rrd 12 Flashcards
(219 cards)
1
Q
small intestines
A
- duodenum
- jejunum
- ileum
2
Q
large intestines
A
- aka colon
- cecum
- ascending colon
- transverse colon
- descending colon
- sigmoid colon
- rectum
3
Q
gastrointestinal tract
A
- mouth
- pharynx
- esophagus
- stomach
- small intestines
- large intestines
- accessory organs: liver, gallbladder, pancreas, spleen
4
Q
5 anatomic sections used to assess abdomen and GI organs
A
- epigastric
- RUQ
- LUG
- RLQ
- LLQ
- umbilical region/periumbilical area
5
Q
epigastric
A
- area across upper abdomen just below sternum + ribs
- pyloric area of stomach, duodenum, part of pancreas
6
Q
RUQ
A
- right upper quad
- liver + gallbladder, part of pancreas, part of transverse colon
7
Q
LUQ
A
- left upper quad
- part of stomach, spleen, part of transverse colon
8
Q
RLQ
A
- right lower quad
- cecum + appendix
- part of ascending colon
9
Q
LLQ
A
- left lower quad
- part of descending colon
- sigmoid colon
10
Q
umbilical region
A
- lower duodenum
- jejunum
- ileum
11
Q
endoscopy
A
gen term for passing scope into GI tract for direct visualization
12
Q
esophagogastroduodenoscopy (EGD)
A
visualization of the esophagus, stomach, duodenum
13
Q
colonscopy
A
- visualization of the rectum, colon and distal small bowel
- important tool in detecting colon cancer early
14
Q
gastroesophageal reflux disorder (GERD)
A
- reflux of HCl + pepsin from the stomach into esophagus
15
Q
GERD may be due to?
A
relaxation of the lower esophageal sphincter (LES) and/or delayed emptying of the stomach
16
Q
GERD S/S
A
- heartburn
- epigastric pain
- coughing
w/in 1 hr of eating
17
Q
GERD S/S worsen when?
A
- lying down
- aggravated by ETOH
- coffee
- smoking
18
Q
Barrett’s esophagus is a relatively uncommon disorder almost always caused by?
A
GERD
19
Q
Barrett’s esophagus
A
- certain areas in esophagus tissue becomes dysplastic
- left untreated: esophageal cancer
20
Q
hiatal hernia
A
herniation of the stomach thru the diaphragm so that it protrudes into the thoracic cavity
21
Q
S/S hiatal hernia
A
- GERD
- epigastric pain
- dysphagia
- also can have no S/S at all
22
Q
tx hiatal hernia
A
may need surgury
23
Q
gastritis
A
an inflammation that affects gastric mucosa and can cause erosions (superficial areas of wearing away of mucosa)
24
Q
gastritis S/S
A
- pain or burning over epigastric area
- occasional bleeding (acute hemorrhagic gastritis)
25
layers of stomach from inside to out
- mucosa (mucous membrane)
- submucosa (connective tissue)
- layers of muscle
26
acute gastritis
- from overuse of NSAIDS (suppress protective prostaglandins) or ETOH (direct chem damage)
- heals spontaneously once offending agent removed
27
chronic gastritis
- aka atrophic gastritis
- autoimmune etiology
- mainly in elderly
- causes atrophy of gastric mucosa
- result: develop pernicious anemia bc loss of intrinsic factor
28
peptic refers to _____, which along with _____ (_____ + ____ = ______) digests food in stomach and duodenum
- pepsin
- HCl
- pepsin + HCl = peptic acid
29
if the mucosa is disturbed by ________, the balance is _____ and acid can get down to the ________.
- aggressive change factors
- disrupted
- vulnerable tissue underneath
30
peptic ulcer disease (PUD)
- chronic inflammatory condition of stomach + proximal duodenum
- disturbance of their mucosal lining allows acid to ulcerate the underlying tissue -> gastric and/or duodenal ulcers
31
what aggressive change factors can cause mucosal disturbance and/or increase tissue vulnerability to ulceration?
- ASA and other NSAID use
- chronic steroid use
- heavy ETOH use
- cig smoking
- chronic diseases
- severe psychological stress
- (+) for H. pylori
32
why does ASA/NSAID/steroid use cause PUD?
decrease prostaglandin synthesis -> protects stomach lining
33
what chronic diseases can cause PUD?
- chronic gastritis
- liver disease
- CKD
- diabetes
- COPD
34
Helicobacter pylori (H. pylori)
bacterium that can be ingested via food, drinking water, or other oral/fecal route
35
H. pylori infection more common in?
- same families
- crowded conditions
36
once H. pylori is ingested, can swim thru _____, burrow thru and disrupt the ________, and attach to _________ and ________ (can survive in ______)
- HCl
- mucous layer of stomach
- surface epithelial cells
- colonize
-- HCl
37
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.
- do not
- vulnerability to injury
- pepsin + HCl
38
S/S PUD
- painless ulcers sometimes
- ulcers that cause burning epigastric pain 1-3 hr after meals
- pain that awakens person during the night
39
in PUD, if ulcer beings eroding blood vessels, the pt can have?
GI bleed of various degrees depending on size of vessel
40
tx PUD
- antacids
- H2-blockers (Zantac, Pepcid)
- PPIs (proton pump inhibitors - Nexium, Prevacid)
- eradication of H. pylori w/ antibx regimen
41
colorectal cancer
- #3 killer amongst all cancers
- almost always arises from pre-existing benign neoplasm -> polyp form (stalk-like growth on colon wall) -> becomes malignant
42
colorectal cancer risk factors
- age over 50
- high fat diet, obesity, sedentary lifestyle
- smoking & ETOH over-consumption
- family hx
43
S/S colorectal cancer
- blood in stool, either visible or occult
- change in bowel habits
44
colorectal cancer dz most often done by?
colonoscopy
45
tx colorectal cancer
- 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
46
inflammatory bowl disease
chronic disorder characterized by inflammation of the lining + walls of intestines
47
two main types of IBD
- Crohn's disease
- ulcerative colitis
48
IBD common characteristics
- 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
49
possible causes of IBD
- infectious agents (bacteria, viruses)
- links to familial occurrence
- autoimmune response
50
IBD: formation of ______ against glycoproteins in intestinal walls -> ________.
- autoantibodies
- inflammation
51
IBD: sometimes pts has manifestation of _______ autoimmune features: ________.
- systemic
- arthritis , vasculitis, iritis
52
where does the intestinal obstruction in IBD come from?
chronic inflammation + scarring
53
fistula formation in IBD
abnormal channels or tracts that develops in the presence of inflammation and infection
54
tx IBD
- control inflammation by giving steroids + other meds
- sometimes surgery to remove parts of bowl
55
IBD vs IBS
- IBS: less serious disorder; abdominal pain, diarrhea, and/or constipation
- IBS: no inflammation, no blood in stool
- IBD: inflammation + bloody stools hallmark
56
Crohn's disease
- 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
57
S/S Chron's disease
- malabsorption
- malnutrition
- wt loss
bc most nutrients absorbed in small intestines, esp duodenum
58
ulcerative colitis
- severe inflamm + ulcerations begin in rectum and progress to involve entire colon (only colon)
- confluent, effected segments
- do not extend beyond submucosa
59
S/S ulcerative colitis
- dehydration risk more severe bc colon main site of water reabsorption
- not as high risk for nutritional deficiency
60
intestinal obstruction
occlusion of either the small or large intestine that can be partial or complete in nature
61
pathogenesis + S/S intestinal obstruction
1. obstruction
2. sequestration of gas + fluid proximal to obstruction
3. abdominal distention (swollen/stretched)
62
S/S intestinal obstruction
- severe, colicky abdominal cramping
- N&V
- constipation or w/ partial obstruction, diarrhea
63
intestinal obstructions can develop secondary to?
- adhesions
- hernia
- tumor in lumen of intestine
- intussusception
- volvulus
- paralytic ileus
64
adhesions
scar tissue from surgery or from chronic inflammation such as IBD
65
hernia
intestine protrudes thru weakness in the abdominal muscle or thru inguinal ring
66
intussusception
- telescoping of one portion of the bowel into the other, causing strangulation of blood supply
- more common in infants
67
volvulus
- aka torsion
- twisting of the intesstine with occlusion of blood supply
68
paralytic ileus
- aka ileus
- loss of peristaltic motor activity in the intestine
69
paralytic ileus is not a physical obstruction, but a _____ one bc all peristalsis ______ & fluids, gasses, etc build up, causing ________>
- functional
- stops
- distention, constipation, pain, etc
70
paralytic ileus is associated w/?
- immobility
- post-anesthesia effects
- surgery (esp abdominal)
- peritonitis
- electrolyte imbalances
- spinal trauma
71
paralytic ileus prevention
increasing pt mobility as soon as possible
72
diverticulum (pleural: diverticula)
herniations or saclike outpouchings of mucosa from muscle layer of the intestine that protrude from the intestine
73
diverticula most commonly occur in the?
sigmoid colon
74
diverticulosis
asymptomatic diverticular disease
75
diverticulitis
inflammation/infection of the diverticula
76
S/S diverticulitis
- pain (most often in LLQ)
- fever
- leukocytosis
77
diverticulitis can result in ____ if not treated adequately.
- abscess formation
- rupture
- peritonitis
78
tx diverticulitis
- increase dietary fiber
- avoid certain foods like seeds and nuts
- sometimes antibx
- occasionally surgery if required
79
appendicitis
- inflammation most often caused by fecal matter getting caught in lumen of appendix -> infection + inflammation
- slight genetic predisposition
80
tx appendicitis
appendectomy
81
S/S appendicitis
- norm pain pattern
- N/V/D, anorexia
- fever, leukocytosis
- not tx quick: inflammation to peritoneum -> peritonitis -> potential sepsis + other complications
82
pain pattern of appendicitis
- epigastric/periumbilical pain that migrates to become RLQ pain
- pain exacerbated upon movement
- rebound tenderness sometimes
83
peritoneum
membranous-like covering of abdominal organs
84
upper GI (UGI) bleed
from esophagus, stomach, duodenum
85
lower GI (LGI) bleed
from jejunum, ileum, colon
86
most common causes of UGI bleed
- acute hemorrhagic gastritis
- esophageal varices
- peptic ulcers
87
esophageal varices
large torturous veins in the esophagus caused by liver dz that can be easily irritated and caused to bleed
88
emesis, vomitus
product of vomiting
89
S/S that tell you bleeding is coming from UGI area of gut
- hematemesis
- blood in stools
90
hematemesis
- sudden vomiting of blood
- can be visible/frank or occult
91
visible/frank hematemesis
- 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
occult bleeding w/ hematemesis
- vomitus looks norm but
- small amt of hidden blood from slower, maybe chronic bleeding situation
93
blood in stools type
- occult bleeding
- melena
94
occult bleeding in stools
- 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
melena w/ bloody stool
- loose
- dark and tarry
- indicates blood partially digested in stomach or duodenum
- like coffee ground but blacker and pastier
96
most common causes of LGI bleed (hematochezia)
- IBD
- diverticulitis
- neoplasms
97
occult bleeding S/S that tell you bleeding is coming from LGI area of gut
- 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
frank bleeding w/ LGI bleed
- red blood mixed w/ stool
- no melena
99
objective of bilirubin cycle
to get unconjugated bilirubin into conjugated form so that it can be used to make bile
100
unconjugated bilirubin
comes out of spleen as water-insoluble substance so must have a protein carrier to get it to the liver to become conjugated
101
conjugated bilirubin
bilirubin becomes water-soluble so can be easily be incorporated into bile
102
stages of bilirubin cycle
1. prehepatic
2. hepatic stage
3. posthepatic
103
prehepatic stage
- unconjugated bili (indirect bilirubin): water insoluble + released from spleen
- proteins carry it to liver via bloodstream
104
hepatic stage
process of making unconjugated bili conjugated (direct bilirubin): water soluble
105
posthepatic
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
jaundice is not a disease in itself, but rather?
a manifestation of various disease states
107
bilirubin is the product of?
RBC break-down
108
there is normally a small amt of bilirubin in the blood, but most is excreted as?
- a waste product
- in the stool: gives stool its norm brownish color
- in the urine as urobilinogen
109
jaundice (icterus)
- alteration in norm bilirubin cycle -> accumulates in blood -> pathologically deposited thruout body
- yellow -green pigment
110
usual pigmented areas w/ jaundice
- skin
- sclera
- under tongue
- palate of mouth
111
causes of jaundice groups
- prehepatic jaundice
- hepatic jaundice
- posthepatic (obstructive) jaundice
112
prehepatic jaundice
- 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
prehepatic jaundice occurs because of?
increase in unconjugated bilirubin (aka indirect bilirubin)
114
most common causes of prehepatic jaundice is?
hemolytic conditions
115
increased unconjugated bili occurs when?
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
prehepatic jaundice can result in various forms of?
hemolytic anemia
117
hemolytic anemia
- decreased RBCs due to excess destruction of them
- certain drugs can cause excess breakdown of RBCs
118
erythroblastosis fetalis
hemolytic anemia of a newborn
119
erythroblastosis fetalis can happen in the ______ pregnancy when mother is _____ and fetus is _____ (and mom didn't receive ____ w/ previous similar pregnancy)
- second (or more)
- Rh neg
- Rh pos
- Rhogam
120
the baby becomes severely _____ as the mother's ____ to Rh factor _______ the fetus's RBCs
- jaundiced
- antibodies
- hemolyzes
121
physiologic jaundice is due to?
immaturity of the conjugating enzyme glucuronyl transferase
122
tx physiologic jaundice
- 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
post-hepatic jaundice
- 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
posthepatic (obstructive) jaundice occurs because of?
increase in conjugated bilirubin (direct bilirubin) in the blood
125
problem w/ posthepatic jaundice is with the?
flow of bilirubin making its ways to the intestines due to obstruction and/or inflammation (ex: cholecystitis, choledocholithiasis, tumor of the area, etc.)
126
in posthep j: ____ bilirubin have no where else to go -> _______ -> begins to leak from _____ back into ________ -> ______
- conjugated
- backs up
- liver cells
- circulation
- jaundice
127
hallmark sign of obstructive jaundice is?
- stool that is grey-colored bc lack of pigment from bilirubin (less bilirubin going to intestines)
128
hepatic jaundice
- sick liver
- cannot conjugate norm amts of unconjugated bilirubin
- bili gets deposited under skin + elsewhere
129
hepatic jaundice occurs because of?
increase in unconjugated bili
130
if hepatocyes are diseased, such as in hepatitis and cirrhosis, the liver?
cannot conjugate the unconjugated bilirubin that arrives
131
hepat j: the unconjugated bilirubin remains in ______ = ________ level of indirect bilirubin in the ______
- blood
- higher than normal
- blood
132
pts with hepatic jaundice will additionally have _____ conjugated bili.
low
133
blood test results that reflect prehepatic jaundice
- total serum bili: HIGH
- serum indirect bilirubin: HIGH
- serum direct bilirubin: normal
134
blood test results that reflects posthepatic jaundice
- total serum bilirubin: HIGH
- indirect bilirubin: NORMAL
- direct bilirubin: HIGH
135
blood test results that reflect hepatic jaundice
- total serum bili: HIGH or NORMAL
- serum indirect bilirubin: HIGH
- serum direct bilirubin: LOW
136
cholecystitis
inflammation of the gall bladder
137
cholecystitis is almost always caused by?
- irritation of stones inside gall bladder itself (cholelithiasis)
- stones in nearby duct like common bile duct (choledocholithiasis)
138
gallbladder purpose
stores bile that is secreted into intestine to help emulsify fats
139
patho cholelithiasis/cholecystitis
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
S/S cholecystitis
- 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
RUQ/epigastric pain from cholecystitis is often manifested as?
- painful spasms/contractions of the GB + bile ducts
- biliary colic
142
RUQ/epigastric pain from cholecystitis most commonly comes on or worsens?
- 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
risk factors of cholecystitis
- 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
why do women have higher risk of GB stones?
estrogen reduces synthesis of bile acid + increase liver secretiono f cholesterol into bile
145
5 Fs of GB disease
- female
- fat
- forty
- fertile
- fair *more typical in whites
146
GB problem labs
- often leukocytosis from inflamm + sometimes infection
- high direct bilirubin levels
147
dx GB problems
- ultrasound to detect small stones (1-2cm)
- CAT scan
148
tx GB
- GB inflamed enuf -> remove it (cholecystectomy)
149
acute pancreatitis
severe, life-threatening disorder associated w/ escape of pancreatic enzymes into pancreas + surrounding tissues -> autodigestion + hemorrhage
150
cause of acute pancreatitis
- gallstones -> pancreatic duct obstruction and/or biliary reflux activate enzymes in pancreatic duct system
- alcohol -> potent stimulator of pancreatic secretions
151
S/S acute pancreatitis
--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
dx acute pancreatitis and pancreatic cancer
- serum amylase + lipase elevated
- maybe leukocytosis
- abdominal CT (CAT scan)
153
pancreatic cancer
- one of most deadly malignancies
- risk increases w/ age
- most occurs 60 - 80 yrs
154
pancreatic cancer cause
- unknown but has risk factors
- smoking
- diet high in fat, meat, salt, dehydrated foods, fried foods, refined sugars
- genetic risk
155
S/S pancreatic cancer
- 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
cystic fibrosis
autosomal recessive disease in which S/S develop by age 6months
157
w/ cystic fibrosis: _____ of a gene causes abnormality in the ______ present on the surface of many types ____ cells: _______.
- mutation
- chloride channel
- epithelial
- airways, sweat ducts, pancreases
158
chloride channels' primary jobs is to?
help mediate flow of sodium + water in/out of cells -> maintain appropriate salt/water balance in the cells
159
when cellular Na/H2O balance is disturbed....
secretions are thickened and can block passageways in the lungs, skin, and pancreas
160
cystic fibrosis: blocked lung passageways
- viscous secretions + mucous plugs occlude bronchi + bronchioles
- thick secretions breeding grounds for bacteria -> CF pts high risk for infection
161
cystic fibrosis: blocked skin passaggeways
sweat gland secretions saltier compared to healthy ppl
162
cystic fibrosis: blocked pancreatic passa=ageways
viscous secretions disable pancreas' ability to release pancreatic enzymes into gut to help w/ digestion
163
dx cystic fibrosis
- sweat test: (+) when sweat on skin too salty = CF
164
tx cystic fibrosis
- lungs: vigorous pulm toilet, antibx as needed
- pancreas: must take pancreatic enzymes b4 each meal
165
hepatitis
inflammation of the liver
166
causes of hepatitis
- autoimmune probs
- microbes
- idiopathic
167
S/S hepatitis vary and may include?
- aching
- fatigue
- malaise
- N/V/D
- jaundice
168
3 most common strains of viral hepatitis
- A (HAV)
- B (HBV)
- C (HCV)
169
HAV S/S
- fairly acute onset (fever, malaise, jaundice)
- mild w/ full recovery
170
HAV often transmitted ______. example?
- enterally
- tainted food like oysters
171
HAV vaccine ___ available. can also get ______ shot if not been vax + suspect been exposed.
- now
- immunoglobulin
172
HBV and HCV transmitted ______ (from ______ the gut) via?
- parenterally
- outside
- IV drug abuse, receiving blood, needlestick of infected pt, sexually
173
HBV and HCV _____ onset w/ potentially devastating destruction of ______
- insidious
- liver cells
- insidious: pt exist w/o S/S many years while being passed onto others unknowingly
174
vaccine + immunoglobulin available for _____, but not for ____.
- HBV
- HCV
175
cirrhosis
end-stage, irreversible disease of liver
176
cirrhosis usually begins w/ some ______ initiation, which eventually leads to most of normal architecture of entire liver being ________ and replaced with _________.
- inflammatory
- destroyed
- fibrous tissue + abnormal nodules
177
cirrhosis causes norm ____ fxn to cease and disrupts flow in _________>
- hepatocyte
- vascular channels + biliary duct systems
178
some damage to the liver can be _____ - but when cirrhosis is finally diagnosed, have reached ______ stage.
- reversed
- irreversible
179
how well or badly a pt with cirrhosis does depends on?
how much normal tissue is remaining
180
the major, most common cause of cirrhosis is?
- excessive ETOH intake
- alcohol's toxic metabolites gradually destroy hepatocytes -> replace by fibrotic tissue + fat cells
181
toxic rxn to drugs + chemicals
1. too much acetaminophen
2. overtaxes liver's ability to metabolize it
3. damaged hepatocytes
4. cirrhosis
182
viral hepatitis and other microbes can also cause?
cirrhosis
183
diseases of the bile ducts such as __________ (an autoimmune dz) or _______ from obstruction of bile flow (_______) can cause cirrhosis
- primary biliary cirrhosis
- secondary biliary cirrhosis
- chronic cholecystitis, etc.
184
_____ disorders can also cause cirrhosis
genetic
185
patho and S/S of cirrhosis can be categorized as problems of?
- diminished hepatocyte fxn
- related to portal hypertension
186
w/p proper hepatocyte fxn, liver cannot perform?
norm metabolic fxn
187
S/S diminished hepatocyte fxn
- 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
nutritional problems w/ diminished hepatocyte fxn due to impaired...
- 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
protein depletion problems with diminished hepatocyte fxn
- decreased levels of plasma proteins
- decreased levels of clotting factors
190
decreased levels of plasma proteins contributes to?
fluid shift problems such as ascites + generalized edema
191
ascites
- 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
decreased levels of clotting factors
- 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
contributing to bleeding problems will be _______ from _______.
- thrombocytopenia
- splenomegaly (hypersplenism)
194
decreased ability to break down ammonia into ______, resulting in?
- urea
- increased blood ammonia levels
195
at toxic levels, the ammonia affects?
CNS -> brain inflammation called hepatic encephalopathy
196
S/S hepatic encephalopathy
- range from lack of mental alertness to confusion to coma
- blurred vision
- tremors
- szres
- asterixis: liver flap; flapping tremor of hands
197
w/ diminished hepatocyte fxn, sex hormones can't be broken down, so men may get ______ and women may get _____.
- gynecomastia (breast growth in men)
- hirsutism (abnormal hair growth)
198
dim hepatocyte fxn: glucocorticoids can't be broken down...
hypercortisolism -> Cushing's syndrome
199
dim hepatocyte fxn: aldosterone can't be broken down...
hyperaldosteronemia -> salt + fluid retention -> ascites + general edema
200
dim hepatocyte fxn: drugs can't be broken down + not enuf albumin to bind to....
increased effect of drugs due to accumulation in the blood
201
portal system
system of veins + venous flow btw organs in the abdomen - spleen, stomach, liver, pancreas, intestines
202
patho of portal HTN
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
patho that causes portal HTN leads to 3 main problems, which are?
- ascites
- splenomegaly
- varices: hemorrhoidal, esophageal
204
ascites by portal HTN due to?
1. increased back pressure in portal veins
2. increased hydrostatic pressure in all veins of the area
3. fluid forced into abdominal cavity
205
splenomegaly
shunting of blood into splenic veins enlarges spleen
206
hypersplenism
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
sequelae of hypersplenism
- anemia
- thrombocytopenia
- leukopenia
208
S/S of anemia/thrombocytopenia/leukopenia
- fatigue + SOB
- easy bleeding/bruising
- increased susceptibility to infection
209
varices
enlarged, thin-walled veins
210
varices can occur in?
esophagus, rectum (hemorrhoids), umbilicus area
211
worst varices to have is ____ because?
- esophageal varices
- easily rupture -> pt bleed to death from huge outpouring of blood into esophagus
212
lab tests specific for liver cirrhosis
- elevated indirect serum bilirubin; sometimes low direct bilirubin also
- elevates serum liver enzymes
213
patho of high indirect bili lab results for cirrhosis
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
patho of low direct bili lab results for cirrhosis
diseases liver cells canonot conjugate bilirubin -> low serum direct bili
215
what liver enzymes are elevated with cirrhosis?
- AST (aspartate aminotransferase)
- ALT (alanine aminotransferase)
- ALP (alkaline phosphatase)
216
tx liver disease
- enhance nutrition + no alc
- restablish appropriate fluid balance
- control ammonia
- protection against infection, trauma, drug overdose
- liver transplant
217
how do you reestablish fluid balance to treat liver disease?
- 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
how do you control ammonia to treat liver disease?
low protein diet + certain drugs
219
with liver disease tx, you want to ____ protein molecules in the bloodstream but ____ dietary protein.
- increase
- decrease
