Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

nur 326 > liver: patho and pharm > Flashcards

liver: patho and pharm Flashcards

(53 cards)

Start Studying
1
Q

prevention: vax - hep A

A

2 doses 6 mo apart
rec: all children beginning at 12 mo, special high risk pops (health care, traveling, handle food, not requirement)

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

prevention: vax - hep B

A

3 doses at least 4 mo apart
rec: all infants beginning as newborns, titer for healthcare

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

classes for chronic HBV

A

different strains, mutate, some more resistant so we use 2 classes - usually combo
interferons
nucleoside analogs

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

hbv treatment

A

only for high risk pt - evidence that liver is suffering:
elevated AST, hepatic inflam (US or CT), advanced fibrosis
lots of drugs, changes constantly

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

hbv treatment: disadvantages

A

prolonged therapy
costs and adverse effects - interfere with a lot of drugs and each other and SE
high relapse - develop back into having an acute attack, treatment not great

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

hcv treatment

A

only recommended for chronic - however this is changing with newer and more effective drugs (treat anyone with detectable viral loads)
now easily treatable and eliminated in most
treat with direct acting antiviral therapy and interferon based regiments (some also need nucleoside analogue)
cost! but beneficial bc work well
note!: can take acetaminophen but <2g/day! (avoid NSAIDS all together if in liver fail), help with fatigue and malaise

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

pharm for cirrhosis/liver disease

A

lactulose
rifaximin

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

lactulose

A

hyperosmotic laxative
I: reduce ammonia abd in hepatic encephalopathy, also constipation
moa: creates acidic env to reduce blood ammonia levels by converting ammonia to ammonium (water sol and trapped in intestines = not abs)
PO or enema/rectal

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

lactulose: nc

A

can be given to titrate by # of stools (2-3/day) or by ammonia levels - not just given for high ammonia levels though - must have s/s of encephalopathy
make sure pt is NOT hypoK - increases renal ammonia production (monitor levels)
can take at home to treat LOC changes

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

rifaximin

A

2nd line if lactulose isnt working, so for hepatic encephalopathy
moa: inhibit bacterial rna synthesis by binding to bacterial DNA (initially used as an abx for GI)
sometimes preventative - hcp pref
PO

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

rifaximin: SE

A

peripheral edema, n, ascites, dizzy, fatigue, pruritis, skin rash, abd pain, anemia
has been associated with increased risk of c diff - monitor

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

liver function

A

met and/or storage of: fat, CHO, P, vits and min
blood volume reservoir: distend (compress to alter circulating BV)
blood filter: purify blood -> remove billy (hgb breakdown)
blood clotting factors -> proT and fibrinogen
drug metabolism and detox

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

liver anatomy

A

lobes = funcitonal units, made of hepatocytes, arranges around central vein, can regrow/generate
kupfer cells line inner liver caps/sinusoids, remove bacteria and toxins from blood

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

liver: portal circulation

A

blood into liver from stomach, intestines, spleen, pancreas (rich in nutrients), enters via portal vein
absorbed products of digestion come directly to liver and sent to lobules -> 1st pass effect

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

LFT: ALT, AST, alk phos

A

enzymes
not great indicator of disease severity
abn is elevated

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

LFT: billy

A

total, conjugated, direct, unconjugated (indirect)
abn is elevated

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

LFT: serum ammonia

A

liver breaks down
abn is elevated

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

LFT: serum P

A

liver makes
abn is decreased

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

LFT: serum albumin

A

abn is decreased

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

LFT: proT time

A

abn is elevated

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

jaundice

A

icterus
sclera! palms and soles, mucus membranes
caused by elevates billy in blood -> usually causes problems and is noticeable with total billy >2-2.5, look at conjugated v unconjugated to determine cause
yellowish discoloration of skin and deep tissues
3 classifications

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

jaundice: hemolytic

Study These Flashcards
A

increased breakdown of RBCs
bleeding or polycythemic

23
Q

jaundice: hepatocellular

Study These Flashcards
A

liver unable to take buildup of billy from blood or unable to conjugate
liver not doing its job

24
Q

jaundice: obstructive

Study These Flashcards
A

decreased or obstructed flow of bile (billy cant get out)
r/t gallstones

25
bilirubin
by product of heme breakdown - mainly hbg direct = conjugated indirect = unconjugated elevations of indirect billy = billy overP or impaired liver F elevations of direct = liver working out cant get out -> bile obstruction, gallstone
26
jaundice: cm
urine = darker liver E = elevated stools = normal or clay colored (infection or obstruction) pruritus = billy buildup - general or [] in palms and soles
27
hepatitis
viral systemic, mainly affects liver -> inflamm various strains cause different types -> A, B, C, can also be caused by epstein barr virus and cytomegalovirus (just inflam, not infection) hepatitis (just inflam, not infection), can also occur from OH abuse, drugs, chm, bacteria E is v dangerous for preg
28
hepatitis: patho
viral infection -> immune inflam mediators -> lysis of infected cells -> edema and tissues swelling -> tissue hypoxia -> hepatocyte death
29
hepatitis: cm
similar btw all types many cases of all types are asymptomatic -> but can range from none, mild, liver fail cause abn elevated LFTs -> non consistent with cellular liver damage prodromal -> icteric -> recovery
30
hepatitis: cm - prodromal
2 weeks after exposure fatigue, anorexia, malaise, n/v, HA, hyperalgesia, cough, low grade fever HIGHLY transmissible
31
hepatitis: cm - icteric
begins with jaundice jaundice, dark urine, clay colored stools liver enlarges and may be painful with palpation fatigue abd pain persists or increases in severity
32
recovery
resolution of jaundice 6-8 wks after exposure, S diminish liver remains enlarged/tender
33
hepatitis: complications
most recover w/o higher mortality in elderly and comorbidities chronic hep, liver cirrhosis, liver cancer, fulminant ural hep-acute liver fail
34
hep A
feral -> oral, parental (drugs), sexual acute onset with fever, mild severity, no chronic hep, usually children and adults, HH, vax -> high risk and travel with low sanitation
35
hep B
parental, sexual insidious onset (60-180 days), severe - can be prolonged or develop chronic, any age group, HBV vax (kids and hc workers), safe sex, hygeine
36
hep C
parental, sexual, mom -> fetus insidious onset, mild-severe S, can develop to chronic, any age, screen blood, hygiene, no vax, leads to hepatocellular carcinoma (new treatments and more widely avail), liver transplant
37
cirrhosis
can progress from hep, cirhosis is scarring and irreversible but hep is not irreversible, inflam, fibrotic liver disease -> higher death rate structural change from injury (OH/viruses) and fibrosis -> infiltration of leukocytes and active inflam chaotic fibrosis leads to obstructive biliary channels and BF -> jaundice and portal htn regeneration disrupted by hypoxia, necrosis, atrophy, liver fail -> this is why it is irreversible severity and rate of progression depend on cause
38
cirrhosis: common causes
hep B+C, accessive OH, idiopathic, non OH fatty liver disease, autoimmune, hereditary metabolism
39
cirrhosis: common causes - alcoholism and liver disease
OH -> acetylhide (excessive amounts alter hepatocyte F and activate hepatic stelocyte cells -> fibrosis acetylehide inhibits export of P and alters met of vits and mins -> malN OH cirrhosis most common but still onyl 25% various stages/spectrum: fatty liver -> steatohepatits -> cirrhosis kuffer cells attract neutrophils -> inflam -> toxins accumulate from gut bacteria -> cell mediated immunity
40
OH and liver disease: fatty liver
mildest, asymp reversible fat deposits increase lipogenesis
41
OH and liver disease: steatohepatitis
precursor to cirrhosis, inflam, degen of hepatocytes increased hepatic fat storage, stim irreversible fibrosis anorexia, n, jaundice, edema
42
OH and liver disease: cirrhosis
fibrosis and scaring alter liver structure immune issues
43
cirrhosis: patho
liver cells destroyed -> try to regen -> disorganized process -> abn growth -> poor blood flow and scar tissue -> hypoxia -> liver fail
44
cirrhosis: cm - early
insidious GI: n/v, anorexia, flatulence, change in bowel habits fever, weight loss, palpable liver
45
cirrhosis: cm - late
jaundice, peripheral edema bc low albumin and loss of pulling power (3rd spacing), low PT (protein), ascites (3rd spacing and portal htn), skin lesions (spider angiomata vascular), hematologic problems (anemia, bleed -> CF; portal htn = veins burst) endocrine issues: small testes, amenorrhea, impotence, infertile esophageal and anorectal varices: distended veins, portal htn, burst -> bleed, mortality encephalopathy: toxins -> confusion, coma, death
46
cirrhosis: cm - portal htn
resistant portal BF: varices and ascites, all blood has to go through liver, fibrosis blocks free flow and causes buildup cause: sustemic hypoT, vascular underfilling, stim of vasoconstrictive S (RAAS), plasma V expansion, increased CO -> ascites asymp until complications: variceal hemorrhage, ascites, peritonitis (gut bacteria), hepatorenal S (liver and kidney fail), cardiomyopathy (HF) tm: liver transplant, reversible, treat s and complications
47
cirrhosis: cm - hepatic encephalopathy
LOC primary diagnosis grade by severity correlated with liver labs -> mainly ammonia (primary chem driver of LOC changes)
48
hepatic encephalopathy: minimal
abn results on psychometric or neurophysical testing without cm
49
hepatic encephalopathy: grade 1
changes in behavior, mild confusion, slurred speech, disordered sleep
50
hepatic encephalopathy: grade 2
lethargy, mod confusion
51
hepatic encephalopathy: grade 3
marked confusion (stupor), incoherent speech, sleeping but arousable
52
hepatic encephalopathy: grade 4
coma, unresponsive to pain
53
acute liver fail
fulminent liver fail separate liver failure not caused by cirrhosis or other liver disease most common cause -> acetaminophen OD, treat with acetylcysteine patho: edematous hepatocytes and patchy areas of necrosis and inflam cell infiltrates and disrupts liver tissues 6-8 wks after viral hep or met liver disease -> rapid onset, 5 days -> 8 wks after acetaminophen OD s similar to cirrhosis, just without cellular changes tm: not much, liver transplant

nur 326 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions