Brainscape's Knowledge GenomeTM

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


See full index

nurs pathophysiology > rrd 12 > Flashcards

rrd 12 Flashcards

1
Q

small intestines

A
  • duodenum
  • jejunum
  • ileum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

large intestines

A
  • aka colon
  • cecum
  • ascending colon
  • transverse colon
  • descending colon
  • sigmoid colon
  • rectum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

gastrointestinal tract

A
  • mouth
  • pharynx
  • esophagus
  • stomach
  • small intestines
  • large intestines
  • accessory organs: liver, gallbladder, pancreas, spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

5 anatomic sections used to assess abdomen and GI organs

A
  • epigastric
  • RUQ
  • LUG
  • RLQ
  • LLQ
  • umbilical region/periumbilical area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

epigastric

A
  • area across upper abdomen just below sternum + ribs
  • pyloric area of stomach, duodenum, part of pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RUQ

A
  • right upper quad
  • liver + gallbladder, part of pancreas, part of transverse colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

LUQ

A
  • left upper quad
  • part of stomach, spleen, part of transverse colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RLQ

A
  • right lower quad
  • cecum + appendix
  • part of ascending colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

LLQ

A
  • left lower quad
  • part of descending colon
  • sigmoid colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

umbilical region

A
  • lower duodenum
  • jejunum
  • ileum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

endoscopy

A

gen term for passing scope into GI tract for direct visualization

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

esophagogastroduodenoscopy (EGD)

A

visualization of the esophagus, stomach, duodenum

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

colonscopy

A
  • visualization of the rectum, colon and distal small bowel
  • important tool in detecting colon cancer early
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

gastroesophageal reflux disorder (GERD)

A
  • reflux of HCl + pepsin from the stomach into esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

GERD may be due to?

A

relaxation of the lower esophageal sphincter (LES) and/or delayed emptying of the stomach

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

GERD S/S

A
  • heartburn
  • epigastric pain
  • coughing
    w/in 1 hr of eating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

GERD S/S worsen when?

A
  • lying down
  • aggravated by ETOH
  • coffee
  • smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Barrett’s esophagus is a relatively uncommon disorder almost always caused by?

A

GERD

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

Barrett’s esophagus

A
  • certain areas in esophagus tissue becomes dysplastic
  • left untreated: esophageal cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hiatal hernia

A

herniation of the stomach thru the diaphragm so that it protrudes into the thoracic cavity

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

S/S hiatal hernia

A
  • GERD
  • epigastric pain
  • dysphagia
  • also can have no S/S at all
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

tx hiatal hernia

A

may need surgury

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

gastritis

A

an inflammation that affects gastric mucosa and can cause erosions (superficial areas of wearing away of mucosa)

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

gastritis S/S

A
  • pain or burning over epigastric area
  • occasional bleeding (acute hemorrhagic gastritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

layers of stomach from inside to out

A
  • mucosa (mucous membrane)
  • submucosa (connective tissue)
  • layers of muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

acute gastritis

A
  • from overuse of NSAIDS (suppress protective prostaglandins) or ETOH (direct chem damage)
  • heals spontaneously once offending agent removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

chronic gastritis

A
  • aka atrophic gastritis
  • autoimmune etiology
  • mainly in elderly
  • causes atrophy of gastric mucosa
  • result: develop pernicious anemia bc loss of intrinsic factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

peptic refers to _____, which along with _____ (_____ + ____ = ______) digests food in stomach and duodenum

A
  • pepsin
  • HCl
  • pepsin + HCl = peptic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

if the mucosa is disturbed by ________, the balance is _____ and acid can get down to the ________.

A
  • aggressive change factors
  • disrupted
  • vulnerable tissue underneath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

peptic ulcer disease (PUD)

A
  • chronic inflammatory condition of stomach + proximal duodenum
  • disturbance of their mucosal lining allows acid to ulcerate the underlying tissue -> gastric and/or duodenal ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what aggressive change factors can cause mucosal disturbance and/or increase tissue vulnerability to ulceration?

A
  • ASA and other NSAID use
  • chronic steroid use
  • heavy ETOH use
  • cig smoking
  • chronic diseases
  • severe psychological stress
  • (+) for H. pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

why does ASA/NSAID/steroid use cause PUD?

A

decrease prostaglandin synthesis -> protects stomach lining

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

what chronic diseases can cause PUD?

A
  • chronic gastritis
  • liver disease
  • CKD
  • diabetes
  • COPD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Helicobacter pylori (H. pylori)

A

bacterium that can be ingested via food, drinking water, or other oral/fecal route

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

H. pylori infection more common in?

A
  • same families
  • crowded conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

once H. pylori is ingested, can swim thru _____, burrow thru and disrupt the ________, and attach to _________ and ________ (can survive in ______)

A
  • HCl
  • mucous layer of stomach
  • surface epithelial cells
  • colonize
    – HCl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

majority of ppl infected w/ H. pylori _____ develop ulcers. By damaging the mucosa, the organism creates more ________ by _______ when a person has other risk factors.

A
  • do not
  • vulnerability to injury
  • pepsin + HCl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

S/S PUD

A
  • painless ulcers sometimes
  • ulcers that cause burning epigastric pain 1-3 hr after meals
  • pain that awakens person during the night
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

in PUD, if ulcer beings eroding blood vessels, the pt can have?

A

GI bleed of various degrees depending on size of vessel

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

tx PUD

A
  • antacids
  • H2-blockers (Zantac, Pepcid)
  • PPIs (proton pump inhibitors - Nexium, Prevacid)
  • eradication of H. pylori w/ antibx regimen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

colorectal cancer

A
  • # 3 killer amongst all cancers
  • almost always arises from pre-existing benign neoplasm -> polyp form (stalk-like growth on colon wall) -> becomes malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

colorectal cancer risk factors

A
  • age over 50
  • high fat diet, obesity, sedentary lifestyle
  • smoking & ETOH over-consumption
  • family hx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

S/S colorectal cancer

A
  • blood in stool, either visible or occult
  • change in bowel habits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

colorectal cancer dz most often done by?

A

colonoscopy

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

tx colorectal cancer

A
  • if confines to polyp: polypectomy during colonoscopy
  • more widespread: colectomy (remove part colon) and sometimes colostomy (opening created in abdomen for stool); chemothx
  • prevention: high fib diet, lifestyle changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

inflammatory bowl disease

A

chronic disorder characterized by inflammation of the lining + walls of intestines

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

two main types of IBD

A
  • Crohn’s disease
  • ulcerative colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

IBD common characteristics

A
  • inflammation: episodes of bloody diarrhea + abdominal cramps w/ patterns of exacerbation + remission bc stress
  • no proven primary etiology
  • intestinal obstruction
  • fistula formation
  • sometimes perforation of intestinal wall + spillage of intestinal contents into abdominal cavity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

possible causes of IBD

A
  • infectious agents (bacteria, viruses)
  • links to familial occurrence
  • autoimmune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

IBD: formation of ______ against glycoproteins in intestinal walls -> ________.

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

IBD: sometimes pts has manifestation of _______ autoimmune features: ________.

A
  • systemic
  • arthritis , vasculitis, iritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

where does the intestinal obstruction in IBD come from?

A

chronic inflammation + scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

fistula formation in IBD

A

abnormal channels or tracts that develops in the presence of inflammation and infection

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

tx IBD

A
  • control inflammation by giving steroids + other meds
  • sometimes surgery to remove parts of bowl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

IBD vs IBS

A
  • IBS: less serious disorder; abdominal pain, diarrhea, and/or constipation
  • IBS: no inflammation, no blood in stool
  • IBD: inflammation + bloody stools hallmark
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Crohn’s disease

A
  • pattern of intestinal involvement majority of time involve duodenum, ileum, and/or cecum
  • all bowel layers (entire wall) involved = transmural involvement
  • patchy pattern: random inflamed tissue segments separated by norm tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

S/S Chron’s disease

A
  • malabsorption
  • malnutrition
  • wt loss
    bc most nutrients absorbed in small intestines, esp duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

ulcerative colitis

A
  • severe inflamm + ulcerations begin in rectum and progress to involve entire colon (only colon)
  • confluent, effected segments
  • do not extend beyond submucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

S/S ulcerative colitis

A
  • dehydration risk more severe bc colon main site of water reabsorption
  • not as high risk for nutritional deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

intestinal obstruction

A

occlusion of either the small or large intestine that can be partial or complete in nature

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

pathogenesis + S/S intestinal obstruction

A
  1. obstruction
  2. sequestration of gas + fluid proximal to obstruction
  3. abdominal distention (swollen/stretched)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

S/S intestinal obstruction

A
  • severe, colicky abdominal cramping
  • N&V
  • constipation or w/ partial obstruction, diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

intestinal obstructions can develop secondary to?

A
  • adhesions
  • hernia
  • tumor in lumen of intestine
  • intussusception
  • volvulus
  • paralytic ileus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

adhesions

A

scar tissue from surgery or from chronic inflammation such as IBD

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

hernia

A

intestine protrudes thru weakness in the abdominal muscle or thru inguinal ring

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

intussusception

A
  • telescoping of one portion of the bowel into the other, causing strangulation of blood supply
  • more common in infants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

volvulus

A
  • aka torsion
  • twisting of the intesstine with occlusion of blood supply
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

paralytic ileus

A
  • aka ileus
  • loss of peristaltic motor activity in the intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

paralytic ileus is not a physical obstruction, but a _____ one bc all peristalsis ______ & fluids, gasses, etc build up, causing ________>

A
  • functional
  • stops
  • distention, constipation, pain, etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

paralytic ileus is associated w/?

A
  • immobility
  • post-anesthesia effects
  • surgery (esp abdominal)
  • peritonitis
  • electrolyte imbalances
  • spinal trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

paralytic ileus prevention

A

increasing pt mobility as soon as possible

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

diverticulum (pleural: diverticula)

A

herniations or saclike outpouchings of mucosa from muscle layer of the intestine that protrude from the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

diverticula most commonly occur in the?

A

sigmoid colon

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

diverticulosis

A

asymptomatic diverticular disease

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

diverticulitis

A

inflammation/infection of the diverticula

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

S/S diverticulitis

A
  • pain (most often in LLQ)
  • fever
  • leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

diverticulitis can result in ____ if not treated adequately.

A
  • abscess formation
  • rupture
  • peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

tx diverticulitis

A
  • increase dietary fiber
  • avoid certain foods like seeds and nuts
  • sometimes antibx
  • occasionally surgery if required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

appendicitis

A
  • inflammation most often caused by fecal matter getting caught in lumen of appendix -> infection + inflammation
  • slight genetic predisposition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

tx appendicitis

A

appendectomy

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

S/S appendicitis

A
  • norm pain pattern
  • N/V/D, anorexia
  • fever, leukocytosis
  • not tx quick: inflammation to peritoneum -> peritonitis -> potential sepsis + other complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

pain pattern of appendicitis

A
  • epigastric/periumbilical pain that migrates to become RLQ pain
  • pain exacerbated upon movement
  • rebound tenderness sometimes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

peritoneum

A

membranous-like covering of abdominal organs

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

upper GI (UGI) bleed

A

from esophagus, stomach, duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

lower GI (LGI) bleed

A

from jejunum, ileum, colon

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

most common causes of UGI bleed

A
  • acute hemorrhagic gastritis
  • esophageal varices
  • peptic ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

esophageal varices

A

large torturous veins in the esophagus caused by liver dz that can be easily irritated and caused to bleed

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

emesis, vomitus

A

product of vomiting

89
Q

S/S that tell you bleeding is coming from UGI area of gut

A
  • hematemesis
  • blood in stools
90
Q

hematemesis

A
  • sudden vomiting of blood
  • can be visible/frank or occult
91
Q

visible/frank hematemesis

A
  • bright red: very acute prob like esophageal bleeding or artery erosion related to peptic ulcer
  • coffee ground: brownish-red w/ flecks; acute bleed but partially digested in stomach or duodenum
92
Q

occult bleeding w/ hematemesis

A
  • vomitus looks norm but
  • small amt of hidden blood from slower, maybe chronic bleeding situation
93
Q

blood in stools type

A
  • occult bleeding
  • melena
94
Q

occult bleeding in stools

A
  • stool may look norm but
  • small amt of hidden blood from slower, chronic bleeding situation like cancer irritating walls of UGI structure
  • detected by using hemoccult test
95
Q

melena w/ bloody stool

A
  • loose
  • dark and tarry
  • indicates blood partially digested in stomach or duodenum
  • like coffee ground but blacker and pastier
96
Q

most common causes of LGI bleed (hematochezia)

A
  • IBD
  • diverticulitis
  • neoplasms
97
Q

occult bleeding S/S that tell you bleeding is coming from LGI area of gut

A
  • stool may look norm but has small amt of hidden blood from slower, chronic bleeding situation such as cancer or diverticulitis
  • detected by hemoccult test
98
Q

frank bleeding w/ LGI bleed

A
  • red blood mixed w/ stool
  • no melena
99
Q

objective of bilirubin cycle

A

to get unconjugated bilirubin into conjugated form so that it can be used to make bile

100
Q

unconjugated bilirubin

A

comes out of spleen as water-insoluble substance so must have a protein carrier to get it to the liver to become conjugated

101
Q

conjugated bilirubin

A

bilirubin becomes water-soluble so can be easily be incorporated into bile

102
Q

stages of bilirubin cycle

A
  1. prehepatic
  2. hepatic stage
  3. posthepatic
103
Q

prehepatic stage

A
  • unconjugated bili (indirect bilirubin): water insoluble + released from spleen
  • proteins carry it to liver via bloodstream
104
Q

hepatic stage

A

process of making unconjugated bili conjugated (direct bilirubin): water soluble

105
Q

posthepatic

A

conjugated bili comes out of liver + incorporated into bile for excretion into small intestine (bile helps to emulsify fat as part of digestive process)

106
Q

jaundice is not a disease in itself, but rather?

A

a manifestation of various disease states

107
Q

bilirubin is the product of?

A

RBC break-down

108
Q

there is normally a small amt of bilirubin in the blood, but most is excreted as?

A
  • a waste product
  • in the stool: gives stool its norm brownish color
  • in the urine as urobilinogen
109
Q

jaundice (icterus)

A
  • alteration in norm bilirubin cycle -> accumulates in blood -> pathologically deposited thruout body
  • yellow -green pigment
110
Q

usual pigmented areas w/ jaundice

A
  • skin
  • sclera
  • under tongue
  • palate of mouth
111
Q

causes of jaundice groups

A
  • prehepatic jaundice
  • hepatic jaundice
  • posthepatic (obstructive) jaundice
112
Q

prehepatic jaundice

A
  • liver is fine; conjugates usual amt of unconjugated bilirubin that is brought to it
  • lots of unconjugated is left over in blood + gets deposited under skin and elsewhere
113
Q

prehepatic jaundice occurs because of?

A

increase in unconjugated bilirubin (aka indirect bilirubin)

114
Q

most common causes of prehepatic jaundice is?

A

hemolytic conditions

115
Q

increased unconjugated bili occurs when?

A

the rate of hemolysis (RBC breakdown) exceeds the liver’s ability to handle the bilirubin load -> too much unconjugated bilirubin in blood and liver cannot conjugate it all

116
Q

prehepatic jaundice can result in various forms of?

A

hemolytic anemia

117
Q

hemolytic anemia

A
  • decreased RBCs due to excess destruction of them
  • certain drugs can cause excess breakdown of RBCs
118
Q

erythroblastosis fetalis

A

hemolytic anemia of a newborn

119
Q

erythroblastosis fetalis can happen in the ______ pregnancy when mother is _____ and fetus is _____ (and mom didn’t receive ____ w/ previous similar pregnancy)

A
  • second (or more)
  • Rh neg
  • Rh pos
  • Rhogam
120
Q

the baby becomes severely _____ as the mother’s ____ to Rh factor _______ the fetus’s RBCs

A
  • jaundiced
  • antibodies
  • hemolyzes
121
Q

physiologic jaundice is due to?

A

immaturity of the conjugating enzyme glucuronyl transferase

122
Q

tx physiologic jaundice

A
  • commonly occurs to some degree in many newborns
  • UV light therapy helps convert unconjugated bilirubin to conjugated
  • wait for baby’s glycuronyl transferase to mature and take over
123
Q

post-hepatic jaundice

A
  • liver fine; conjugates usual amt of unconjugated bilirubin brought to it
  • conjugated bili can’t get into intestine
  • bili backs up into bloodstream + gets deposited under skin and elsewhere
124
Q

posthepatic (obstructive) jaundice occurs because of?

A

increase in conjugated bilirubin (direct bilirubin) in the blood

125
Q

problem w/ posthepatic jaundice is with the?

A

flow of bilirubin making its ways to the intestines due to obstruction and/or inflammation (ex: cholecystitis, choledocholithiasis, tumor of the area, etc.)

126
Q

in posthep j: ____ bilirubin have no where else to go -> _______ -> begins to leak from _____ back into ________ -> ______

A
  • conjugated
  • backs up
  • liver cells
  • circulation
  • jaundice
127
Q

hallmark sign of obstructive jaundice is?

A
  • stool that is grey-colored bc lack of pigment from bilirubin (less bilirubin going to intestines)
128
Q

hepatic jaundice

A
  • sick liver
  • cannot conjugate norm amts of unconjugated bilirubin
  • bili gets deposited under skin + elsewhere
129
Q

hepatic jaundice occurs because of?

A

increase in unconjugated bili

130
Q

if hepatocyes are diseased, such as in hepatitis and cirrhosis, the liver?

A

cannot conjugate the unconjugated bilirubin that arrives

131
Q

hepat j: the unconjugated bilirubin remains in ______ = ________ level of indirect bilirubin in the ______

A
  • blood
  • higher than normal
  • blood
132
Q

pts with hepatic jaundice will additionally have _____ conjugated bili.

A

low

133
Q

blood test results that reflect prehepatic jaundice

A
  • total serum bili: HIGH
  • serum indirect bilirubin: HIGH
  • serum direct bilirubin: normal
134
Q

blood test results that reflects posthepatic jaundice

A
  • total serum bilirubin: HIGH
  • indirect bilirubin: NORMAL
  • direct bilirubin: HIGH
135
Q

blood test results that reflect hepatic jaundice

A
  • total serum bili: HIGH or NORMAL
  • serum indirect bilirubin: HIGH
  • serum direct bilirubin: LOW
136
Q

cholecystitis

A

inflammation of the gall bladder

137
Q

cholecystitis is almost always caused by?

A
  • irritation of stones inside gall bladder itself (cholelithiasis)
  • stones in nearby duct like common bile duct (choledocholithiasis)
138
Q

gallbladder purpose

A

stores bile that is secreted into intestine to help emulsify fats

139
Q

patho cholelithiasis/cholecystitis

A
  1. stones from cholesterol increase (chol norm in bile) or less water in body (dehydration)
  2. formation of small (2-8mm) to large (3-4cm) stones made of cholesterol + bilirubin precipitant
  3. chem irritation of conc bile in gallstones cause GB swell + inflamm in biliary area
140
Q

S/S cholecystitis

A
  • pain in RUQ + epigastric area
  • referred pain to back, above waistline + esp to R shoulder, R scapula
  • N/V
  • obstructive jaundice + gray stools if large stone completely blocks common bile duct
141
Q

RUQ/epigastric pain from cholecystitis is often manifested as?

A
  • painful spasms/contractions of the GB + bile ducts
  • biliary colic
142
Q

RUQ/epigastric pain from cholecystitis most commonly comes on or worsens?

A
  • after high fat meal
  • more fat in intestines = more need for bile to emulsify it -> secretion of bile puts on inflamed GB + causes pain
143
Q

risk factors of cholecystitis

A
  • obesity -> more cholesterol in body
  • women, esp on contraceptive or have had multiple pregnancies
  • starvation, rapid weight loss -> increase GB sludge -> thickened GB mucoprotein
  • genetics
144
Q

why do women have higher risk of GB stones?

A

estrogen reduces synthesis of bile acid + increase liver secretiono f cholesterol into bile

145
Q

5 Fs of GB disease

A
  • female
  • fat
  • forty
  • fertile
  • fair *more typical in whites
146
Q

GB problem labs

A
  • often leukocytosis from inflamm + sometimes infection
  • high direct bilirubin levels
147
Q

dx GB problems

A
  • ultrasound to detect small stones (1-2cm)
  • CAT scan
148
Q

tx GB

A
  • GB inflamed enuf -> remove it (cholecystectomy)
149
Q

acute pancreatitis

A

severe, life-threatening disorder associated w/ escape of pancreatic enzymes into pancreas + surrounding tissues -> autodigestion + hemorrhage

150
Q

cause of acute pancreatitis

A
  • gallstones -> pancreatic duct obstruction and/or biliary reflux activate enzymes in pancreatic duct system
  • alcohol -> potent stimulator of pancreatic secretions
151
Q

S/S acute pancreatitis

A

–epigastric pain: abrupt onset of post-prandial or post-alc-ingestion epigastric pain that is severe + radiates to back
- jaundice maybe if biliary obstruction/inflamm

152
Q

dx acute pancreatitis and pancreatic cancer

A
  • serum amylase + lipase elevated
  • maybe leukocytosis
  • abdominal CT (CAT scan)
153
Q

pancreatic cancer

A
  • one of most deadly malignancies
  • risk increases w/ age
  • most occurs 60 - 80 yrs
154
Q

pancreatic cancer cause

A
  • unknown but has risk factors
  • smoking
  • diet high in fat, meat, salt, dehydrated foods, fried foods, refined sugars
  • genetic risk
155
Q

S/S pancreatic cancer

A
  • insidious onset
  • pain, jaundice wt loss
  • close to common duct + ampula of Vater -> obstruct bile flow -> jaundice frequent symptom but pt usually metastasized by then
156
Q

cystic fibrosis

A

autosomal recessive disease in which S/S develop by age 6months

157
Q

w/ cystic fibrosis: _____ of a gene causes abnormality in the ______ present on the surface of many types ____ cells: _______.

A
  • mutation
  • chloride channel
  • epithelial
  • airways, sweat ducts, pancreases
158
Q

chloride channels’ primary jobs is to?

A

help mediate flow of sodium + water in/out of cells -> maintain appropriate salt/water balance in the cells

159
Q

when cellular Na/H2O balance is disturbed….

A

secretions are thickened and can block passageways in the lungs, skin, and pancreas

160
Q

cystic fibrosis: blocked lung passageways

A
  • viscous secretions + mucous plugs occlude bronchi + bronchioles
  • thick secretions breeding grounds for bacteria -> CF pts high risk for infection
161
Q

cystic fibrosis: blocked skin passaggeways

A

sweat gland secretions saltier compared to healthy ppl

162
Q

cystic fibrosis: blocked pancreatic passa=ageways

A

viscous secretions disable pancreas’ ability to release pancreatic enzymes into gut to help w/ digestion

163
Q

dx cystic fibrosis

A
  • sweat test: (+) when sweat on skin too salty = CF
164
Q

tx cystic fibrosis

A
  • lungs: vigorous pulm toilet, antibx as needed
  • pancreas: must take pancreatic enzymes b4 each meal
165
Q

hepatitis

A

inflammation of the liver

166
Q

causes of hepatitis

A
  • autoimmune probs
  • microbes
  • idiopathic
167
Q

S/S hepatitis vary and may include?

A
  • aching
  • fatigue
  • malaise
  • N/V/D
  • jaundice
168
Q

3 most common strains of viral hepatitis

A
  • A (HAV)
  • B (HBV)
  • C (HCV)
169
Q

HAV S/S

A
  • fairly acute onset (fever, malaise, jaundice)
  • mild w/ full recovery
170
Q

HAV often transmitted ______. example?

A
  • enterally
  • tainted food like oysters
171
Q

HAV vaccine ___ available. can also get ______ shot if not been vax + suspect been exposed.

A
  • now
  • immunoglobulin
172
Q

HBV and HCV transmitted ______ (from ______ the gut) via?

A
  • parenterally
  • outside
  • IV drug abuse, receiving blood, needlestick of infected pt, sexually
173
Q

HBV and HCV _____ onset w/ potentially devastating destruction of ______

A
  • insidious
  • liver cells
  • insidious: pt exist w/o S/S many years while being passed onto others unknowingly
174
Q

vaccine + immunoglobulin available for _____, but not for ____.

A
  • HBV
  • HCV
175
Q

cirrhosis

A

end-stage, irreversible disease of liver

176
Q

cirrhosis usually begins w/ some ______ initiation, which eventually leads to most of normal architecture of entire liver being ________ and replaced with _________.

A
  • inflammatory
  • destroyed
  • fibrous tissue + abnormal nodules
177
Q

cirrhosis causes norm ____ fxn to cease and disrupts flow in _________>

A
  • hepatocyte
  • vascular channels + biliary duct systems
178
Q

some damage to the liver can be _____ - but when cirrhosis is finally diagnosed, have reached ______ stage.

A
  • reversed
  • irreversible
179
Q

how well or badly a pt with cirrhosis does depends on?

A

how much normal tissue is remaining

180
Q

the major, most common cause of cirrhosis is?

A
  • excessive ETOH intake
  • alcohol’s toxic metabolites gradually destroy hepatocytes -> replace by fibrotic tissue + fat cells
181
Q

toxic rxn to drugs + chemicals

A
  1. too much acetaminophen
  2. overtaxes liver’s ability to metabolize it
  3. damaged hepatocytes
  4. cirrhosis
182
Q

viral hepatitis and other microbes can also cause?

A

cirrhosis

183
Q

diseases of the bile ducts such as __________ (an autoimmune dz) or _______ from obstruction of bile flow (_______) can cause cirrhosis

A
  • primary biliary cirrhosis
  • secondary biliary cirrhosis
  • chronic cholecystitis, etc.
184
Q

_____ disorders can also cause cirrhosis

A

genetic

185
Q

patho and S/S of cirrhosis can be categorized as problems of?

A
  • diminished hepatocyte fxn
  • related to portal hypertension
186
Q

w/p proper hepatocyte fxn, liver cannot perform?

A

norm metabolic fxn

187
Q

S/S diminished hepatocyte fxn

A
  • nutritional probs
  • protein depletion
  • probs w/ metabolism (breakdown) of substances like ammonia, drugs, hormones
  • Kupffer cells don’t fxn properly to filer out bacteria + leukopenia from splenomegaly = increased risk of infection
  • jaundice from inability to conjugate bilirubin
188
Q

nutritional problems w/ diminished hepatocyte fxn due to impaired…

A
  • production of bile salts -> unable to absorb fat + fat-soluble vitamins = vit deficiencies, wt loss
  • fat + cholesterol metabolism -> impaired synthesis of lipoproteins + altered cholesterol levels
  • glycogenolysis + gluconeogenesis -> hypoglycemia
189
Q

protein depletion problems with diminished hepatocyte fxn

A
  • decreased levels of plasma proteins
  • decreased levels of clotting factors
190
Q

decreased levels of plasma proteins contributes to?

A

fluid shift problems such as ascites + generalized edema

191
Q

ascites

A
  • shifting of fluid FROM portal veins thuout abdomen INTO the abdominal cavity
  • skin stretches to accommodate
  • protuberant abdomen
  • waves of fluid can be seen beneath skin
192
Q

decreased levels of clotting factors

A
  • low fibrinogen, prothrombin, other factors partially due to inability to create them
  • result: bleed easily + abnormal labs w/ clotting times (ex: PT, PTT will be prolonged)
193
Q

contributing to bleeding problems will be _______ from _______.

A
  • thrombocytopenia
  • splenomegaly (hypersplenism)
194
Q

decreased ability to break down ammonia into ______, resulting in?

A
  • urea
  • increased blood ammonia levels
195
Q

at toxic levels, the ammonia affects?

A

CNS -> brain inflammation called hepatic encephalopathy

196
Q

S/S hepatic encephalopathy

A
  • range from lack of mental alertness to confusion to coma
  • blurred vision
  • tremors
  • szres
  • asterixis: liver flap; flapping tremor of hands
197
Q

w/ diminished hepatocyte fxn, sex hormones can’t be broken down, so men may get ______ and women may get _____.

A
  • gynecomastia (breast growth in men)
  • hirsutism (abnormal hair growth)
198
Q

dim hepatocyte fxn: glucocorticoids can’t be broken down…

A

hypercortisolism -> Cushing’s syndrome

199
Q

dim hepatocyte fxn: aldosterone can’t be broken down…

A

hyperaldosteronemia -> salt + fluid retention -> ascites + general edema

200
Q

dim hepatocyte fxn: drugs can’t be broken down + not enuf albumin to bind to….

A

increased effect of drugs due to accumulation in the blood

201
Q

portal system

A

system of veins + venous flow btw organs in the abdomen - spleen, stomach, liver, pancreas, intestines

202
Q

patho of portal HTN

A
  1. fibrotic liver tissue from cirrhosis cause liver to be resistant to norm portal venous flow
  2. venous pressure in liver area increases as venous flow tries to overcome resistance -> portal HTN
  3. venous back pressure increases
  4. veins going into liver filate
  5. liver + surrounding area engorged w/ larger-than-norm amt of venous blood
203
Q

patho that causes portal HTN leads to 3 main problems, which are?

A
  • ascites
  • splenomegaly
  • varices: hemorrhoidal, esophageal
204
Q

ascites by portal HTN due to?

A
  1. increased back pressure in portal veins
  2. increased hydrostatic pressure in all veins of the area
  3. fluid forced into abdominal cavity
205
Q

splenomegaly

A

shunting of blood into splenic veins enlarges spleen

206
Q

hypersplenism

A

stasis of blood in abnorm large spleen causes RBCs, thrombocytes, and WBCs to undergo more breakdown than usual due to prolonged time in spleen

207
Q

sequelae of hypersplenism

A
  • anemia
  • thrombocytopenia
  • leukopenia
208
Q

S/S of anemia/thrombocytopenia/leukopenia

A
  • fatigue + SOB
  • easy bleeding/bruising
  • increased susceptibility to infection
209
Q

varices

A

enlarged, thin-walled veins

210
Q

varices can occur in?

A

esophagus, rectum (hemorrhoids), umbilicus area

211
Q

worst varices to have is ____ because?

A
  • esophageal varices
  • easily rupture -> pt bleed to death from huge outpouring of blood into esophagus
212
Q

lab tests specific for liver cirrhosis

A
  • elevated indirect serum bilirubin; sometimes low direct bilirubin also
  • elevates serum liver enzymes
213
Q

patho of high indirect bili lab results for cirrhosis

A
  1. norm level of unconjugated bili enters liver
  2. diseased hepatocytes cannot conjugate it
  3. remains in blood as unconjugated
  4. higher level of indirect bilirubin in blood
214
Q

patho of low direct bili lab results for cirrhosis

A

diseases liver cells canonot conjugate bilirubin -> low serum direct bili

215
Q

what liver enzymes are elevated with cirrhosis?

A
  • AST (aspartate aminotransferase)
  • ALT (alanine aminotransferase)
  • ALP (alkaline phosphatase)
216
Q

tx liver disease

A
  • enhance nutrition + no alc
  • restablish appropriate fluid balance
  • control ammonia
  • protection against infection, trauma, drug overdose
  • liver transplant
217
Q

how do you reestablish fluid balance to treat liver disease?

A
  • diuretics to mobilize fluid from tissue to blood to urine
  • IB albumin to increase protein in blood so water won’t be going out from blood to tissues
218
Q

how do you control ammonia to treat liver disease?

A

low protein diet + certain drugs

219
Q

with liver disease tx, you want to ____ protein molecules in the bloodstream but ____ dietary protein.

A
  • increase
  • decrease

nurs pathophysiology (13 decks)

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