gi disorders Flashcards

1
Q

Upper and lower GI :

A

Upper : Esophagus, Stomach, Beginning of small intestines

Lower GI: Small intestines, colon (large intestines), rectum/anus

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

upper GI problems

A

esophageal:
- GERD
- Hiatial Hernia

Inflammatory disorders of stomach:

  • gastritis
  • acute gastroenteritis
  • PUD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

dysphagia definition

A

Defined: Difficulty swallowing
Begins with solids and progresses to liquids

Common Causes:

  1. Mechanical obstruction
    - Stenosis or stricture
    - Diverticula
    - Tumors
  2. Neuromuscular dysfunction, intubation or trach
    - CVA
    - Achalasia
    – LES (lower esophageal sphincter) can’t open properly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is GERD?

A
  • gastroesophageal reflux disease
  • upper GI problem
  • esophageal disorder
  • Backflow of gastric acid from the stomach into the esophagus
  • Occurs via the lower esophageal sphincter (LES)
  • Highly ACIDIC material!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

gerd etiology

A
Anything that alters closure strength of LES or increases abdominal pressure
Examples:
Fatty foods
Spicy foods
Tomato based foods
Citrus foods
Caffeine
Large amounts of alcohol
Cigarette smoking
Sleep position
Obesity
Pregnancy
Pharmacologic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

gerd clinical manifestations

A
Heartburn (pyrosis)
Dyspepsia - indigestion
Regurgitation
Chest pain
Dysphagia
Pulmonary symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

gerd complications

A

Complications:
ulceration
scarring
strictures
Barrett esophagus (development of abnormal metaplastic tissue - premalignant)
**Three-fold increased risk of developing adenocarcinoma of the esophagus
Overall survival only 17%

**longterm GERD = increased risk esophageal

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

hiatal hernia

A

A defect in the diaphragm that allows part of the STOMACH to pass into the THORAX

Two Main Types:
1. Sliding hernia – usually small and often do not need treatment** less severe
2. Paraesophageal hernia- part of the stomach pushes through the diaphragm and stays there- peritonial becomes thin
**more severe
3-4. mix of type 1 & 2 and increase with severity

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

hiatal hernia: pathophysiology

A

Exact cause is unknown
Age related Injury or other damage may weaken the diaphragm muscle
Repeatedly putting too much pressure on the muscles around the stomach
- Severe coughing
- Vomiting
- Constipation and straining to have a bowel movement

**obesity increases risk

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

risk factors hiatal hernia

A

age
obesity
smoking

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

clinical manifestations hiatal hernia

A

Asymptomatic
Belching
Dysphagia
Chest or epigastric pain

**common for hiatal hernia and GERD to coexist

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

hiatal hernia tx

A

Mostly a conservative treatment
Teaching: small, frequent meals, avoid lying down after eating
Avoid tight clothing and abdominal supports
Weight control for obese individuals
Antacids for the GERD/esophagitis symptoms
Surgery if the conservative treatments do not work

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

what is gastritis

A

inflammatory condition of the stomach

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

acute gastritis

A

Defined: TEMPORARY inflammation of the STOMACH lining only (intestines NOT affected)
Generally last from 2-10 days

Etiology:
Irritating substances (**alcohol
Drugs (NSAIDs) - stop prostaglandin secretion in stomach
Infectious agents - h. pylori

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

chronic gastritis

A

PROGRESSIVE disorder with chronic inflammation in the stomach
Can last weeks to years

Complications: PUD, bleeding ulcers, anemia, gastric cancers
Two main etiologies:
Autoimmune - Attacks parietal cells
H. pylori infection - acute or chronic

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

what is h. pylori

A

Helicobacter pylori bacterium- gram negative spiral bacteria
Acidic environment
Destructive pattern of persistent inflammation
- Can cause chronic gastritis, PUD, and stomach cancer

How is it transmitted?

  • Person to person via saliva, fecal matter, or vomit
  • Contaminated food or water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

clinical manifestations acute/chronic gastritis?

A
Sometimes none
Anorexia
N/V
Postprandial (after eating) discomfort
Intestinal gas
Hematemesis
Tarry Stools
Anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is acute gastroenteritis

A

Inflammation of stomach & SMALL INTESTINE

Etiology:
Viral infections: Norovirus and rotavirus
Bacterial infections: E. col, salmonella, campylobacter
Parasitic infections

Usually lasts 1-3 days but may last as long as 10 days

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

clinical manifestations and complications acute gastroenteritis

A

Clinical manifestations
*Watery Diarrhea
May be bloody if bacterial

Abdominal pain
N/V
Fever, malaiseComplication: fluid volume deficits
** decreased fluid = increased dehydration

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

what is peptic ulcer disorder (PUD)?

A

Ulcerative disorder of the upper GI tract

  1. Esophageal
  2. Stomach - gastric ulcers
  3. Duodenum - peptic ulcer in the first part of the small intestine

Develops when the GI tract is exposed to acid and h. pylori

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

what are factors that influence healthy GI balancing?

A

aggressive factors (causing ulcers)

  • h. pylori
  • NSAIDs
  • acid
  • pepsin
  • smoking

defensive factors

  • mucus
  • bicarbonate
  • increased blood flow
  • prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

peptic ulcer disease etiology

A

H. pylori
Injury-causing substances
**NSAIDs, ASA, alcohol
Excess secretion of acid
SmokingFamily history
Stress - remember there is increased gastric acid secreted with the stress response
**can worsen the response not the actual cause tho

23
Q

risk factors NSAIDs PUD

A

**inhibits prostaglandin synthesis and decreases mucus protection in stomach
Age
Higher doses of NSAIDs
History of PUD
Use of corticosteroids and anticoagulants
Serious systemic disorders
H. pylori infection

24
Q

PUD pathogenesis

A

Mucosa is damaged
Histamine is secreted, resulting in:
Increase in acid and pepsin secretion
– causes further tissue damage

Vasodilation
– causes edema
***If blood vessels are destroyed, this results in BLEEDING

25
Q

PUD classification - Duodenal ulcer

A
***Most common type
Age – any; early adulthood
Gastric/peptic ulcer
Age – peak 50 - 70
Why?   Increased use of NSAIDS, corticosteroids, anticoagulants and more likely to have serious systemic illnesses
26
Q

PUD clinical manifestations

A
Sometimes none
N/V, anorexia
Weight loss
Bleeding
Burning Pain - in middle of abdomen that is usually worse when the stomach is empty
27
Q

describe gastric ulcers

A

burning, cramping, gas-like
epigastric, back
1-2 hours after eating

28
Q

describe duodenal ulcers

A

burning, cramping, gas-like
epigastrium, back
***2-4 hours after eating

29
Q

how to best decipher btw gastric and duodenal PUD?

A

timing!!
gastric - 1-2 hrs after eating
duodenal - 2-4 hrs after eating

30
Q

PUD complications (HOP)

A
“HOP” 
Complications
H – Hemorrhage
O – Obstruction - scarring tissue bondage
P – Perforation and Peritonitis
31
Q

what are the lower GI disorders

A

appendicitis
peritonitis
irritable bowel disorder

inflammatory bowel disorder
- Crohn’s and ulcerative colitis

diverticulosis/diverticulitis

32
Q

appendicitis

A

Inflammation of the appendix
**RLQ pain

Etiology
Appendix is OBSTRUCTED

Leads to INFLAMMATION

Complications
Gangrene
Abscess formation
**PERITONITIS

33
Q

appendicitis and pain

A

Classic Pain: RLQ in periumbilical area

Rebound Pain
Sudden pain relief may indicate rupture
- Peritonitis

Rebound Pain = Pain is SEVERE after release of palpating hand over the RLQ

34
Q

what is peritonitis

A

Inflammation of the PERITONEUM (abdominal cavity)

Serous membrane that lines abdominal cavity & covers visceral organs (like the pleura for lungs)What happens to the peritoneum?

  • INFLAMMATION
  • Fluid shifts

– THIRD SPACING
- Can lead to hypovolemic shock and sepsis

DECREASED PERISTALSIS
- Can lead to paralytic ileus and intestinal obstruction

35
Q

causes peritonitis

A
perforated ulcer
ruptured gallbladder
pancreatitis
ruptured spleen
ruptured bladder
ruptured appendix
non-asepsis during peritoneal dialysis
36
Q

clinical manifestations peritonitis

A
Usually sudden and severe
Abdominal pain* severe
***Tenderness
Rigid “board-like” abdomen
 **hard to touch**
N/V
Others:
Fever
Elevated WBC
HR \_\_\_\_\_increased\_\_\_\_
BP \_\_\_\_decreased\_\_\_\_\_
37
Q

lower GI problems

A

irritable bowel syndrome (IBS)

inflammatory bowel disease (IBD)

38
Q

IBS - irritable bowel syndrome

A

Chronic condition characterized by:
alterations in bowel pattern due to changes in intestinal motility,
Chronic and frequent constipation (IBSC)
Chronic and frequent diarrhea (IBSD)

39
Q

symptoms IBS

A

Symptoms: vary by individual
Abdominal distension, fullness, flatus, and bloating
Intermittent abdominal pain exacerbated by stress and ***RELIEVED BY DEFECATION
Bowel urgency
Intolerance to certain foods (sorbitol, lactose, gluten)
Non-bloody stool that may contain mucous

40
Q

stress and IBS

A

IBS is almost never the result of primarily psychological causes
“Emotional stress did not cause my illness”
IBS can be exacerbated by stress

“Emotional stress can make my illness worse.”
IBS can cause stress and psychological problems

“My IBS is stressful to live with and may cause me to have emotional problems.”
Cause UNKNOWN but thought to be “triggered” by stress, food, hormone changes, GI infections, menses

41
Q

inflammatory bowel disease - 2 types?

A

A group of life-changing, chronic illnesses
TWO SEPARATE DISORDERS:
Crohn’s disease
Ulcerative colitis

Characterized by:
Chronic inflammation of the intestines
Exacerbation and remissions

More common in WOMEN, Caucasians, persons of Jewish descent, and smokers

Etiology? Genetically
AUTOIMMUNE activated by an infection

42
Q

crohn’s disease - pathogenesis

A

Lymph structures of the GI tract are blocked
Tissue becomes engorged and inflamed
Deep linear FISSURES and ULCERS develop in a ”patchy” pattern in the bowel wall
—SKIP LESIONS—COBBLESTONE APPEARANCE

Complications:
Malnutrition
Anemia
Scar tissue and obstructions
Fistulas- connections btw 2 structure that's not           normal
 Cancer
43
Q

crohn’s disease clinical manifestations

A

Crampy lower Abdominal pain (RLQ)
Watery diarrhea

SYSTEMIC: Weight loss, fatigue, no appetite, fever, malabsorption of nutrients
Palpable abdominal mass (RLQ)
Mouth ulcers

S/S of fistulas - location dependent
granulomas and skip lesions*

44
Q

ulcerative colitis definition

A

Inflammation of the mucosa of the RECTUM AND COLON
Usually develops in the third decade of life

More common in white people of European descent, esp. Ashkenazi Jewish descent
Occasionally in Black/African Americans
Rare in Asians

45
Q

ulcerative colitis pathogenesis**crypt abscesses

A

Inflammation begins in the rectum and extends in a CONTINUOUS segment that may involve the ENTIRE colon
Inflammation leads to large ulcerations

Necrosis of the epithelial tissue can result abscesses – CRYPT ABSCESSES

Colon and rectum try to repair the damage with new granulation tissue
Why is this a problem? Tissue is fragile and bleeds easily

46
Q

ulcerative colitis clinical manifestations

A

Abdominal pain
***Bloody diarrhea - not typical with crohns

Systemic:
Weight loss, fatigue, no appetite, fever

47
Q

complications ulcerative colitis

A
Hemorrhage - bc of new granulation tissue
Perforation
Cancer
Malnutrition
Anemia
Strictures
FISSURES
ABSCESSES - rectal, colon, anal
TOXIC MEGACOLON – a rapid dilation of the large intestine that can be life-threatening

COLORECTAL CARCINOMA
Liver Disease – from inflammation and scarring of bile ducts
Fluid, electrolyte and PH imbalances
-increase risk vte/dvt

48
Q

diverticular disease pathogenesis

A

Development of diverticula:
Small pouches in lining of colon that bulge outward through weak spots

May be CONGENITAL or ACQUIRED
Thought to be caused by low fiber diet with resulting chronic constipation

Usual location: DESCENDING COLON

49
Q

diverticulosis vs diverticulitis

A

diverticulosis - not inflamed

diverticulitis - inflammed

50
Q

diverticulosis clinical manifestations

A

Usually asymptomatic

Discovered accidently or with presentation of acute diverticulitis

51
Q

diverticulitis

A
INFLAMMATION of one or more of the pouches (diverticula)
Usually from retained fecal material
Clinical manifestations
Abdominal pain – LLQ	
Fever
WBC’s \_\_increased_
Constipation or diarrhea
Acute – passage large quantity of frank blood
May resolve spontaneously

Complications
Perforation
Peritonitis
Obstruction

52
Q

pyrosis?

A

heartburn

53
Q

dyspepsia?

A

indigestion