & constipation

52
Q

Intussusception is…

A

Most common in kids

53
Q

Slide 24

A
54
Q

Slide 25

A
55
Q

Manifestations of intestinal obstructions

A

-May be sudden and dramatic symptoms of pain (intermittent), vomiting, distention, borborygmus (rumbling bowel sounds)**, peristaltic rushes, restlessness and awareness of peristaltic movements

56
Q

Tx of intestinal obstructions

A

Tx is based on the cause, it may respond to decompression but may require surgery

57
Q

Stomach & intestinal dysfunction key assessment points

A

-aBowel sounds, N/V, anorexia, distention & aLab values
-GI pain

58
Q

Intestinal dysfunction GI pain

A

-Usually sharp or burning
-May be steady or intermittent
-May be referred

59
Q

Slide 29

A
60
Q

Slide 30

A
61
Q

Hepatitis A pathophysiology

A

-Widespread inflammation of the liver tissue
-Liver damage is mediated by cytotoxic cytokines and natural killer cells that cause lysis of infected hepatocytes
-Damage results from liver necrosis
-Inflammation of periportal areas interrupts flow of bile

62
Q

Transmission of hepatitis A

A

-Transmitted through feces (fecal-oral route; contaminated water and food; blood)

63
Q

Incubation period of hepatitis A

A

2-7 weeks

64
Q

Manifestations of hepatits A

A

-Fatigue, fever, N/V, hepatomegaly, jaundice, dark urine, anorexia, rash
-Usually a mild disease

65
Q

Hepatitis A…

A

Interrupts flow of bile out of the liver

66
Q

Fulminant viral hepatitis

A

-Results in severe impairment or necrosis of the liver cells commonly caused by tyelenol OD
-May occur with hepatitis B or C virus

67
Q

Fulminant viral hepatitis pathophysiology

A

-Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the parenchyma
-Acute liver failure develops within 6-8 weeks after initial symptoms of hepatitis

68
Q

Manifestations of fulminant viral hepatitis

A

Anorexia, vomiting, abdominal pain, progressive jaundice, followed by ascites and GI bleed

69
Q

Jaundice

A

-May occur as a result of liver dysfunction
-Results from 1. Extrahepatic (post-hepatic) obstruction to bile flow, 2. Intrahepatic obstruction, 3. Prehepatic excessive production of unconjugated bilirubin

70
Q

Pathophysiology of jaundice

A

Conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts stools become light or clay coloured

71
Q

Jaundice can lead to…

A

-Pruritis which occurs d/t bile salts accumulating under the skin
-Dark brown/reddish urine

72
Q

Slide 34

A
73
Q

Portal HTN pathophysiology + intrahepatic

A

Results from vascular remodelling with intrahepatic shunts, thrombosis, inflammation or fibrosis such as in cirrhosis of the liver, viral hepatitis, or schistosomiasis (parasitic infection)

74
Q

Portal HTN pathophysiology + posthepatic

A

Causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart (RV HF); blood backs up and there is increased pressure in the portal system

75
Q

Portal HTN pathophysiology + prehepatic

A

Causes occur with narrowing of the hepatic portal vein

76
Q

Longterm complications of portal HTN

A

Varices, splenomegaly, hepatopulmonary syndrome and portopulmonary hypertension

77
Q

Manifestations of portal HTN

A

Most common clinical manifestation is vomiting of blood from bleeding esophageal varices, then slow, chronic bleeding from varices causes anemia or melena

78
Q

Prehepatic, intrahepatic, & posthepatic are…

A

All right sided heart issues

79
Q

Progression of portal HTN

A

-Backup leads to varices, ascites and right sided HF
-Varices can result in profound bleed: Melena, frank red blood & vomiting

80
Q

Tx of portal HTN

A

-Rapid treatment needed: Volume replacement, drugs, endoscopy, balloon tamponade & surgery (portacaval shunt)

81
Q

Non-alcoholic fatty liver disease (NAFLD) & non-alcoholic steatohepatitis (NASH)

A

These present as cirrhosis but are in the absence of ETOH

82
Q

Slide 37

A
83
Q

Cirrhosis of the liver pathophysiology

A

-Irreversible inflammatory, fibrotic liver disease
-Occurs d/t a disorganized regenerative process
-Overgrowth of new & fibrous tissue distorts the structure, resulting in lobules of irregular size and shape impeding blood flow
-Leads to poor cellular nutrition, and hypoxia causing inadequate flow and scar tissue decreasing the function of the liver

84
Q

Manifestations of liver cirrhosis + labs

A

-Abnormal AST, ALT, GGT, & Alk Phos
-Normal blood values; albumin, bilirubin (initially low but then increase), PTT

85
Q

Initial manifestations of liver cirrhosis

A

Abdominal pain, fatigue, slight weight loss, and enlargement of the liver & spleen

86
Q

Manifestations as liver cirrhosis progresses

A

Jaundice, skin lesions, peripheral neuropathy, portal HTN, esophageal and gastric varices, edema, ascites, hepatic encephalopathy & hepatorenal syndrome

87
Q

Liver failure leads to…

A

Kidney failure

88
Q

Ascites

A

-Sodium, water and protein accumulate in peritoneal cavity due to pressure changes in lymphatic system capillaries. -Oncotic and osmotic pressures rise

89
Q

Tx of ascites

A

-May require paracentesis as abdominal pressures increase
-Sodium restriction & diuretics
-Colloids to increase oncotic pressure

90
Q

Ascites decrease…

A

Alveoli expansion

91
Q

Slide 42

A
92
Q

Ascites is the most…

A

Common complication of cirrhosis but can also occur with right sided HF, abdominal malignancies, nephrotic syndrome & malnutrition

93
Q

Pathophysiology of ascites

A

Contributing factors include: Portal HTN, decreased synthesis of albumin by the liver, splanchnic arterial vasodilation, and renal sodium and water retention

94
Q

Ascites may cause

A

Bacterial peritonitis (fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid)

95
Q

Slide 44

A
96
Q

Hepatic encephalopathy is AKA

A

Portosystemic encephalopathy

97
Q

Pathophysiology of hepatic encephalopathy

A

-Complex neurologic syndrome characterized by impaired cognitive function, asterixis, and EEG changes
-Increased amounts of Ammonia and GABA (inhibitory transmitter) may contribute to reduced LOC
-May develop rapidly and become an EMERGENCY situation quickly

98
Q

Manifestations of hepatic encephalopathy

A

aGait & personality, memory loss, irritability, lethargy and sleep disturbances
-Symptoms can progress to confusion, flapping tremor of the hands, stupor, convulsions and coma

99
Q

Tx of hepatic encephalopathy

A

& when you weren’t looking, I added some lactulose

100
Q

Liver dysfunction can lead to…

A

Hepatic encephalopathy

101
Q

Gallbladder structure

A

Saclike organ

102
Q

Function of the gallbladder

A

-Store and concentrate bile between meals
-Aids in digestion of fats
-Bile is released in response to food
-Conditions slowing or obstructing flow of bile out of the gallbladder lead to gallbladder disease

103
Q

About bile

A

Bile is an alkaline, bitter tasting, yellowish green fluid that contains bile salts, cholesterol, bilirubin, electrolytes, and water

104
Q

Pathophysiology of gallbladder cholelithiasis (gallstones)

A

-Gallstones are formed from impaired metabolism of cholesterol, bilirubin and bile salts
-Form when there is decreased motility and biliary stasis
-Stones may lay dormant and silent until they become lodged in the cystic or common duct, causing pain when the gallbladder contracts

105
Q

Types of gallstones

A

Cholesterol (most common), pigmented (black-hard, brown-soft) and mixed

106
Q

Manifestations of gallbladder cholelithiasis

A

-Often asymptomatic
-Epigastric and RUQ pain and intolerance to fatty foods are cardinal manifestations
-Heartburn, flatulence, epigastric discomfort, pruritus, jaundice and food intolerances to fats and cabbage
-Biliary colic (pain) occurs 30 min to several hours after eating a fatty meal

107
Q

Pathophysiology of gallbladder cholecystitis

A

-Caused by the lodging of a gallstone in the cystic duct causing distention & inflammation
-Colic pain but decreased blood flow can result in ischemia, necrosis, and perforation of the gallbladder

108
Q

Manifestations of gallbladder cholecystitis

A

-Fever, leukocytosis, rebound tenderness and guarding
-Serum bilirubin and alkaline phosphatase (ALP) may be elevated

109
Q

Slide 52

A
110
Q

Diagnostic tests associated with gallbladder disorder

A

-Endoscopic Retrograde Cholangiopancreatography (ERCP)
-Radiographic and endoscopic; diagnosis & treatment
-X-rays, ultrasound, CT, scintigraphy (nuclear scanning)

CV487 (15 decks)

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