GI (Exam 3) Flashcards

(113 cards)

1
Q

Cleft lip

A

failure of the maxillary processes and nasal elevations or upper lip to fuse during development

MALES TWICE AS LIKELY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cleft palate

A

failure of the hard and soft palate to fuse in development, creating an opening between the oral and nasal cavity

COMMON MULTIFACTORIAL CONGENITAL DEFECTS OF THE MOUTH AND FACE THAT ARE APPARENT AT BIRTH AND VARY IN SEVERITY; USUALLY DEVELOP AT 4-7 WEEKS GESTATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can cleft lip and cleft palate lead to?

A

feeding issues, speech problems, ear infections, hearing problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cleft palate demographics

A

associated with GENETIC MUTATIONS, DRUGS, TOXINS, VIRUSES, VITAMIN DEFICIENCIES, CIGARETTE SMOKING

most frequent in NATIVE AMERICANS, HISPANICS, AND ASIANS; AAs least likely

FEMALES TWICE AS LIKELY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Esophageal atresia

A

incomplete formation of the esophagus; fairly common congenital defect (Type C)

rarest and most severe is Type D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Possible causes of esophageal atresia?

A

EXACTLY CAUSE UNKNOWN

VACTERL (Vertebral anomalies, Anal atresia, Cardiac malformations, Tracheoesophageal fistula, Renal anomalies, Limb anomalies)
heart defects
mental/physical developmental delays
genital hypoplasia
ear abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk factors of esophageal atresia?

A

increased paternal age
maternal use of assisted reproduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Manifestations/complications of esophageal atresia

A

excessive secretions
coughing
vomiting
cyanosis after feeding

C: aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pyloric stenosis (infantile hypertrophic pyloric stenosis)

A

narrowing and obstruction of the pyloric sphincter

muscle fibers become thick and stiff, making it difficult for the stomach to empty food into small intestine

MAY BE PRESENT AT BIRTH/DEVELOP LATER, MOST CASES PRESENT AT 3 WEEKS OLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes/demographics of pyloric stenosis

A

EXACTLY CAUSE UNKNOWN (MULTIFACTORIAL), MOST COMMON IN MALES AND WHITES

EXPOSURE TO MACROLIDES (ANTIBIOTICS) IN EARLY INFANCY THOUGHT TO INCREASE RISK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Manifestations of pyloric stenosis

A

hard mass in abdomen
regurgitation
projectile vomiting
wavelike stomach contractions
small and infrequent stools
failure to gain weight
dehydration
irritability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Esophageal abnormality Causes of dysphagia

A

congenital atresia
esophageal stenosis/stricture
esophageal diverticula
tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neurological Causes of dysphagia

A

stroke
cerebral damage
parkinson’s
alzheimer’s
muscular dystrophy
huntingtons
cerebral palsy
MS
ALS
Guillan-Barre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Manifestations of dysphagia

A

sensation of food being stuck in throat
choking
coughing
pocketing food in cheeks
difficulty forming a food bolus
delayed swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hiatal hernia

A

a section of the stomach protrudes upward through opening in diaphragm

RISK FACTORS ARE ADVANCING AGE AND SMOKING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of hiatal hernia

A

weakening of diaphragm muscle
increased intrathoracic pressure (coughing, vomiting, straining during BM)
increased intra-abdominal pressure (pregnancy, obesity)
trauma
congenital defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hiatal hernia manifestations

A

indigestion
heartburn
frequent belching
nausea
chest pain
strictures
dysphagia
soft upper abdominal mass (protruding stomach pouch)

WORSENS WITH RECUMBENT POSITIONING, EATING ESPECIALLY AFTER LARGE MEALS, BENDING OVER, AND COUGHING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Gastroesophageal Reflux Disease (GERD)

A

chyme or bile periodically backs up from the stomach into the esophagus, irritating the esophageal mucosa

often confused with angina and may warrant ruling out cardiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of GERD

A

certain foods (chocolate, caffeine, carbonated beverages, citrus, tomatoes, spicy or fatty foods, peppermint)
alcohol or nicotine
history of hiatal hernia
obesity
pregnancy
certain medications (corticosteroids, beta blockers, calcium-channel blockers, anticholinergics)
delayed gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Manifestations of GERD

A

heartburn
epigastric pain (usually after meal or when recumbent)
dysphagia
dry cough
laryngitis
pharyngitis
regurgitation of food
sensation of lump in throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complications of GERD

A

esophagitis
strictures
ulcerations
esophageal cancer
chronic pulmonary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Gastritis

A

inflammation of the stomachs mucosal lining (may involve the entire stomach or region)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute gastritis

A

can be a mild transient irritation or it can be severe ulceration with hemorrhage

usually develops suddenly and likely to be accompanied by nausea and epigastric pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chronic gastritis

A

develops gradually; may be asymptomatic but usually accompanied by a dull epigastric pain and a sensation of fullness after minimal intake

can be further categorized as erosive or nonerosive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Helicobacter pylori
MOST COMMON CAUSE OF CHRONIC GASTRITIS *embeds itself in the mucous layer, activating toxins and enzymes that cause inflammation* **genetic vulnerability and lifestyle behaviors like smoking or stress may increase susceptibility**
26
Other causes of gastritis
food and water contamination long term use of NSAIDs excessive alcohol use severe stress autoimmune conditions
27
Gastritis manifestations
indigestion heartburn epigastric pain abdominal cramping nausea vomiting anorexia fever malaise **hematemesis and dark, tarry stools can indicate ulceration and bleeding**
28
Complications of chronic gastritis
peptic ulcers gastric cancer hemorrhage
29
Gastroenteritis
inflammation of the stomach and intestines, usually because of an infection or allergic reaction
30
Peptic Ulcer Disease (PUD)
erosive lesions affecting stomach lining or duodenum; develops from an imbalance between destructive forces and protective mechanisms **vary in severity from superficial erosions to complete penetration**
31
Risk factors for PUD
male advancing age NSAIDs H. Pylori infections certain gastric tumors risk factors for GERD (*smoking, alcohol, etc.*)
32
Duodenal ulcers (PUD)
MOST COMMON (*associated with excessive acid or H.Pylori*) **typically present with epigastric pain that is relieved in the presence of food**
33
Gastric ulcers (PUD)
LESS FREQUENT BUT DEADLIER (*associated with malignancy and NSAIDs*) **pain typically worsens with eating**
34
Stress ulcers (PUD)
develop because of a major physiological stressor on the body due to **local tissue ischemia, tissue acidosis, bile salts entering the stomach and decreased GI motility** curlings and cushing’s ulcers
35
Curlings ulcers
stress ulcers associated with burns
36
Cushing’s ulcers
stress ulcers associated with head injuries
37
Stress ulcers complications
GI hemorrhage obstruction perforation peritonitis
38
Stress ulcers manifestations
epigastric or abdominal pain abdominal cramping heartburn indigestion nausea vomiting
39
Cholelithiasis (gallstones)
common condition that varies in severity based on **size of stone** but affects both genders and all ethnic groups equally **may instruct bile flow and cause *gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma*** cholecystitis
40
Cholecystitis
inflammation or infection in the biliary system caused by calculi
41
Risk factors for cholelithiasis
advancing age obesity diet rapid weight loss pregnancy hormone replacement long-term parenteral nutrition
42
Manifestations of cholelithiasis
biliary colic abdominal distention nausea vomiting jaundice fever leukocytosis
43
Hepatitis
inflammation of the liver *can be acute, chronic or fulminant; active or nonactive* **can result in *hepatic cell destruction, necrosis, autolysis, hyperplasia, scarring***
44
Hepatitis causes
infections (*usually viral*) alcohol medications (*acetaminophen, antiseizure agents, antibiotics*) autoimmune disease
45
Nonviral hepatitis
noncontagious and most will recover (*toxicity related to meds*) **may develop *liver failure, liver cancer or cirrhosis***
46
Viral hepatitis
contagious but most will recover with sufficient time **advancing age and comorbidity increase the likelihood that *liver failure, liver cancer or cirrhosis* will develop**
47
Hepatitis A (HAV)
spread through food, drink, and close contact with infected person
48
Hepatitis B (HBV)
spread from mother to baby, sexual transmission, sharing needles and contact with the blood of an infected person
49
Hepatitis C (HCV)
spreads through childbirth, sharing needles, tattoos in unregulated shops
50
Hepatitis D (HDV)
can only be contracted if you have HBV
51
Hepatitis E (HEV)
transmitted via food or water
52
Acute hepatitis
four phases; **asymptomatic incubation phase, 3 symptomatic phases**
53
Chronic hepatitis
continued hepatic disease lasting longer than 6 months **symptom severity and diseases progression vary depending on degree of liver damage; can quickly deteriorate with declining liver integrity**
54
Cirrhosis
chronic, progressive, irreversible, diffuse damage to the liver resulting in decreased liver function; may develop after 40 yrs even if underlying cause is addressed **leads to *fibrosis, nodule formation, impaired blood flow, bile obstruction that can result in liver failure***
55
Cirrhosis causes
HCV chronic alcohol abuse
56
Cirrhosis manifestations
portal hypertension ascites jaundice varicosities enlarged organs slow/severe bleeding clotting changes muscle wasting hyperlipidemia hyper/hypoglycemia toxin and bile accumulation clay-colored stools and dark urine intense itchiness altered hormone regulation (*decreased estrogen absorption*) esophageal varices
57
Pancreatitis causes
cholelithiasis alcohol abuse biliary dysfunction hepatotoxic drugs metabolic disorders trauma renal failure endocrine disorders pancreatic tumors penetrating peptic ulcer
58
Pancreatitis
pancreatic injury causes enzymes to leak into pancreatic tissue and initiates autodigestion, resulting in *edema, vascular damage, hemorrhage, and necrosis* **pancreatic tissue is replaced by fibrosis which causes exocrine and endocrine changes and dysfunction of the islets of Langerhans**
59
Acute pancreatitis
medical emergency; mortality increases with advancing age and comorbidity
60
Complications of acute pancreatitis
acute respiratory distress syndrome diabetes mellitus infection shock disseminated intravascular coagulation renal failure malnutrition pancreatic cancer pseudocyst abscess
61
Acute pancreatitis manifestations
**usually sudden and severe** upper abdominal pain that radiates to the back, worsens after eating and is somewhat relieved by leaning forward of pulling knees to chest nausea and vomiting mild jaundice low grade fever BP and pulse changes
62
Chronic pancreatitis manifestations
**insidious** upper abdominal pain indigestion losing weight w/o trying steatorrhea constipation flatulence
63
Intestinal obstruction
sudden or gradual and partial or complete blockage of intestinal contents in intestines; mechanical and functional obstructions **chyme and gas accumulate at site of blockage; saliva, gastric juices, bile, and pancreatic secretions begin to collect as blockage lingers and can cause abdominal distention and pain**
64
Mechanical obstructions (intestinal)
foreign bodies tumors adhesions hernias intussusception volvulus strictures IBS fecal impaction
65
Functional obstructions (paralytic ileus) (intestinal)
neurologic impairment intra-abdominal surgery complications chemical, electrolyte, and mineral disturbances infections blood supply impairment (*strangulation, necrosis, contents seep into abdomen*) meds (*narcotics*)
66
Intestinal obstruction complications
perforation pH imbalance fluid disturbances shock death
67
Manifestations of intestinal obstruction
abdominal distention abdominal cramping and colicky pain nausea and vomiting constipation or diarrhea intestinal rushes decreased/absent bowel sounds restlessness diaphoresis tachycardia progressing to weakness confusion and shock
68
Appendicitis
inflammation of the vermiform appendix, most often caused by infection
69
Appendicitis pathogenesis
1. inflammation triggers local tissue edema, which obstructs small structure 2. as fluid builds up inside appendix, microorganisms proliferate 3. appendix fills with purulent exudate and area blood vessels become compressed 4. ischemia and necrosis develop; bacteria and toxins leak out to surrounding structures
70
Complications of appendicitis
abscesses peritonitis gangrene sepsis death
71
Appendicitis manifestations
**vary from asymptomatic to sudden and severe** nausea, vomiting, abdominal distention, bowel pattern changes indications of inflammation and infection (*fever, chills, leukocytosis*) indications of peritonitis (*abdominal rigidity, tachycardia, hypotension*) sharp abdominal pain develops, gradually intensifies (over 12-24 hrs) and becomes localized to LRQ of abdomen (**McBurney point**) pain may occur anywhere in abdomen and will temporarily subside when appendix ruptures then return and escalate
72
Peritonitis
inflammation of the peritoneum that activates several protective mechanisms
73
Peritonitis: Protective mechanisms
1. thick, sticky exudate that bonds nearby structures and temporarily seals them off 2. abscesses may form to wall off infections 3. peristalsis may slow down in response to inflammation, decreasing spread of toxins
74
Causes of peritonitis
chemical irritation (*ruptured gallbladder or spleen*) direct organism invasion (*appendicitis, peritoneal dialysis*)
75
Peritonitis manifestations
**usually sudden and severe** ABDOMINAL RIGIDITY abdominal tenderness and pain decreased peristalsis intestinal obstruction nausea and vomiting large volumes of fluid leak into peritoneal cavity indicators of infection, sepsis or shock
76
Celiac disease
celiac sprue or gluten sensitivity enteropathy; inherited, autoimmune, malabsorption disorder **most common in whites and women, a childhood disease but can develop any time**
77
Celiac disease causes
1. combination of immune response to an environment factor (*gliadin*) and genetic predisposition 2. defect in intestinal enzymes that prevents further digestion of gliadin (*a product of gluten digestion*) **intestinal villi with atrophy and flatten, causing decreased enzyme production, decreasing surface area available for nutrient absorption**
78
Celiac disease manifestations
in infants, generally appear as cereals are added to diet (4-6 months) abdominal pain/distention bloating gas indigestion constipation diarrhea lactose intolerance nausea steatorrhea weight loss irritability lethargy malaise behavioral changes
79
Complications of celiac disease
anemia arthralgia myalgia bone disease dental enamel defects and discoloration intestinal cancers depression growth and development delays in kids hair loss hypoglycemia mouth ulcers increased bleeding tendencies neurologic disorders skin disorders vitamin/mineral deficiency endocrine disorders
80
Inflammatory Bowel Disease (IBD)
chronic inflammation of the GI tract, usually intestines; exacerbations and remissions and **can be painful, debilitating, and life-threatening** *women, whites, jewish people, and smokers* thought to be caused by genetically associated autoimmune state that has been activated by infection **immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the function and neural activity of the secretory and smooth muscle cells** FLUID, ELECTROLYTE, pH IMBALANCES DEVELOP
81
Crohn’s disease (IBD)
insidious, slow developing, progressive condition often develops in adolescence **patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations (skip lesions); wall is thick/rigid and lumen is narrowed**
82
Crohn’s disease pathogenesis
1. form fissures developed by nodules, giving the intestinal wall a cobblestone appearance 2. granulomas develop on intestinal wall and nearby lymph nodes 3. damaged intestinal wall loses ability to digest and absorb 4. inflammation also stimulates intestinal motility, decreasing digestion and absorption
83
Crohn’s disease manifestations
abdominal cramping and pain (*RLQ*) diarrhea steatorrhea constipation palpable abdominal mass melena anorexia weight loss indications of inflammation (*fever, fatigue, arthralgia, malaise*)
84
Complications of crohn’s disease
malnutrition anemia (*iron deficiency*) fistulas adhesions abscesses intestinal obstruction perforation anal fissure delayed growth and development fluid, electrolyte, pH imbalances
85
Ulcerative colitis (IBD)
progressive condition of the rectum and colon mucosa, usually developing in 20s-30s **ulcers merge = inadequate surface area for absorption**
86
Ulcerative colitis pathogenesis
1. inflammation triggered by T cell accumulation in colon mucosa which causes epithelium loss, surface erosion, and ulceration that begins in rectum and extends to entire colon 2. mucosa becomes inflamed, edematous, and frail 3. necrosis of the epithelial tissue can result in abscesses; granulation tissue formed is fragile
87
Ulcerative colitis manifestations
diarrhea (*frequent, as many as 20x daily*) watery stools (*with blood and mucus*) proctitis abdominal cramping nausea and vomiting weight loss indications of inflammation (*fever, fatigue, arthralgia, malaise*)
88
Ulcerative colitis complications
malnutrition anemia hemorrhage perforation strictures fistulas toxic megacolon colorectal carcinoma liver disease fluid, electrolyte, and pH imbalances
89
Irritable bowel syndrome (IBS)
chronic, noninflammatory GI condition with exacerbations associated with stress **includes alterations in bowel pattern and abdominal pain not explained by structural or biochemical abnormalities** *less serious than IBD and doesn’t cause permanent intestinal damage; MORE COMMON IN WOMEN*
90
3 theories of IBS etiology
1. altered GI motility 2. visceral hyperalgesia (increased sensitivity to pain) 3. psychopathology **intensified response to stimuli with increased intestinal motility and contractions means low tolerance for stretching and pain in intestinal smooth muscle**
91
Complications of IBS
hemorrhoids nutritional deficits social issues sexual discomfort
92
Manifestations of IBS
stress, mood disorders, food, and hormone changes often worsen symptoms abdominal distention, fullness, flatus, and bloating intermittent abdominal pain exacerbated by eating and relieved with shitting chronic and frequent constipation or diarrhea usually with pain non bloody stool that may contain mucus bowel urgency intolerance to certain foods (*gas-forming; sorbitol, lactose, gluten*) emotional distress anorexia
93
Diverticular Disease
conditions related to the development of diverticula, outwardly bulging pouches of intestinal wall that occur when mucosa secretions or large intestine submucosa layers herniate through a weakened muscular layer; may be congenital or acquired
94
Diverticular disease causes
low-fiber diet and poor bowel habits resulting in chronic constipation (*muscular wall can become weakened from the prolonged effect of moving hard stools*) **more common in developed countries with shitty diets**
95
Diverticulosis
asymptomatic diverticular disease, multiple diverticula present
96
Diverticulitis
diverticula become inflamed, usually because of retained fecal matter (often asymptomatic until it becomes serious) **potential for fatal obstruction, infection, abscess, perforation, peritonitis, hemorrhage, shock**
97
Diverticular disease manifestations
abdominal cramping passing frank blood low-grade fever abdominal tenderness (*LLQ*) abdominal distention/mass constipation obstipation nausea leukocytosis
98
Oral Cancer
most cases involve squamous cell carcinomas of the tongue and mouth floor; very treatable if caught early but most cases are advanced upon diagnosis *usually appears as one or more painless, whitish thickenings that develop into a nodule or an ulcerative lesion that persists, doesn’t heal and bleeds easily* **a lump, thickening or soreness in the mouth, throat, or tongue as well as difficulty chewing or swallowing**
99
Risk factors of oral cancer
smoked and smokeless tobacco alcohol consumption viral infections (*HPV*) immunodeficiency inadequate nutrition poor dental hygiene chronic irritation exposure to UV light **often metastasizes to neck lymph nodes and esophagus**
100
Esophageal cancer
usually squamous cell carcinoma in distal esophagus; most common in men and associated with chronic irritation **tumors grow the circumference of the esophagus, creating a stricture, or they can grow out into the lumen of the esophagus creating an obstruction**
101
Complications of esophageal cancer
esophageal obstruction respiratory compromise esophageal bleeding
102
Manifestations of esophageal cancer
**usually asymptomatic early, delaying treatment** dysphagia chest pain weight loss hematemesis (vomiting blood)
103
Gastric cancer
occurs in several forms but adenocarcinoma (*an ulcerative lesion*) is most frequent incidence and mortality rates declined in US but very prevalent in Japan
104
Risk factors of gastric cancer
**STRONGLY ASSOCIATED WITH INTAKE OF SALTED, CURED, PICKLED, PRESERVED, AND SMOKED FOOD** low fiber diet constipation family history H.Pylori infections smoking pernicious anemia chronic atrophic gastritis gastric polyps
105
Manifestations of gastric cancer
**asymptomatic early stages delay diagnosis and treatment** abdominal pain/fullness epigastric discomfort palpable abdominal mass melena dysphagia that worsens over time excessive belching anorexia nausea vomiting hematemesis premature abdominal fullness after meals unintentional weight loss weakness fatigue
106
Liver Cancer
most commonly occurs as a second tumor that has metastasized from breast, lung or other GI structures; rates in US have tripled since 1980 **causes of primary tumors are chronic cirrhosis and hepatitis**
107
Liver cancer manifestations
anorexia fever jaundice nausea vomiting abdominal pain (*RUQ*) hepatomegaly splenomegaly portal hypertension edema third spacing ascites paraneoplastic syndrome diaphoresis weight loss
108
Pancreatic cancer
aggressive malignancy that quickly metastasizes, usually adenocarcinoma most frequent in men and AA’s
109
Pancreatic cancer risk factors
family history obesity chronic pancreatitis long-standing diabetes mellitus cirrhosis alcohol abuse tobacco use
110
Pancreatic cancer manifestations
**often asymptomatic until well advanced** progressive upper abdomen pain that may radiate to back jaundice dark urine clay-colored stools indigestion anorexia weight loss depression malnutrition hyperglycemia increased clotting tendencies
111
Colorectal cancer
very common and fatal **associated with fatty, caloric, low fiber diets with red meat, processed meal, and alcohol**
112
Risk factors for colorectal cancer
male AA family history advancing age obesity tobacco use physical inactivity IBD
113
Colorectal cancer manifestations
**asymptomatic until advanced** lower abdominal pain and tenderness blood in stool (*occult or frank*) diarrhea constipation intestinal obstruction narrow stools unexplained anemia (*usually iron deficiency*) unintentionally weight loss