PhyS: LIVER Flashcards

1
Q

Name all the functions of the liver (6)

A
Carbohydrate metabolism
Protein synthesis 
Lipid metabolism
Drugs metabolism
Hormone metabolism
Bile production
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2
Q

glads are derived from the

A

alimentary epithelium

including the gallbladder which comes from the common hepatic duct

and they contribute to the process

mout: saliva
gut: liver and pancreas are accessory organs that facilitate the process

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3
Q

movement of bile from production to absorption

A

made in the liver
stored in gallbladder
travels through sphincter of Oddi to get to the duadenum and emulsify fat

90% bile salts reabsorbed in ileum as URObilinogen
circulates back through blood stream protal vein and back to the liver

10% bile salts lost in faeces as STEROcobilinogen

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4
Q

proteins made by the liver

A

clotting factors
albumine
lipoproteins

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5
Q

we get bilirubin from

A

Bilirubin comes mostly from hemoglobin 85%
also comes from myoglobin breakdown in muscle 15%

(break down of blood) gives stool it’s color

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6
Q

before becoming bilirubin haemoglobin and myoglobin and broken down into

A

biliverdin before becoming unconjugated bilirubin and albumin

this occurs from RBC breakdown after 120 days

this is absorbed by hepatocytes in the liver

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7
Q

bilirubin is conjugated in the and then become

A

liver and then become part of bile

If liver is impaired, then you would have elevated unconjugated bilirubin bc the liver is not able to do its job

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8
Q

if you have an abnormality in bilirubin what questions should you be asking

A

production problem?
too much made ?

that would mean
Bleeding
Hemolysis at abnormal rate

is it conjugated or unconjugated?

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9
Q

three physiological processes that would lead to hyper unconjugated bilirubin

A

can’t absorb because impaired uptake
making so much of it liver can’t keep up
reduced enzymatic activity

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10
Q

what would lead to impairment in bilirubin uptake

A

drugs
newborn
heptocellular injury: hepatitis

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11
Q

what would lead to an over production of bilirubin

A

bleeding
Erythroblastosis
Congenital RBC dz: sickle sell
Immune hemolysis

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12
Q

when would we see high bilirubin leading to

A

Newborns: hepatocytes not ready to go

Gilbert syndrome

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13
Q

why would you see hyper conjugatebilirubin

A

i. Build up from blockage

1. Stone

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14
Q

why are LFTs inappropriately named

A

AST and ALT are transaminase enzymes within the hepatocytes

they test liver health (of hepatocytes) not function

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15
Q

more appropriate name for LFTS

what exactly are they testing

A

necrosis index (amt. of damage done to hepatocytes)

these enzymes are usually not in the blood (AST mitochondria)
(ALT are found in cytosol)

they end up in blood after damage

ii. When ALT, AST, and LDH goes up, you are talking about liver cell death

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16
Q

amines and how they relate to transaminase enzymes in the liver

A

amines are nitrogen containing molecules that come from proteins

gluconeogenesis
3 carbon protein taken out of protein and made into glucose
nitrogen group is taken my a transaminase

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17
Q

which one is usually higher ALT or AST

A

ALT

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18
Q

what is a cholestasis index

A

ALP and GGT

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19
Q

what is a common drug that would cause an increase in liver enzymes

A

tylenol

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20
Q

Severity index

A

looks at how severe liver damage is

albumin mostly
this is actually a liver FUNCTION test

PT is also a function test because this is a function of the liver

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21
Q

what is cholestasis

A

refers to a decrease in the bile flow through the intraheptic cancaliculi (stones)

liver is trying to secrete bile through the SI

can be intraheptic (hepatic cell problem) or extrahepatic (biliary tree)

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22
Q

what lab values would we see with cholestasis

A

increase in cholesterol bilirubin and bile acids in the blood

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23
Q

bile lakes

A

intraductil build up of bile

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24
Q

bile pigment

A

seen as the result of intracellular accumulation

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25
what's are complications of cholestasis
fibrosis | cirrhosis
26
causes of cholelithiasis
``` bile stones drugs biliary cirrhosis atresia scelrosing cholangitis cholagipcarcinoma ```
27
one of the most common forms of prehepatic jaundice and the common causes
HEMOLYTIC (PREHEPATIC ``` Blood transfusion reactions Hereditary red cell disorders Sickle cell, polycytopenia Acquired hemolytic disorders Autoimmune hemolytic anemia Hemolytic disease of newborn ```
28
what is hepatocellular jaundice what labs would you see
i. Decreased bilirubin uptake ii. Decreased conjugation iii. Hepatocellular liver damage iv. Drug induced, frequently Disproportionate elevation in the alkaline phosphatase compared with the serum aminotransferases
29
sxs of cholestasis
``` pruritus jaundice skin xanthoma alk phos ADEK deficiencies ```
30
why do we see pruritus with cholestasis
build up of bile salts
31
why do we see a ADEK deficiency
we need bile to break down lipids and absorb them for the absorption of these fat soluble vitamins
32
other than classic viral hepatitis what can cause hepatitis
a. Malaria (plasmodium falciparum) b. Staphylococcal bacteremia c. Salmonellosis d. Candidiasis (disseminated dz in immunocomp'd like in DM) e. Amebiasis (100,000 deaths/yr - trohpozooites from ingested cysts infest liver, lung, brain) f. Miliary TB - when TB travels
33
Massive hepatic necrosis
Fulminant hepatitis:
34
chronic hepatitis is considered what duration
Duration greater than 6 months
35
Patient has no clinical disease, but has positive serum markers for virus production and we assume them to be infectious
x. Carrier state:
36
Subclinical infection
Asymptomatic infection or anicteric "flu like" syndrome usually only noted to be hepatitis by identifying HBsAb at a later date.
37
only DNA hepatitis why is this important
B more stable (carrier state)
38
50% of us are sero positive for which hepatitis
hep A
39
feco oral hepatitis
hep A and hep E
40
shortest incupation of hep A and E
2-5 weeks A 2-9 E
41
Travellers dz | Self-limiting
o Hepatitis A
42
has a carrier state and is associated with liver cancer
Hep B
43
incubation period of hep D
4-7 weeks
44
incubation of hep C
6-12 weeks
45
incubation of hep B
4-26 weeks
46
chronic carrier state is seen MC in
hep c
47
Pt with what hepatitis get hep D
hep B
48
vaccines exist for what viral hepatitis .
hep A | Hep B
49
HBsAg
Hepatitis B Surface Antigen).
50
First serum marker to rise
HBsAg
51
when would HBsAg be indicative of chonric hep b
After 6 months
52
HBeAg
Hepatitis B "E" antigen second marker as well as HBV DNA Inside the virus, "the core" - indicates acute infection w/ high titers of HBV
53
INDICATES VIRAL REPLICATION AND INFECTIVITY
HBeAg
54
Anti-HBc
anti hepatitis b Core proteins IgM- made 1st (Mmediate) or IgG- lasting immunity
55
indicates pt is RECOVERING; Non-infective hep b
IgM Anti-HBc
56
indicates non-infective hep b; protected from future infxn
IgG Anti-HBc can also be indicative of chronic
57
Anti-HBs/HBsAb
Antibody to Hepatitis B Surface Antigeno
58
indicative of SUCCESSFUL VACCINATION.
Anti-HBs/HBsAb
59
what would you expect to see + in a acute infection with hep b
o HBsAG --> Positive o HBeAg --> Positive o HBV DNA --> Positive o Anti-HBc (IgM) --> Positive
60
window" phase
o Anti-HBc (IgM) í positive
61
" Pt had HBV, non-infective, protected from future infxn
o Anti-HBc (IgG) í positive | o Anti-HBs í positive
62
Vaccinated pt
Anti HBs --> positive (no other Ab present)
63
causes of chronic hepatitis
``` o Chronic viral hepatitis. o Chronic alcoholism. o Drugs Isoniazideí TB Methyldopaí cardiac Methotextrate í arthritis o Autoimmunity. ```
64
clinical features of chronic hepatitis
o Fatigue. o Malaise. o Bouts Of jaundice --> don't forget pruritus o Loss Of appetite.
65
labs characteristic of chronic hepatitis
o Prothrombin Time (PT) - thin blood --> d/t clotting not working as well o Hyperbilirubinemia. o Mild in alkaline phosphatase. o of serum transaminases depends on the degree of damage.
66
Why can you see normal AST ALT in chronic hepatitis
because there aren't any hepatocytes left and these aren't liver function tests
67
Involves an extrahepatic biliary obstruction outside the liver
intrahepatic biliary disorder: Secondary Biliary Cirrhosis
68
what is Primary Biliary Cirrhosis
o Autoimmune See antibodies o See lymphocytic infiltration o Females > Males
69
who do we usually see Primary Sclerosing Cholangitis
o Males > Females
70
who do we usually see primary biliary cirrhosis in
females
71
what intrahepatic biliary disorder is characterized by high levels of globulins
See high levels of globulins sclerosing cholangitis this is an infection of the bile duct
72
what is characteristic of all types of intrahepatic biliary disease
obstructive jaundice
73
hepatocytes are taken over by fats in this liver dz
alcoholic induced liver disease
74
what are the stages of alcoholic liver disease and the sxs
hepatitis: i. Jaundice ii. Tender liver, pain, anorexia, ascites, fever cirrhosis 1. Asymptomatic 2. Portal hypertension 3. Liver failure 4. spleen gets enlarged
75
causes of cirrhosis
1. Alcoholism 2. Hepatitis B and C 3. Hemochromatosis - congenital disorder 4. Wilson disease
76
physiology of portal hypertension
a. All of the abdomen drains into the portal vein including lower part of the esophagus b. When you have a back up of pressure it is going to back up to these vessels the feed
77
clinical features of liver failure
Liver makes clotting factors -->Multiple coagulation defects Liver makes albumin --> Hypoalbuminemia Liver conjugates bilirubin -->Jaundice Liver breaks down estrogen --> Hyperestrinism Hepatic encephalopathy--> neurological impairments from build up of toxins
78
what hormonal impacts do we see as result of liver failure
``` Gynecomastia. Spider angiomata. Palmar erythema í redness of palms Testicular atrophy. Female distribution of hair ```
79
pancreatic secretions
bicarbonate proteins starch lipase
80
role of bicarbonate produced by the pancrease
- Buffers chyme exiting the stomach
81
proteins secreted by the pancrease
Trypsin and chymotrypsin
82
three triggers of the pancreas and where they come from
``` o Acetylcholine -PSNS o Cholecystokinin (CCK)- duodenum o Secretin-small intestine ```
83
what does fat simulate in the gallbladder in the duodenum in the pancreas
When fat comes out of the stomach into duodenum -->CCK release and gallbladder stimulated to secrete bile Stimulates pancreas to secrete its enzymes
84
bicarbonate release from the pancreas causes what what is the most potent trigger for this?
acid production to slow down acid in chyme