Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Week 5 (ch. 17) > Flashcards

Week 5 (ch. 17) Flashcards

1
Q

Gut wall: Mucosa

A

Epithelium, including mucous producing cells

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

Gut wall: submucosa

A

CT - including blood vessels, nerves, lymphatics, secretory glands

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

Gut wall: serosa

A

visceral peritoneum

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

What are the structures of the gut wall

A

mucosa, submucosa, circular smooth muscle layer, longitudinal smooth muscle layer, serosa

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

What are the structures in the upper GI tract and accessory

A 
Oral cavity
Esophagus 
Stomach
Liver 
Pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

salivary amylase

A

starts chemical breakdown of carbohydrates in oral cavity

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

Deglutition

A

swallowing

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

Esophagus

A

Closed except during swallowing, skeletal muscle at superior end - followed by smooth muscle

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

Describe what happens in the upper GI tract during swallowing

A

a. soft palate is pulled upward
b. vocal cords are approximated
c. epiglottis covers the larynx
d. respirations ceases
e. bolus is seized by the constricted pharynx
f. bolus of food moves into esophagus

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

how many muscle layers does stomach have

A

3

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

What are some functions of the stomach

A

a. Mixing and churning food
b. Initial digestion of proteins
c. production of intrinsic factor
d. formation of chyme
e. absorption of smell and lipid-soluble molecules

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

What chemical digests proteins and how is this chemical formed?

A

Pepsin (in the stomach)

– formed by combination of pepsinogen and HCl

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

Why is intrinsic factor important in stomach?

A

essential for absorption of vitamin B12 in ileum

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

Liver receives blood from where

A

hepatic portal vein

- from intestine to liver

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

What stores nutrients in the liver?

A

Hepatocytes

- play role in carbs, proteins, fat metabolism

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

What are some functions of the liver

A

a. production of plasma proteins and clotting factors
b. breakdown of old and damages erythrocytes
c. bile production

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

Pancreas is what

A

Exocrine pancreas arranged in lobules

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

Pancreas secretes digestive enzymes such as?

A 
Trypsin
Chymotrypsin 
carboxypeptidase
ribonuclease 
pancreatic amylase 
bicarbonate ions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the pancreatic duct join to enter the duodenum

A

bile duct

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

What structures are in the lower GI tract?

A

Small intestine

Large intestine

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

What are the structures of the SI

A

Duodenum, jejunum and ileum

- villi / microvilli

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

villi and microvilli

A 
villi = folds of mucosa 
microvilli = folds of cell membranes

Both increase surface area for absorption

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

SI is major site of what

A

absorption

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

SI is the site of what production?

A

mucus

enterokinase, peptidases, nucleosidases, lipase, sucrase, maltase, lactase, cholecystokinin (hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

SI is lacteal, meaning what?

A

lymphatic vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Large intestine functions

A

Fluid/electrolyte reabsorption

formation of solid feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Large intestine has resident flora, which does what?

A

Breakdown of certain food material

Vitamin K synthesis by bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Large intestine has Peyer patches, which are?

A

lymphatic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

PNS: stimulation and effect

A

Primarily though vagus nerve

  • increased motility
  • increased secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

SNS stimulation and effects

A

Stimulated by factors such as fear, anger

  • inhibits GI activity
  • causes vasoconstriction
  • reduced secretions and regeneration of epithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What do facial nerve and glossopharyngeal nerves do

A

maintain continuous flow of saliva in mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Effects of distention and stretching of stomach

A
  • PNS activation

- increase peristalsis and gastric secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how often does stomach empty

A

2-6 hours after meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Gastrin: formation

A

Secreted by mucosal cells (stomach) in response to distention of stomach or partially digested substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

gastrin: function

A

increase gastric motility, relaxes pyloric and ileocecal sphincters - promotes stomach emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Histamine

A

increased secretion of HCl acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Secretin

A

Decreases gastric secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Cholecystokinin

A

inhibits gastric emptying; stimulates contraction of gall bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Digestion and Absorption: carbohydrates

A

Digestion starts in mouth followed by digestion in small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Digestion and Absorption: proteins

A

digestions starts in stomach, continues in SI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Digestion and Absorption: lipids

A

Emulsified by bile prior to chemical breakdown. Action of enzymes form monoglycerides and free fatty acids.

Formation of Chlyomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Digestion and Absorption: Fat soluble vitamin

A

vitamins A, D, E K

– absorbed with fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Digestion and Absorption: Water soluble vitamins

A

B and C

– diffuse into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Digestion and Absorption: electrolytes

A

absorbed by active transport or diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where are drugs primarily absorbed?

A

stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where is aspirin usually absopbed?

A

stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is water absorbed

A

primarily osmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how much water is secreted into digestive tract each day

A

about 700 mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how much fluid is ingested in good and fluids each day

A

about 2300 mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

how much fluid leaves the body in feces

A

only 50-200mL

– vomiting and diarrhea disrupt this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Common manifestations of Digestive Disorders

A

Anorexia, nausea, vomiting and bulimia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

where is the vomiting center located in the body

A

medulla

  • coordinates activities involved in vomiting
  • protects airway during vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is commonly effected from bulimia? Why?

A

Oral mucosa, teeth, esophagus

– damage is caused by recurrent vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Vomiting Center Activation: what is effected?

A

a. distention / irritation of digestive tract
b. vestibular apparatus of inner ear (motion)
c. increased intracranial pressure
- - sudden projective vomiting without previous nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Vomiting Reflex Activities

A 
Deep inspiration
Closing glottis, raising soft palate
Ceasing respiration
Relaxation of gastroesophageal sphincter
Contracting abdominal muscles
Reversing peristaltic waves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Characteristics of Vomitus: Presence of blood

A

Hematemesis

  • coffee grounds vomitus; brown glandular material indicates actions of HCl on hemoglobin
  • hemorrhage - red blood may be in vomitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Characteristics of Vomitus: yellow or green

A

bile from duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Characteristics of Vomitus: deeper brown color

A

may indicate content from lower intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Characteristics of Vomitus: recurrent vomiting of undigested food

A

problem with gastric emptying or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Large volume diarrhea (secretory or osmotic)

A

Watery stool resulting from increased secretions into intestine from the plasma

Often related to infection

Limited reabsorption because of reversal of normal carriers for sodium and/or glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Small-volume diarrhea

A

Often caused by inflammatory bowel disease

  • stool may contain blood, mucus and pus
  • may be accompanied by abdominal cramps and tenesmus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Steatorrhea

A

“fatty diarrhea”

  • frequently bulky, greasy, loos stools
  • foul order
  • characteristics of malabsorption syndromes
  • fat usually the first dietary component affects
  • abdomen often distended
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What syndromes may have Steatorrhea

A

Celiac disease, cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why is fat usually the first dietary component affected leading to Steatorrhea ?

A

presence interferes with digestion of other nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Blood in stool: Frank blood

A

Red blood - usually from lesions in rectum or anal canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Blood in stool: Occult blood

A

Small hidden amounts, detectable with stool tests

may be caused by small bleeding ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Blood in stool: Melena

A

Dark-colored, tarry stool

May result from significant bleeding in upper digestive tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Causes of excessive gas

A

Eructation
Borborygmus
Abdominal distention and pain
Flatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Gas results from

A

swallowed air (drinking through straw)
Bacterial action on food
foods or alterations in motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Constipations

A

less frequent bowel movements than normal

  • small or hard stools
  • acute or chronic issue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Chronic constipation may cause what

A

hemorrhoids, anal fissures, diverticulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Causes of constipation

A 
Weakness of smooth muscle fibers (age/illness)
low fiber intake
low fluid intake
failure to response to defecation reflex
immobility
neurological disorders
drugs
some antacids, iron meds
obstruction caused by tumors or strictures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Common complications of digestive tract disorders

A

dehydration and hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Digestive tract disorders: Metabolic Alkalosis

A

Results from loss of hydrochloric acid with vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Digestive tract disorders: metabolic acidosis

A

Severe vomiting causes a change to metabolic acidosis because of the loss of bicarbonate of duodenal secretions.

Diarrhea causes loss of bicarbonate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Visceral pain digestive tract: Burning sensation

A

inflammation and ulceration in upper digestive tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Visceral pain digestive tract: dull, aching pain

A

typical result of stretching of liver capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Visceral pain digestive tract: cramping or diffuse pain

A

inflammation, distention, stretching of intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Visceral pain digestive tract: Colicky, often severe pain

A

Recurrent smooth muscle spasms or contraction

- response to severe inflammation or obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Somatic pain receptors are directly linked to what

A

spinal nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

rebound tenderness

A

Identified over area of inflammation when pressure is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Somatic pain digestive tract:

A

Steady, intense, often localized

  • may cause reflex spasms of overlying abdominal muscles
  • involvement or inflammation of parietal peritoneum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

referred pain

A

Pain is perceived at a site different from origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

referred pain results from what

A

when visceral and somatic nerves converse at one spinal cord level

  • source of visceral pain is perceived as the same as that of the somatic nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Causes if limited malnutrition - specific problem

A

Vitamin B12 deficiency

Iron deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Causes of generalized malnutrition

A 
Chronic anorexia, vomiting, diarrhea
Other systemic causes
- chronic inflammatory bowel disorders
- cancer treatment
- wasting syndrome
- lack of available nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Sigmoidoscopy and colonoscopy

A

Diagnostic test

- biopsy and removal of polyps may be done

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Laboratory analysis of stool specimens

A

check for infections, parasites and ova, blooding, tumors, malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Disorders of Oral cavity: Cleft lip / palate

A

Congenital abnormality

  • arise 6-7 week of gestation
  • multifactorial origin
  • high risk of aspiration
  • speech impaired (speech therapy)
  • feeding problems in infant
  • surgical repair asap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Disorders of Oral cavity: Herpes Simplex 1 infection

A

HSV-1

  • kissing/close contact
  • dormant virus on sensory ganglion
  • cause: stress, trauma, infection
  • antiviral medication
  • can spread to eyes (conjunctivitis and keratitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Disorders of Oral cavity: Syphilis

A

Cause: Treponema pallidum

  • oral lesions
  • highly contagious during 1st and 2nd stages
  • treated with long-acting penicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Primary Stage Syphilis

A

Chancre, a painless ulcer on tongue lip or palate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Secondary syphilis

A

Red macules or papules on palate - highly infections

heals spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Disorders of Oral cavity: Aphthous ulcers

A

Steptococcus sanguis may be involved
- part of oral resident flora

Small painful lesions on

  • movable mucosa
  • buccal mucosa
  • floor or mouth
  • soft palate
  • lateral borders of tongue

usually heals spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Disorders of Oral cavity: Dental caries

A

Streptococcus mutans - initiating microbe
Lactobacillus follows in large numbers
–> bacteria break down sugards and produce large amount of lactic acid which dissolves mineral in tooth enamel which can lead to tooth erosion and formation of caries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

anti-caries treatment

A

fluoride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what promotes the growth of dental caries

A

sugars and acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Disorders of Oral cavity: Gingivities

A

Changes in Gingivae may lead to a local or systemic problems.
- inflammation of the gingiva –> tissue become red, soft, swollen, bleed easily. This may result from too much plaque, bad hygiene or toothbrush trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Disorders of Oral cavity: Periodontal disease

A

organisms enter the gingival blood vessels and travel to the connective tissues and bone of the dental arch.

Resorption of bone and loss of ligament fibers result in weakened attachment of teeth.

May result in total loss of tooth from socket

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Periodontal disease treatment

A

Treated by antimicrobials, local surgery of gingiva, and improved dental hygiene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Disorders of Oral cavity: Hyperkeratosis

A

Whitish plaque or epidermal thickening of mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Where does Hyperkeratosis occur

A

buccal mucosa, palate, lower lip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Hyperkeratosis may be related to what

A

smoking or chronic irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Why do Hyperkeratosis lesions require monitoring

A

Epithelial dysplasia beneath plaque may develop into squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Hyperkeratosis example

A

Leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

common types of cancer of oral cavity

A 
Squamous cell carcinoma 
Kaposi sarcoma (AIDs patients)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Oral cancer predisposing factors

A

smoking, alcohol abuse, preexisting leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Sialadenitis

A

Inflammation of salivary glands

  • infectious and non-infectious
  • parotid gland most affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Salivary gland disorders: Mumps

A

Infectious parotitis

  • viral infection
  • vaccine available
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Salivary gland disorders: noninfectious parotitis

A

often seen in older adults who lack adequate fluid intake and mouth care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are most malignant tumors of salivary glands?

A

mucoepidermoid carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Caused of dysphagia

A 
neuro deficit
- infection, stoke, brain damage, achalasia
muscular disorder
- impairment from muscular dystrophy) 
mechanical obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

achalasia

A

failure of the lower esophageal sphincter to relax because of lack of innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

left off on slide 46

A

g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Dysphagia: congenital atresia

A

developmental anomaly

upper and lower esophageal segments are separated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Dysphagia: stenosis

A

narrowing of esophagus

117
Q

Dysphagia: esophageal diverticula

A

out-pouchings of esophageal wall

- congenital or acquired following inflammation

118
Q

Dysphagia: tumors

A

may be internal or external

119
Q

esophageal cancer: what kind of cells

A

primarily squamous cell carcinoma

120
Q

esophageal cancer: location

A

usually distal esophagus

121
Q

esophageal cancer is associated with chronic inflammation because?

A
  • chronic esophagitis
  • achalasia
  • hiatal hernia
  • alcohol abuse, smoking
122
Q

hiatal hernia

A

part of stomach protrudes into thoracic cavity

123
Q

sliding hernia

A

most common

- portions of the stomach and gastroesophageal junction slide up above the diaphragm

124
Q

rolling or paraesophageal hernia

A

part of the fundus of the stomach moves up through the enlarged or weak hiatus in the diaphragm and may become trapped

125
Q

what happens when food lodges and becomes trapped in hernia

A

inflammation of mucosa
reflux of food up esophagus
chronic esophagaitis

126
Q

signs of hernia

A

heartburn pr pyrosis
belching
discomfort when lying down
substernal pain that radiates to should or jaw

127
Q

gastroesophageal reflux disease (GERD)

A

Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation

128
Q

GERD often seen with with other disease

A

hiatal hernia

129
Q

what may be a factor of GERD

A

delayed gastric emptying

130
Q

GERD: avoid what

A

Caffeine, fatty and spicy foods, alcohol, smoking, certain drugs

131
Q

Acute Gastritis: what

A

gastric mucosa is inflammed

- may be ulcerated and bleeding

132
Q

Acute gastritis may result from?

A 
Infection by microorganisms
Allergies to foods
Spicy or irritating foods
Excessive alcohol intake
Ingestion of aspirin or other NSAIDs 
Ingestion of corrosive or toxic substances
Radiation or chemotherapy
133
Q

Basic signs of gastrointestinal irritation

A
  • Anorexia, nausea, vomiting may develop
  • Hematemesis caused by bleeding
  • Epigastric pain, cramps or general - discomfort
  • With infection, diarrhea may develop.
134
Q

Acute gastritis is usually self-limiting, meaning

A

Complete regeneration of gastric mucosa

Supportive treatment with prolonged vomiting

May require treatment with antimicrobial drugs

135
Q

Chronic gastritis: what

A

Characterized by atrophy of stomach mucosa

  • loss of secretory glands
  • reduced production of intrinsic factor
136
Q

What is often present in Chronic gastritis

A

Helicobacter pylori

137
Q

sings of Chronic gastritis

A

may be vague

- Mild epigastric discomfort, anorexia, intolerance for certain foods

138
Q

increased risk of what with Chronic gastritis

A

peptic ulcers and gastric carcinoma

139
Q

gastroenteritis

A

inflammation of stomach and intestines

- usually caused by infection or allergic reactions to food or drugs

140
Q

gastroenteritis: describe the effect that microbes have as they are transmitted by fecally contaminated food, soil or water

A

a. most infections self limiting
b. serious illness may result in compromised house or virulent organisms
c. may cause epidemic outbreaks in refugee or disaster settings
d. safe sanitation essential for prevention

141
Q

Peptic ulcer (gastric and duodenal): cause

A

most caused by H. pylori infection

142
Q

Where do peptic ulcers usually occur

A

proximal duodenum and antrum of stomach

143
Q

Describe how the development of gastric ulcers begin

A
  1. breakdown of mucosal barrier
  2. decreased mucosal defense
    - more common in gastric ulcer development
144
Q

What is a predominant factor in duodenal ulcers

A

increased acid secretion

145
Q

damage to mucosal barrier predisposes someone to the development of ulcers and is associated with what?

A
  • Inadequate blood supply (vasoconstriction)
  • excessive glucocorticoid secretion / meds
  • ulcerogenic substances break down mucous layer (aspirin, NSAID, alcohol)
  • atrophy of gastric mucosa
146
Q

increase acid pepsin related to gastric ulcers may also lead to what?

A
  • Increased gastrin secretion
  • Increased vagal stimulation
  • Increased sensitivity to vagal stimuli
  • Increased number of acid pepsin secretory cells in the stomach (genetic anomaly)
  • Increased stimulation of acid pepsin secretion d/t Alcohol, caffeine, certain foods
  • Interference with normal feedback mechanisms
  • Rapid gastric emptying
147
Q

Complications of peptic ulcer: hemorrage

A

Caused by erosion of blood vessels

May be the first sign of a peptic ulcer

148
Q

Complications of peptic ulcer: perforation

A

Ulcer erodes completely through the wall.

Chyme can enter the peritoneal cavity.

Results in chemical peritonitis

149
Q

Complications of peptic ulcer: obstruction

A

may result later because the formation of scar tissue

150
Q

peptic ulcer s/s

A

epigastric burning or localized pain, usually following stomach emptying

151
Q

peptic ulcer diagnostic test

A

Fiberoptic endoscopy
Barium x-ray
Endoscopic biopsy

152
Q

peptic ulcer treatment

A

Combination of antimicrobial and proton pump inhibitor to eliminate H. pylori

Reduction of exacerbating factors

153
Q

Stress ulcers associated with

A

severe trauma or systemic problems

  • burns, head injuries
  • hemorrhage or sepsis
154
Q

stress ulcers: rapid onset

A

multiple ulcer (usually gastric) may form within hours of precipitating event

155
Q

first indicator of stress ulcer

A

hemorrhage and severe pain

156
Q

Gastric cancer: where

A

mucous glands mostly in antrum or pyloric area

157
Q

Gastric cancer: early carcinoma

A

confirmed to mucosa and submucosa

158
Q

gastric cancer: later stages

A

involves muscularis

eventually invades serosa and spreads to lymph node

159
Q

gastric cancer: prognosis

A

poor bc asymptomatic in early stages

160
Q

key factor of gastric cancer

A

diet

- smoked foods, nitrates, nitrites

161
Q

survival rate of gastric cancer

A

less than 20%

162
Q

gastric cancer treatment

A

surgery and chemo

163
Q

Dumping syndrome

A

Control gastric emptying is lost and gastric contents are “dumped” into duodenum without complete digestion

164
Q

Dumping syndrome may follow

A

gastric resection

165
Q

Dumping syndrome: Hyperosmolar chyme draws fluid from vascular compartment into intestine, which can cause

A

Intestinal distention

Increased intestinal motility

Decreased blood pressure → anxiety and syncope

166
Q

Dumping syndrome occurs when

A

during or shortly after meals

167
Q

Dumping syndrome s/s

A

adb. cramps, nausea, diarrhea

168
Q

Dumping syndrome: hypoglycemia 2-3 hours after meals, why

A

High blood glucose levels in chyme stimulate increased insulin secretion → drop in blood glucose levels.

169
Q

Dumping syndrome: treatment

A

dietary changes (frequent small meals high in protein, low in simple carbs)

often resolves over time

170
Q

pyloric stenosis

A

Narrowing and obstruction of pyloric sphincter

171
Q

pyloric stenosis signs / symptoms

A

Signs appear within several weeks after birth

  • Projectile vomiting immediately after feeding
  • Firm mass can be palpated at pylorus.
  • Infant fails to gain weight, dehydration, persistent hunger
172
Q

pyloric stenosis treatment

A

surgery

173
Q

signs of pyloric stenosis if acquired lated in life

A

Persistent feeling of fullness

Increased incidence of vomiting

174
Q

pyloric stenosis cause

A

developmental anomaly

175
Q

Cholelithiasis

A

formation of gallstones

176
Q

cholecystitis

A

inflammation of gall bladder and cystic duct

177
Q

cholangitis

A

inflammation usually related to infection of bile ducts

178
Q

Choledocholithiasis

A

Obstruction of the biliary tract by gallstones

179
Q

gallstones may consist of

A

Cholesterol or bile pigment

Mixed content with calcium salts

180
Q

small vs large gallstones

A

small: may be silent and excreted in bile
larger: obstruct flow of bile through gallbladder

181
Q

possible locations of gallstones

A

Biliary Ducts & Pancreas

182
Q

Gallstone risk factors / causes

A 
Women 
High cholesterol in bile
High cholesterol intake 
Obesity 
Multiparity
Oral contraceptives or estrogen supplements
Hemolytic anemia
Alcoholic cirrhosis
Biliary tract infection
183
Q

Gallstones can cause obstruction of a duct by large calculi, which causes what

A

sudden, severe waves of radiating pain

184
Q

gallstone treatment

A

laparoscopic surgery

low fat diet

185
Q

why might jaundice develop from gallstones

A

bile backs up into liver and blood

186
Q

pain related to gallstones decreases if gallstones move where

A

duodenum

187
Q

Prehapatic jaundice

A

results of excessive destruction of RBC

188
Q

What diseased might you see prehepatic jaundice

A

hemolytic anemias or transfusion reactions

189
Q

intra-hepatic jaundice

A

occurs with disease or damage to hepatocytes

190
Q

what disease might you see intra-hepatic jaundice

A

hepatitis or cirrhosis

191
Q

Posthepatic jaundice

A

caused by obstruction of bile into gallbladder or duodenum

192
Q

what disease might you see posthepatic jaunduce

A

tumor or cholelithiasis

193
Q

bilirubin measurements: direct or conjugated bilirubin

A

cause be measured in blood

194
Q

bilirubin measurements: total bilirubin

A

measured in blood

195
Q

bilirubin measurements: how do you get indirect or unconjugated bilirubin

A

Total bilirubin - direct bilirubin

196
Q

Type of jaundice indicated how ?

A

by increase in serum bilirubin level and changes in stools

197
Q

bilirubin measurement for prehepatic jaundice?

A

Unconjugated bilirubin level elevated

198
Q

bilirubin measurement for Intrahepatic jaundice

A

Both unconjugated and conjugated bilirubin levels may be elevated.

199
Q

bilirubin measurement for posthepatic jaundice

A

increase conguated bilirubin level

- light colored stool caused by absense of bile

200
Q

hepatitis

A

inflammation of liver

201
Q

viral hepatitis

A

cell injury results in inflammation and necrosis in liver

- liver is edematous and tender

202
Q

viral hepatitis: causative agents

A 
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
203
Q

Hepatitis A virus (HAV): type is virus

A

small RNA virus

- acute but self-limiting infection

204
Q

Hepatitis A virus (HAV): transmission

A

Fecal-oral route

  • areas of bad sanitation / hygiene
  • often from contaminated water or shellfish
  • sexually transmitted (anal)
205
Q

Hepatitis A virus (HAV): carrer or chronic state?

A

no

206
Q

Hepatitis A virus (HAV): what happens before onset of signs

A

fecal shedding of virus

207
Q

Hepatitis A virus (HAV): vaccine

A

available for travelers, food care workers, and health care workers

208
Q

Hepatitis C virus (HCV): type of virus

A

single-stranded RNA virus

209
Q

Hepatitis C virus (HCV): transmission

A

most common type transmitted by blood transfusion

210
Q

Hepatitis C virus (HCV): carrier / chronic state

A

May exist in carrier state

about 50% of pt. enter chronic state

211
Q

Hepatitis C virus (HCV): increased risk of what

A

hepatocellular carcinoma

212
Q

Hepatitis C virus (HCV): treatment

A

interferon injections

213
Q

Hepatitis D virus (HDV): virus type

A

incomplete RNA virus

214
Q

Hepatitis D virus (HDV): requires what

A

HBV to replicate and produce active infection

215
Q

Hepatitis D virus (HDV): effect on HBV

A

increases severity of HBV

216
Q

Hepatitis D virus (HDV): transmission

A

blood

217
Q

Hepatitis E virus (HEV): virus type

A

single-stranded RNA virus

218
Q

Hepatitis E virus (HEV): transmission

A

oral-fecal

219
Q

Hepatitis E virus (HEV): chronic or carrer state

A

no

220
Q

Hepatitis: Preicteric stage s/s

A

Fatigue and malaise
Anorexia and nausea
General muscle aching

221
Q

Hepatitis: Icteric stage s/s

A

Onset of jaundice

Stools light in color, urine becomes darker

Liver tender and enlarged, mild aching pain

222
Q

Hepatitis: Posticteric stage - recovery stage s/s

A

Reductions in signs

Weakness persists for weeks

223
Q

Viral hepatitis: bodies defense

A

only body defense is formation of antibodies via vaccination

224
Q

Viral hepatitis: supportive measures

A

Rest, diet high in protein, carbohydrate, and vitamins

225
Q

Chronic hepatitis can be treated with interferon: what does this do?

A

Decrease viral replication

  • effective 30-40% ind.
  • drug combination (slow-acting interferon plus antiviral drugs) more effective
226
Q

Toxic or nonviral Hepatitis

A

Variety of hepatotoxins can cause inflammation and necrosis of the liver.

May result from sudden exposure to large amounts or from lower dose and long-term exposure

227
Q

drugs and chemicals that can cause Toxic or nonviral Hepatitis

A

Drugs include:
Acetaminophen, halothane, phenothiazines, tetracycline

Chemicals include:
Carbon tetrachloride (not used currently), toluene, ethanol
228
Q

Cirrhosis

A

Progressive destruction of liver

229
Q

Cirrhosis causes

A

alcoholism
biliary cirrhosis
postnectrotic cirrhosis
metabolic abnormalities

230
Q

biliary cirrhosis associated with

A

associated with immune disorders

231
Q

Postnectrotic cirrhosis

A

Linked with chronic hepatitis or long-term exposure to toxic materials

232
Q

Cirrhosis leads to

A

Extensive diffuse fibrosis

  • Interferes with blood supply
  • Bile may back up.

Loss of lobular organization

Degenerative changes may be asymptomatic until disease is well advanced.

233
Q

Cirrhosis diagnosis

A

Liver biopsy and serologic test to determine cause and extent of damage

234
Q

Cirrhosis (Alcoholic Liver Disease): initial stage

A

Fatty liver

  • enlargement of liver
  • Asymptomatic and reversible with reduced alcohol intake
235
Q

Cirrhosis (Alcoholic Liver Disease): second stage

A

Alcoholic Hepatitis

a. inflammation / cell necrosis
b. fibrous tissue formation (irreversible)

236
Q

Cirrhosis (Alcoholic Liver Disease): third stage

A

End stage cirrhosis

a. fibrotic tissue replaces normal tissue
b. little normal function remains

237
Q

slide 80: functional loss with cirrhosis

A

go look

238
Q

Cirrhosis: initial manifestations

A

Mild and vague

  • chronic infection s/s
  • dull aching pain may be present in upper right abdominal quadrant
239
Q

Advanced cirrhosis s/s

A 
Ascites and peripheral edema
increased bruising 
esophageal varies 
jaundice
encephalopathy
240
Q

Cirrhosis treatment

A 
Avoidance of alcohol
Supportive or symptomatic treatment
Dietary restriction 
Balancing serum electrolytes 
Paracentesis
Antibiotics
Liver transplant
241
Q

Hepatocelluar carcinoma

A

most common primary tumor of liver

- more common in cirrhotic livers

242
Q

Liver cancer: secondary or metastatic cancer

A

Arises from areas served by the hepatic vein or spread along the peritoneal membranes

243
Q

liver cancer: initial signs and diagnosis

A

signs: mild and general
Diagnosis: usually occurs with advanced stages

244
Q

liver cancer treatment

A

possible lobectomy, radio-frequency ablation (RFA) procedure

245
Q

Acute pancreatitis

A

Inflammation of pancreas; results in auto-digestion of tissue

246
Q

causes of acute pancreatitis

A
  • gallstones
  • alc abuse
  • sudden onset may follow large meal or large amount of alcohol
247
Q

pancreatitis can be acute or chronic, what is acute consider?

A

medical emergency

248
Q

describe patho of pancreatitis

A

Pancreas lacks capsule
- substances released by necrotic tissue lead to widespread inflammation

  • destruction may progress into tissue surrounding pancreas
249
Q

Acute pancreatitis

A

Severe epigastric/abdominal pain radiating to back

signs of shock

low grade fever until infection develops

abdominal distention (decreased peristalsis and paralytic ileus)

250
Q

Acute pancreatitis Diagnostic tests

A

Serum amylase levels—first rise, then fall after 48 hours

Serum lipid levels are elevated.
Hypocalcemia
Leukocytosis

251
Q

Acute pancreatitis treatment

A

Oral intake is stopped.

Treatment of shock and electrolyte imbalances

Analgesics for pain relief

252
Q

Pancreatic cancer risk factors

A

smoking

pancreatitis and dietary factors

253
Q

Adenocarcinoma

A

most common type of Pancreatic cancer

  • arises in ducts
254
Q

Pancreatic cancer early manifestions

A

weight loss and jaundice

255
Q

Pancreatic cancer mortality rate

A

metastases occur early

- mortality 95%

256
Q

celiac disease

A

Malabsorption syndrome; genetics

257
Q

celiac disease defect is where

A

intestinal enzyme (gliadin)

  • prevents the breakdown of gluten
  • atrophy of villi in intestine
258
Q

celiac disease: first signs

A

usually as children when cereals are first introduced into the diet

259
Q

celiac disease manifestations

A

Steatorrhea, muscle wasting, failure to gain weight

Irritability and malaise common

260
Q

celiac disease diagnosis

A

blood tests

261
Q

celiac disease treatment

A

gluten free diet, intestinal mucosa returns to normal after a few weeks without gluten

262
Q

Chron disease: where?

A

May affect anywhere in digestive tract, SI most affects

263
Q

Chron disease: describe the inflammatoin

A

inflammation occurs in characterist distribution

-“skip” lesions - affected areas are separated by areas of normal tissue

264
Q

Chron disease: what causes obstructed areas?

A

Progressive inflammation and fibrosis
- damaged walls impair processing and absorption of food

  • inflammation stimulates intestinal motililty
265
Q

Chron disease interferes with digestion and absoption, leading to what?

A

Hypoproteinemia, avitaminosis, malnutrition, possibly steatorrhea

266
Q

complications of Chrons disease

A

Adhesions between loops may form and fistulas may develop.

267
Q

Chrons disease in children: complications

A

delayed growth and sexual maturation

268
Q

Chrons disease treatment

A

Glucocorticoids

269
Q

Ulcerative colitis

A

inflammation starts in rectum and progresses through colon. mucosa and submucosa are inflammed.

270
Q

Ulcerative colitis: tissue destruction inferes with what

A

absorption of fluid and electrolytes in colon

271
Q

Ulcerative colitis: when might megacolon develop

A

severe acute episodes

272
Q

Ulcerative colitis s/s

A

diarrhea, up to 12 a day

  • contains blood and mucus
  • cramps
273
Q

IBS manifestions

A

Lower abdominal pain
Diarrhea
Constipation, alternating with diarrhea
Bloating, nausea

274
Q

IBS diagnosis

A

signs and symptoms

  • Testing for food allergies
  • Testing for bacterial or parasitic infections
  • No single cure for IBS
275
Q

IBS treatment

A 
Team approach
Anti-inflammatory meds
Antimotility agents 
Nutritrional supplements
Antimicrobials 
Immunotherapeutic agents
Surgical resection
276
Q

Appendicitis

A

Obstruction of lumen; fluid builds inside

- purulent exudate, swollen

277
Q

Appendicitis treatment

A

surgical removal and antimicrobial drugs

278
Q

treatment of diverticulitis

A

antimicrobial drugs

dietary modifications to prevent stasis

279
Q

Diverticulitis stasis

A

material trapped in pouch leads to inflammation and infection

280
Q

colorectal cancer: most malignancies develop from what

A

adenomatous polyps

- early diagnosis essential

281
Q

colorectal cancer: risk factors

A

genetics
Long-term ulcerative colitis
environmental factors (low fiber)

282
Q

colorectal cancer. treatment

A

surgical removal with radiation and or chemo

283
Q

intestinal obstruction: what

A

lack of movement of intestinal content through intestine - most common in SI

284
Q

intestinal obstruction: mechanical obstruction

A

Result from tumors, adhesions, hernias, other tangible obstructions

285
Q

intestinal obstruction: functional or adynamic obstructions

A

result from impairment of peristalsis

- spinal cord injry

286
Q

Peritonitis

A

inflammtion of peritoneal membranes

287
Q

Chemical peritonitis may result from

A

Enzymes released with pancreatitis

Urine leaking form a ruptured bladder

Chyme spilled from a perforated ulcer

Bile escaping from the ruptured gallbladder

Blood

Any other foreign material in the cavity

288
Q

Bacterial peritonitis caused by

A

Direct trauma affecting the intestine

Ruptured appendix

Intestinal obstruction and gangrene

289
Q

pelvin inflammatory disease in women

A

when (peritonitis) infection reaches the cavity through fallopian tubes

Pathophysiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions