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Patho - Exam 3 > GI > Flashcards

GI Flashcards

1
Q

Candidiasis

A

Fungal infection caused by candida albicans

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2
Q

Oral Candidiasis

A

Thrush

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3
Q

What is the causative agent of candidiasis?

A

Candida albicans

  • Often part of the resident flora
  • opportunistic organism
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4
Q

Who are Candidiasis found in?

A
  • People receiving broad-spectrum antibiotics
  • During and after cancer therapy
  • Immunocompromised
  • DM
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5
Q

Clinical Manifestations of Candidiasis

A
  • Red swollen areas
  • May be irregular patches of white curd like material on tongue
  • Soreness
  • Problems with swallowing
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6
Q

Treatment of Candidiasis

A

Oral antifungals

Ex: Nystatin

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7
Q

Dysphagia

A

Difficulty swallowing

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8
Q

What are the three types of dysphagia?

A

Oropharyngeal
Esophageal
Functional

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9
Q

Characteristics of esophageal dysphagia

A

Inability to swallow solid food

  • Pain on swallowing
  • Highly indicative of carcinoma
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10
Q

Characteristic of functional dysphagia

A

No organic cause for dysphagia that can be found

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11
Q

What are the two types of causes for dysphagia?

A

Mechanical

Neuromuscular disorders

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12
Q

Examples of mechanical obstruction (dysphagia)?

A

-Tumors, masses, trauma, lesions

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13
Q

Examples of Neuromuscular disorders (dysphagia)?

A

CVA, Parkinson’s brainstem tumors, ALS, MS, peripheral neuropathy, Myasthenia gravis, Myopathies

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14
Q

Signs and Symptoms of Oropharyngeal Dysphagia

A
  • difficulty swallowing or controlling food
  • coughing, choking
  • frequent pneumonia
  • unexplained weight loss
  • gurgly or wet voice after swallowing
  • nasal regurgitation
  • dysphagia-patient complains of difficulty swallowing
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15
Q

Signs and Symptoms of Esophageal Dysphagia

A
  • inability to swallow solid food
  • described as being stuck or held up
  • pain on swallowing is highly indicative of carcinoma
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16
Q

Diagnostic of Oropharyngeal Dysphagia

A

-When asked where the food is stuck, patients usually point to the neck as site of obstruction (but actual site is always at or below where it is perceived)

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17
Q

If undiagnosed or untreated, Dysphagia can lead to

A

Dehydration, malnutrition and renal failure

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18
Q

What is a dysphagia patient at high risk of?

A

Pulmonary aspiration

Subsequent aspiration pneumonia (secondary to food/liquid going the wrong way to the lungs)

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19
Q

Treatment for Dysphagia

A
  • Swallowing therapy with exercises and dietary changes
    • Thickening liquids or mechanically soft diet
  • Surgery or medicine for problems with the esophagus
  • Nasogastric or endoscopic tubes are also used to treat dysphagia
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20
Q

GERD

A

Gastroesophageal Reflux Disease

Chronic reflux of chyme from the stomach to the esophagus

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21
Q

Reflux esophagitis

A

If GERD causes inflammation of the esophagus, it can lead to Barrett’s esophagus

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22
Q

Barrett’s Esophagitis

A

Intestinal metaplasia (change of squamous to intestinal columnar epithelium of distal esophagus)

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23
Q

Causes of GERD

A

Conditions that increase abdominal pressure:
-Ascites
-Constipation
-Pregnancy
-Pancreatitis
Changes in the barrier between the stomach and esophagus
-Abnormal relaxation of the lower esophageal sphincter
Hiatal Hernias

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24
Q

Clinical Manifestations of GERD

A

Chronic symptom of mucosal damage caused by stomach acid into esophagus

  • Heartburn
  • Regurgitation of chyme
  • Pain in upper abdominal/epigastric area after eating
  • Pain relieved by food or antacids
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25
Q

Treatment of GERD

A 
Lifestyle changes
Medications 
-Proton Pump inhibitors (Nexium)
-H2 receptor blockers or antacids with or without algenic acid 
Surgery if no improvement
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26
Q

Peptic Ulcer Disease

A

Break in the lining of the stomach, duodenum, or the lower esophagus

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27
Q

Duodenal Ulcers

A

Most common form of peptic ulcer disease, occur in the duodenum

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28
Q

Gastric Ulcers

A

Ulcers in the stomach

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29
Q

Most common cause of peptic ulcers

A

H. Pylori infection (bacterial)

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30
Q

Causes of Peptic Ulcers (4)

A
  • H. Pylori
  • Hypersecretion of stomach acid or pepsin
  • Use of NSAIDs
  • Acid production by cigarette smoking
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31
Q

Most common symptoms of Peptic Ulcers

A
  • Chronic intermittent pain in the epigastric area 2-3 hours after eating
  • Dull/Burning pain
  • Waking up at night with abdominal pain
  • Upper abdominal pain that goes away with eating
  • Bleeding
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32
Q

If asymptomatic, what might be the first sign of peptic ulcers?

A

Bleeding

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33
Q

Other symptoms of Peptic Ulcer Disease

A
  • Belching
  • Vomiting
  • Weight loss
  • Poor appetite
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34
Q

Complications of Peptic Ulcers

A
  • Bleeding
  • Perforation
  • Obstruction of the duodenum
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35
Q

Acute Manifestations of Peptic Ulcer Disease

A
  • Hematemesis
  • Melena
  • Hematochezia
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36
Q

Hematemesis

A

Vomiting of blood

-associated with upper GI bleed

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37
Q

Melena

A

Black tarry stool caused by GI bleeding

-Hemoglobin in the blood altered by digestive chemicals and intestinal bacteria

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38
Q

Hematochezia

A

Passage of fresh blood through the anus

-associated with lower GI bleed

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39
Q

Chronic Manifestations of Peptic Ulcers

A

Occult bleeding

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40
Q

Occult Bleeding

A

Small amounts of bleeding; detected by fecal occult blood test, signifying an upper GI bleed

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41
Q

Diagnostic tests for Peptic Ulcer Disease

A
  • Barium swallow
  • Endoscopy
  • H. Pylori Test
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42
Q

Goal of Management

A

Relieve the causes and effects of hyperacidity

  • Administer antacids and protein pump inhibitors (Nexium)
  • Antibiotics for H. Pylori
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43
Q

GI Bleed

A

All forms of blood loss from the GI tract (from mouth to rectum)

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44
Q

Causes of upper GI bleed

A
  • Peptic ulcer disease
  • Esophageal varices due to liver cirrhosis
  • Cancer
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45
Q

Causes of lower GI bleed

A
  • Hemorrhoids
  • Cancer
  • IBD
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46
Q

Manifestations of GI Bleed

A 
Vomiting red, black, blood 
Bloody or black stool 
Small amounts of blood loss 
Anemia (from the blood loss)
Fatigue or chest pain (from the anemia)
Low blood volume + anemia can cause abdominal pain, pale skin, or syncope
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47
Q

Diagnostics for GI Bleed

A
  • Medical history and physical exam
  • CBC for hemoglobin and HCT
  • Stool analysis (elimination patterns, characteristics)
  • Endoscopy of upper and lower GI
  • Fecal Occult Blood Test (FOBT) - if testure turns blue, blood is present
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48
Q

Treatment for GI Bleed

A

Resuscitation - IV Fluids, blood transfusions

Medications - PPIs (nexium), Octreotide, antibiotics

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49
Q

IBD

A

Group of autoimmune inflammatory conditions related to colon and small intestine

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50
Q

Two types of IBD

A

Crohn’s and Ulcerative Colitis

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51
Q

Chronic IBD

A

Relapsing IBD of unknown origin

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52
Q

Cause of IBD

A

Autoimmune
Genetics
Alterations of epithelial barrier functions
Abnormal T cell responses

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53
Q

IBD has periods of ____ and ______

A

Remissions and exacerbations

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54
Q

Ulcerative Colitis

A

Chronic inflammatory disease that causes ulcerations in the colonic mucosa in the sigmoid colon and rectum

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55
Q

Causes of Ulcerative Colitis

A

Autoimmune disease in which the T cells infiltrate the colon creating ulcers

May be related to: infection, immunologic (anti-colon antibodies), dietary, genetic

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56
Q

Manifestations of Ulcerative Colitis

A

Periods of exacerbation and remission
Diarrhea (10-20 times a day)
Bloody stools
Cramping

57
Q

Long term complications of Ulcerative colitis

A

Increased risk for colon cancer

Anemia

58
Q

GOAL of ulcerative colitis

A
  • Induce remission with medications
  • Administration of maintenance medication to prevent relapse
  • Broad spectrum antibiotics and steroids
  • Immunosuppressive agents
  • Surgery
59
Q

Crohn’s Disease

A

Idiopathic inflammatory bowel disease that affects both small and large intestines (mostly in terminal ileum)
-can also affect mouth, stomach and anus

60
Q

Cause of Crohn’s Disease

A

Idiopathic

Focal infiltration of neutrophils into the epithelium causes mucosal inflammation
-Chronic mucosal damage and blunting of the intestinal villi

61
Q

Manifestations of Crohn’s

A
  • Transmural pattern of inflammation
  • Skip Lesions
  • Ulcerations can produce longitudinal and transverse inflammatory fissures
  • Periods of exacerbation and remission (but remission may not be possible)
  • Abdominal pain
  • Diarrhea
  • Fever
  • Weight loss
  • Anemia can lead to malabsorption of vitamin B12 and folic acid
62
Q

Long-Term Complications of Crohn’s

A
  • Formulation of a fistula between different areas of the GI tract, between the GI and bladder, vagina, urethra, or skin
  • Intestinal obstruction
  • Abscess formation
  • Pyroderma Gangrenosum
  • Erythem Nodosum
  • Bowel obstruction
  • Greater risk for bowel cancer
63
Q

Pryoderma Gangrenosum

A

Condition that causes tissue to become necrotic, causing deep ulcers that usually occur in the legs

64
Q

Erythem Nodosum

A

Inflammatory condition of the fat cells under the skin, resulting in tender red noodles or lumps that are usually seen on both shins

65
Q

Other complications of Crohn’s

A

Anemia, skin rash, arthritis, inflammation of the eye

66
Q

Treatment of Crohn’s

A
  • No cure
  • Relapse may be prevented with medication, lifestyle and dietary changes

Surgery is contraindicative !

67
Q

Intestinal Obstruction

A

Obstruction of the intestines prevents normal transit of products of digestion

68
Q

Causes of Intestinal Obstruction

A

Simple mechanical causes vs functional causes

  • Tumor
  • Fecal impaction
  • Intussuception
69
Q

Intussuception

A

Part of the intestine folds into another section of the intestinal wall

70
Q

Manifestations of Intestinal Obstruction (general)

A
  • Pain
  • Swollen, distended abdomen
  • Constipation
  • Gassiness, fullness
  • Diarrhea
  • Nausea/vomiting
71
Q

Manifestations of Small Obstructions

A
  • Intermittent cramping/pain
  • Spasms
  • Vomiting BEFORE constipation
  • Proximal obstruction of large bowel may present as a small obstruction
72
Q

Manifestations of Large Obstructions

A
  • Pain in lower abdomen
  • Longer spasms
  • Constipation before vomiting
73
Q

What does Intestinal Obstruction lead to?

A
  • Water and electrolyte imbalance (due to vomiting)
  • Respiratory complications (due to pressure on the diaphragm and aspiration of vomit)
  • Perforation from prolonged dissension or pressure from foreign body
  • Perforation can lead to sepsis
74
Q

Treatment of Intestinal Obstruction

A

Usually surgery/treatment of causative lesions are required

  • Decompression fo abdomen with NG tube
  • Correction of dehydration and electrolyte imbalances
  • Opioids for severe pain
  • Antiemetics for vomiting

Some cases may resolve spontaneously

75
Q

Diverticular Disease

A

Altered structure and function of the large intestine walls with diverticulum

76
Q

Diverticulum

A

Small sac outpouring along the wall of the colon

77
Q

Causes of Diverticular Disease

A

Prolonged pressure on the large intestine wall alters structure and function
-Weakness leads to outpouching

78
Q

Diverticulitis

A

Infected diverticula due to fecal matter getting stuck in the out pouches

79
Q

Manifestations of Diverticular Disease

A

LLQ pain and tenderness

80
Q

Complicated Diverticulitis

A

Subsequently infect the outside of the colon

81
Q

Manifestations of complicated diverticulitis

A
  • Inflamed diverticula burst open
  • Infections spread to lining of abdominal cavity (peritoneum) = peritonitis
  • Narrowing of bowel (from inflamed diverticula)
  • Infected part of colon could adhere to bladder or other organs in pelvic cavity causing a fistula or abdominal connection
82
Q

Diagnostic Tests for Diverticular Disease

A
  • History and physical exam for abdominal tenderness/distension
  • Lab analysis
    • Bloody stools
    • Low Hmg and Hct
    • CBC for infection
  • CT scan
    • Inflamed and or ruptured diverticula = confident diagnostic
    • Localized wall thickening
    • Bariumanima and colonoscopy - but don’t do this in acute phase because of its risk of perforation
83
Q

Prevention of Diverticular Disease

A
  • Low fiber diet
  • Lifestyle alterations
  • Medications (bulk forming laxatives, antispasmodic)
84
Q

Treatment for Diverticular Disease

A

Conservative therapy with bowel rest

  • Control infection
  • Manage symptoms
  • Antibiotics for bacterial infection
  • Prevent complications
  • Surgical correction of perforated diverticula, peritonitis, abscess

Emergency surgery for those with ruptured intestine

85
Q

Appendicitis

A

Blockage of hollow portion of appendix, usually by a calcified stone composed of feces
(Inflammation of the vermiform appendix)

86
Q

Causes of Appendicitis

A

Blockage leads to tissue injury and death

  • obstruction
  • ischemia
  • increased intraluminal pressure
  • infection
  • ulceration
87
Q

3 factors of Appendicitis blockage

A
  • Increases pressure in appendix
  • Decreased blood flow to tissues of appendix
  • Bacterial growth inside the appendix causing inflammation
88
Q

Manifestations of Appendicitis

A

Epigastric and RLQ pain

  • Rebound tenderness
  • Abdominal tenderness
89
Q

Rebound Tenderness

A

Pain upon removal of pressure rather than application of pressure

90
Q

What happens if Appendicitis is not treated?

A
  • Appendix may burst and release bacteria into the abdominal cavity (increases abdominal pain and complications)
  • Perforation can lead to peritonitis and possible sepsis and shock
91
Q

Diagnostic Tests for Appendicitis

A
  • Increase in WBC

- CT scan

92
Q

Treatment for Appendicitis

A

Pain management
Surgery (removal of appendix)
Antibiotics

93
Q

Cholelithiasis

A

Gallstones

-Most common biliary disorder

94
Q

Cholecystitis

A

Inflammation of the gallbladder associated with cholelithiasis

95
Q

What do gallstones develop from?

A

Pigments and cholesterol

96
Q

Risk factors for Cholelithiasis/Cholecystitis

A 
Obesity 
Middle age
Female
Native American 
Diseases of the gallbladder, pancreas, or ileal disease
97
Q

Causes of Cholecystitis

A

Due to blockage of cystic duct with gallstones

  • Build up of bile in the gall bladder increases the pressure, causing RUQ pain
  • Concentrated bile, pressure, and bacterial infection irritate and damage the gallbladder wall leading to ischemia / cell death
98
Q

General Manifestations of Cholelithiasis

A

Will not necessarily develop cholecystitis

  • Biliary colic (severe pain with gallstones)
  • Tachycardia, diaphoresis, exhaustion
  • Residual tenderness in RUQ
  • Attacks 3-6 hours after heavy/fatty meal
99
Q

Manifestations of Cholelithiasis if there is total obstruction

A
  • Steatorrhea (lack of bile causes abnormal amounts of fat in feces)
  • Pruritus
  • Dark, amber urine (excess bilirubin in urine)
  • Jaundice
  • Clay colored stools
  • Fever
100
Q

Complications of Cholelithiasis

A
  • Abscess
  • Pancreatitis
  • Gallbladder rupture
  • Delayed diagnosis increases morbidity and mortality
101
Q

Diagnostic tests for cholelithiasis

A
  • RUQ pain + nausea + vomiting + fever
  • Increased WBC count
  • Elevated bilirubin in urine (dark amber urine, lab analysis)
  • Ultrasound (visualize gallstones, changes in GB wall)
  • CT scan
  • Heaptobiliary scan (HIDA) - radioactive tracer
  • Oral cholecystography
  • ERCP
  • PTC
102
Q

How does HIDA diagnose cholelithiasis?

A
  • Gallbladder visualized within 1 hr of radioactive injection = no disease
  • If gallbladder is not visualized within 4 hrs of injection = cholecystitis or cystic duct obstruction
103
Q

Treatment of Cholelithiasis

A

-Antibioditcs, analgesics, antispasmodics
-NPO until symptoms subside
-Gastric decompression with NG tube
-Avoidance of fatty/fried foods
-Laparoscopic cholecystectomy (GOLD standard)
Cholecystectomy - removal of gallbladder or opening it to remove stones, bile, pus

104
Q

What is the gold standard treatment of Cholelithiasis?

A

Laparoscopic Cholecystectomy

105
Q

What are supportive measures prior to Cholecystectomy?

A

Fluid resuscitation
Pain managemnt
Antibiotics to target enteric organs

106
Q

Pancreatitis

A

Inflammation of the pancreas due to autodigestion of the tissues

107
Q

Chronic Pancreatitis

A

Irreversible histological changes and diminished function of the pancreas
-ETOH USE = major cause

108
Q

Causes of Acute Pancreatitis

A

Alcoholism, biliary tract disease, trauma, infection, drugs, GI surgery post op

*They cause early activation of excessive pancreatic enzymes causing massive inflammation, bleeding, and necrosis

109
Q

How do trypsin, lipase, elastase, and cytokines/prostaglandis cause Pancreatitis?

A

Trypsin - progresses into tissues surrounding the pancreas
Lipase - causes fat necrosis, binding calcium ions
Elastase - erodes blood vessels, causing hemorrhage
Cytokines/Prostaglandis - released by tissue necrosis, inducing an inflammatory response, leading to vasodilation, hypovolemia, and circulatory collapse

110
Q

Causes of Chronic Pancreatitis

A

Serious loss of exocrine and endocrine pancreatic function as well as deterioration of pancreatic structure
-Decreased enzyme production and decreased insulin production lead to malabsorption of fats and proteins

111
Q

Manifestations of Acute Pancreatitis

A
  • Sudden onset of severe epigastric pain after a large meal or ETOH
  • Referred pain to back and left shoulder
  • Jaundice if there is biliary obstruction and accumulation of bile
  • Malaise, restlessness, lung involvement, respiratory distress and decreased urine output
  • Decreased bowel sounds, ascites
  • Abdominal tenderness with guarding
112
Q

Manifestations of Chronic Pancreatitis

A

Periods of exacerbations and remissions

  • Constant dull epigastric pain
  • Steatorrhea
  • Severe weight loss
  • Onset of symptoms of DM because of insufficient production of insulin
113
Q

Diagnostics for Pancreatitis

A
  • History of abdominal pain, risk factors, physical exam, diagnostic findings
  • Increased serum bilirubin
  • Increased liver enzymes
  • Increased WBC
  • Increased serum glucose (lack of insulin)
  • Increased pancreatic enzymes (lipase, amylase, trypsin)
  • Decreased Ca and Mg
  • Ultrasound, CT scan, x rays
114
Q

Treatment for Acute Pancreatitis

A
  • Opioids for pain
  • Decrease pancreatic secretions by decreasing stimulation of the pancreas
    • NPO and NG suctioning
    • Remove irritants
    • Reduce vomiting and gastric distention
  • Control fluid and electrolyte imbalances
    • Maintain adequate blood volume (check I/O)
    • When no longer NPO, have a diet high in CHO and protein and low in fat
  • Antibiotics to prevent infection
115
Q

Treatment for Chronic Pancreatitis

A

Long-term pain management

  • Oral pancreatic enzyme replacement therapy (PERT)
  • Alcohol rehab
  • Treat DM with insulin
  • Nutritional therapy - High calorie, high CHO, high, protein, low fat
  • Surgical interventions if obstruction
116
Q

What are the disorders of the liver?

A

Hepatitis

Cirrhosis

117
Q

Where is Hepatitis A found?

A

Feces, bile, and sera of infected individuals

118
Q

What is the sequence of Acute Hepatitis?

A

Prodromal phase, Icteric phase, Recovery phase

119
Q

Prodromal Phase

A

Begins 2 weeks after exposure with non specific symptoms

120
Q

Icteric phase

A

Lasts 2-6 weeks

121
Q

Recovery phase

A

Improvement of symptoms

122
Q

Hep A (transmission, and where its found)

A

Usually transmitted by fecal-oral route

  • Direct contact
  • Food and beverage
  • Cups and spoons
  • Chronic
123
Q

Risk Factors for Hep A

A

Crowded, unsanitary conditions

Food and water contamination

124
Q

Hep E

A

Fecal-oral transmission

  • Developing countries
  • Similar to hep A but NOT chronic
125
Q

Hep B

A

Contact with infected blood, body fluids, contaminated needles

  • piercing/tattooing
  • vertical transmission (breastfeeding)
  • maternal transmission if mother is infected during 3rd trimester
  • blood transfusion
126
Q

Hep D

A

same transmission route as HBV (blood, fluids, needles)

  • Dependent on HBV for replication
  • Often makes HBV infection worse
127
Q

What does Hep D need to manifest?

A

Hep B

128
Q

Hep C

A

IV drug use through sharing needles, and high risk sexual behavior

  • Maternal transmission is a rare but present case
  • 50-80 % of Hep C results in chronic hepatitis
129
Q

What is the primary mode of transmission of Hep C?

A

IV drug use through sharing needles

130
Q

What is the secondary mode of transmission of Hep C?

A

High risk sexual behavior

131
Q

Symptoms of A & B Hepatitis

A

Nausea, vomiting

132
Q

Complications of Hep B and C

A
  • Chronic hepatitis and cirrhosis
  • End stage liver failure
  • Hepatocellular carcinoma
133
Q

Cirrhosis

A

Irreversible inflammatory disease that disrupts liver function and structure

134
Q

Types of Cirrhosis

A
  • Alcoholic
  • Non-alcoholic fatty liver
  • Biliary (Bile canaliculi)
  • Metabolic
135
Q

Cause of Cirrhosis

A

Inflammation leads to necrosis and fibrosis

-Nodular and fibrotic tissue synthesis leads to decreased hepatic function

136
Q

Manifestations of Cirrhosis - Inflammation

A

Pain, fever, nausea, vomit, anorexia, fatigue

137
Q

Manifestations of Cirrhosis - Necrosis

A
  • Decreased bilirubin metabolism (causes hyperbilirubemia and jaundice)
  • Decreased bile in GI tract (light colored stools)
  • Decreased vitamin K absorption (bleeding)
  • Increased urobilinogen (dark urine)
  • Decreased hormone metabolism
  • Increased androgens and estrogen
  • Liver failure
  • Hepatic encephalopathy
  • Death
138
Q

Manifestations of Cirrhosis - Fibrosis

A 
Edema 
Portal HTN can cause: 
-hepatic necrosis
-esophageal varices
-splenomegaly 
-ascites
139
Q

Other complications of Cirrhosis

A

Endstage liver disease

  • reduced clotting
  • impaired ammonia metabolism
  • impaired bilirubin metabolism
  • hypoglycemia
  • increased aldosterone production

Patho - Exam 3 (4 decks)

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