GI Flashcards

(139 cards)

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
Treatment of GERD
``` Lifestyle changes Medications -Proton Pump inhibitors (Nexium) -H2 receptor blockers or antacids with or without algenic acid Surgery if no improvement ```
26
Peptic Ulcer Disease
Break in the lining of the stomach, duodenum, or the lower esophagus
27
Duodenal Ulcers
Most common form of peptic ulcer disease, occur in the duodenum
28
Gastric Ulcers
Ulcers in the stomach
29
Most common cause of peptic ulcers
H. Pylori infection (bacterial)
30
Causes of Peptic Ulcers (4)
- H. Pylori - Hypersecretion of stomach acid or pepsin - Use of NSAIDs - Acid production by cigarette smoking
31
Most common symptoms of Peptic Ulcers
- 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
32
If asymptomatic, what might be the first sign of peptic ulcers?
Bleeding
33
Other symptoms of Peptic Ulcer Disease
- Belching - Vomiting - Weight loss - Poor appetite
34
Complications of Peptic Ulcers
- Bleeding - Perforation - Obstruction of the duodenum
35
Acute Manifestations of Peptic Ulcer Disease
- Hematemesis - Melena - Hematochezia
36
Hematemesis
Vomiting of blood | -associated with upper GI bleed
37
Melena
Black tarry stool caused by GI bleeding | -Hemoglobin in the blood altered by digestive chemicals and intestinal bacteria
38
Hematochezia
Passage of fresh blood through the anus | -associated with lower GI bleed
39
Chronic Manifestations of Peptic Ulcers
Occult bleeding
40
Occult Bleeding
Small amounts of bleeding; detected by fecal occult blood test, signifying an upper GI bleed
41
Diagnostic tests for Peptic Ulcer Disease
- Barium swallow - Endoscopy - H. Pylori Test
42
Goal of Management
Relieve the causes and effects of hyperacidity - Administer antacids and protein pump inhibitors (Nexium) - Antibiotics for H. Pylori
43
GI Bleed
All forms of blood loss from the GI tract (from mouth to rectum)
44
Causes of upper GI bleed
- Peptic ulcer disease - Esophageal varices due to liver cirrhosis - Cancer
45
Causes of lower GI bleed
- Hemorrhoids - Cancer - IBD
46
Manifestations of GI Bleed
``` 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 ```
47
Diagnostics for GI Bleed
- 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
48
Treatment for GI Bleed
Resuscitation - IV Fluids, blood transfusions | Medications - PPIs (nexium), Octreotide, antibiotics
49
IBD
Group of autoimmune inflammatory conditions related to colon and small intestine
50
Two types of IBD
Crohn's and Ulcerative Colitis
51
Chronic IBD
Relapsing IBD of unknown origin
52
Cause of IBD
Autoimmune Genetics Alterations of epithelial barrier functions Abnormal T cell responses
53
IBD has periods of ____ and ______
Remissions and exacerbations
54
Ulcerative Colitis
Chronic inflammatory disease that causes ulcerations in the colonic mucosa in the sigmoid colon and rectum
55
Causes of Ulcerative Colitis
Autoimmune disease in which the T cells infiltrate the colon creating ulcers May be related to: infection, immunologic (anti-colon antibodies), dietary, genetic
56
Manifestations of Ulcerative Colitis
Periods of exacerbation and remission Diarrhea (10-20 times a day) Bloody stools Cramping
57
Long term complications of Ulcerative colitis
Increased risk for colon cancer | Anemia
58
GOAL of ulcerative colitis
- Induce remission with medications - Administration of maintenance medication to prevent relapse - Broad spectrum antibiotics and steroids - Immunosuppressive agents - Surgery
59
Crohn's Disease
Idiopathic inflammatory bowel disease that affects both small and large intestines (mostly in terminal ileum) -can also affect mouth, stomach and anus
60
Cause of Crohn's Disease
Idiopathic Focal infiltration of neutrophils into the epithelium causes mucosal inflammation -Chronic mucosal damage and blunting of the intestinal villi
61
Manifestations of Crohn's
- 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
Long-Term Complications of Crohn's
- 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
Pryoderma Gangrenosum
Condition that causes tissue to become necrotic, causing deep ulcers that usually occur in the legs
64
Erythem Nodosum
Inflammatory condition of the fat cells under the skin, resulting in tender red noodles or lumps that are usually seen on both shins
65
Other complications of Crohn's
Anemia, skin rash, arthritis, inflammation of the eye
66
Treatment of Crohn's
- No cure - Relapse may be prevented with medication, lifestyle and dietary changes Surgery is contraindicative !
67
Intestinal Obstruction
Obstruction of the intestines prevents normal transit of products of digestion
68
Causes of Intestinal Obstruction
Simple mechanical causes vs functional causes - Tumor - Fecal impaction - Intussuception
69
Intussuception
Part of the intestine folds into another section of the intestinal wall
70
Manifestations of Intestinal Obstruction (general)
- Pain - Swollen, distended abdomen - Constipation - Gassiness, fullness - Diarrhea - Nausea/vomiting
71
Manifestations of Small Obstructions
- Intermittent cramping/pain - Spasms - Vomiting BEFORE constipation - Proximal obstruction of large bowel may present as a small obstruction
72
Manifestations of Large Obstructions
- Pain in lower abdomen - Longer spasms - Constipation before vomiting
73
What does Intestinal Obstruction lead to?
- 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
Treatment of Intestinal Obstruction
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
Diverticular Disease
Altered structure and function of the large intestine walls with diverticulum
76
Diverticulum
Small sac outpouring along the wall of the colon
77
Causes of Diverticular Disease
Prolonged pressure on the large intestine wall alters structure and function -Weakness leads to outpouching
78
Diverticulitis
Infected diverticula due to fecal matter getting stuck in the out pouches
79
Manifestations of Diverticular Disease
LLQ pain and tenderness
80
Complicated Diverticulitis
Subsequently infect the outside of the colon
81
Manifestations of complicated diverticulitis
- 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
Diagnostic Tests for Diverticular Disease
- 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
Prevention of Diverticular Disease
- Low fiber diet - Lifestyle alterations - Medications (bulk forming laxatives, antispasmodic)
84
Treatment for Diverticular Disease
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
Appendicitis
Blockage of hollow portion of appendix, usually by a calcified stone composed of feces (Inflammation of the vermiform appendix)
86
Causes of Appendicitis
Blockage leads to tissue injury and death - obstruction - ischemia - increased intraluminal pressure - infection - ulceration
87
3 factors of Appendicitis blockage
- Increases pressure in appendix - Decreased blood flow to tissues of appendix - Bacterial growth inside the appendix causing inflammation
88
Manifestations of Appendicitis
Epigastric and RLQ pain - Rebound tenderness - Abdominal tenderness
89
Rebound Tenderness
Pain upon removal of pressure rather than application of pressure
90
What happens if Appendicitis is not treated?
- 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
Diagnostic Tests for Appendicitis
- Increase in WBC | - CT scan
92
Treatment for Appendicitis
Pain management Surgery (removal of appendix) Antibiotics
93
Cholelithiasis
Gallstones | -Most common biliary disorder
94
Cholecystitis
Inflammation of the gallbladder associated with cholelithiasis
95
What do gallstones develop from?
Pigments and cholesterol
96
Risk factors for Cholelithiasis/Cholecystitis
``` Obesity Middle age Female Native American Diseases of the gallbladder, pancreas, or ileal disease ```
97
Causes of Cholecystitis
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
General Manifestations of Cholelithiasis
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
Manifestations of Cholelithiasis if there is total obstruction
- 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
Complications of Cholelithiasis
- Abscess - Pancreatitis - Gallbladder rupture - Delayed diagnosis increases morbidity and mortality
101
Diagnostic tests for cholelithiasis
- 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
How does HIDA diagnose cholelithiasis?
- 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
Treatment of Cholelithiasis
-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
What is the gold standard treatment of Cholelithiasis?
Laparoscopic Cholecystectomy
105
What are supportive measures prior to Cholecystectomy?
Fluid resuscitation Pain managemnt Antibiotics to target enteric organs
106
Pancreatitis
Inflammation of the pancreas due to autodigestion of the tissues
107
Chronic Pancreatitis
Irreversible histological changes and diminished function of the pancreas -ETOH USE = major cause
108
Causes of Acute Pancreatitis
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
How do trypsin, lipase, elastase, and cytokines/prostaglandis cause Pancreatitis?
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
Causes of Chronic Pancreatitis
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
Manifestations of Acute Pancreatitis
- 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
Manifestations of Chronic Pancreatitis
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
Diagnostics for Pancreatitis
- 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
Treatment for Acute Pancreatitis
- 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
Treatment for Chronic Pancreatitis
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
What are the disorders of the liver?
Hepatitis | Cirrhosis
117
Where is Hepatitis A found?
Feces, bile, and sera of infected individuals
118
What is the sequence of Acute Hepatitis?
Prodromal phase, Icteric phase, Recovery phase
119
Prodromal Phase
Begins 2 weeks after exposure with non specific symptoms
120
Icteric phase
Lasts 2-6 weeks
121
Recovery phase
Improvement of symptoms
122
Hep A (transmission, and where its found)
Usually transmitted by fecal-oral route - Direct contact - Food and beverage - Cups and spoons - Chronic
123
Risk Factors for Hep A
Crowded, unsanitary conditions | Food and water contamination
124
Hep E
Fecal-oral transmission - Developing countries - Similar to hep A but NOT chronic
125
Hep B
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
Hep D
same transmission route as HBV (blood, fluids, needles) - Dependent on HBV for replication - Often makes HBV infection worse
127
What does Hep D need to manifest?
Hep B
128
Hep C
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
What is the primary mode of transmission of Hep C?
IV drug use through sharing needles
130
What is the secondary mode of transmission of Hep C?
High risk sexual behavior
131
Symptoms of A & B Hepatitis
Nausea, vomiting
132
Complications of Hep B and C
- Chronic hepatitis and cirrhosis - End stage liver failure - Hepatocellular carcinoma
133
Cirrhosis
Irreversible inflammatory disease that disrupts liver function and structure
134
Types of Cirrhosis
- Alcoholic - Non-alcoholic fatty liver - Biliary (Bile canaliculi) - Metabolic
135
Cause of Cirrhosis
Inflammation leads to necrosis and fibrosis | -Nodular and fibrotic tissue synthesis leads to decreased hepatic function
136
Manifestations of Cirrhosis - Inflammation
Pain, fever, nausea, vomit, anorexia, fatigue
137
Manifestations of Cirrhosis - Necrosis
- 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
Manifestations of Cirrhosis - Fibrosis
``` Edema Portal HTN can cause: -hepatic necrosis -esophageal varices -splenomegaly -ascites ```
139
Other complications of Cirrhosis
Endstage liver disease - reduced clotting - impaired ammonia metabolism - impaired bilirubin metabolism - hypoglycemia - increased aldosterone production