Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MPharm Y3S2 > Pharmacology Renal and Hepatic Disease > Flashcards

Pharmacology Renal and Hepatic Disease Flashcards

(81 cards)

Start Studying
1
Q

Describe the basic anatomy of the liver:

A

Left and right lobe
8 segments made up of lobules

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

Describe the lobules of the liver:

A

Each lobule made of central vein, radiating sinusoids (type of blood capillary) bile ducts, hepatocytes and other cells

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

What are the functions of bile ducts in the liver?

A

Join to form common bile ducts which drains bile into the duodenum after storage and concentration in the gall bladder

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

What is the function of the hepatic vein?

A

Deoxygenated blood from liver to heart from inferior vena cava

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

What is the function of the hepatic portal vein?

A

Carrying nutrient rich blood, oxygen poor, coming from GIT so can then travel to the body

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

Describe the vascular structure of the liver:

A

25% of resting CO in the liver (25% of bodies blood in liver at a time)
25% of blood is coming from the hepatic artery to liver (oxygen rich)
75% of blood is coming from the hepatic portal vein to liver (nutrient rich)
Blood leaves by hepatic vein to inferior vena cava to the heart

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

Name the structures in the hepatic lobules:

A

Portal triad
Sinusoidal capillaries
Central vein
Bile canaliculi
Hepatocytes

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

Name the features of the portal triad:

A

Bile duct
Portal vein
Artery

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

Name immune cells in the hepatic lobule:

A

Hepatic stellate cells (HSC)
Kupffer cells (KC)
Fibrocytes

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

What is the function of the HSC in the hepatic lobule?

A

Supporting hepatocyte
Perisinusoidal- very close to the blood capillaries
Antigen presenting role
Responsible for liver fibrosis (scarring) in liver disease
Important physiologically but bad in disease

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

What is the function of the KCs in the hepatic lobule?

A

They are macrophages attached to the endothelium
Phagocytosis of any foreign substances/ bacteria carried from the GIT in the portal vein
During disease can become inflammatory cells
Important physiologically but bad in disease

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

What are the functions of the liver?

A

Metabolism
Immunity
Storage
Detoxification
Synthesis
Catabolism
Activation
Transport
Excretion

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

How does the liver metabolically process carbohydrates?

A

Stores glucose as glycogen:
-up to 24 hrs worth
-not as good as not as energy dense and need water in there so lots of space taken up
Glycogenolysis in fasting
Gluconeogenesis in fasting:
-made from F.A and a.a

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

How does the liver metabolically process lipids?

A

Synthesis of cholesterol in liver
Lipoproteins

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

How does the liver metabolically process proteins?

A

Non-essential a.a synthesis
Breakdown of a.a to ammonia to urea for excretion

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

What is the difference between essential and non-essential a.a?

A

Non- essential= means we can synthesise it ourselves in the body
Essential= comes from the diet

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

Why does detoxification take place in the liver?

A

Conversion of harmful ammonia to urea- major elimination route of nitrogenous waste

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

Name and describe the different phases of drug detoxification and degradation in the liver:

A

Phase I reactions- by cyp450 enzymes
Phase II reactions- conjugation with other compounds to become more hydrophilic e.g gluconosyltransferase

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

What factors can affect metabolism?

A

Age, nutrition and genetics

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

What endocrine activities for modification of some hormones does the liver do?

A

Vit D3 to 25-OH vit D3 then in kidney 1,2 (OH2)D3
Thyroid hormone-> conversion of T4 to more potent T3
Insulin like GFs produced by hepatocytes modify action of growth hormone

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

What endocrine activities for major organ degredation of hormones does the liver do?

A

Insulin and glucagon
Oestrogens, glucocorticoids, growth hormones, PTH
Gastrin and other GI hormones

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

What does the liver store?

A

Fats- can be a problem during obesity, fatty liver
Glycogen
Trace elements- copper, iron
Vitamins A,D,K, some water soluble B vitamins for shorter periods

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

What does the liver synthesise?

A

Hormones
Plasma proteins
Iron transport and metabolism proteins
Acute phase proteins
Bile acids

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

Describe hormones synthesised by the liver:

A

Insulin like GF
Thrombopoietin- stimulates platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe plasma proteins synthesised by the liver:
Coagulation factors Transport for cholesterol (lipoproteins) Transport for steroid and thyroid hormones Angiotensinogen- important for salt conversion
26
Describe iron transport and metabolism proteins synthesised by the liver:
Transferrin- transports iron in the blood Hepatoglobin- bind free Hb blood Hemopexin- bind free heme in blood Hepcidin- inhibits iron uptake by gut
27
How is hemopexin involved in inflammation?
Important as can't have free iron in the blood as its a pro-oxidant During infection bacteria is attracted to this
28
Describe bile acids synthesised by the liver:
Primary: -cholic acid -chenodeoxycholic acid Secondary: -deoxycholic acid -lithocholic acid
29
Where is bile secreted and stored?
Actively secreted by liver and actively diverted to gall bladder between meals After a meal it enters the duodenum Stored and concentrated in gall bladder
30
What is the composition of bile acids?
Aqueous alkaline fluid containing: -bile salts -cholesterol -lecithin -bilirubin
31
Describe excretion in the liver:
Excretion of cholesterol and bilirubin through bile secretion Secreted bile salts consist of 95% of old recycled bile salts and 5% newly synthesised bile salts
32
How are bile salts recycled?
Re-absorbed in terminal ileum into the hepatic portal vein and into liver
33
Describe the first stages of removal of RBCs and heme breakdown until it enters the liver:
1. senescent red cells are major source of heme proteins 2. breakdown of heme into bilirubin, occurs in macrophages for the reticula-endothelial system 3. the unconjugated bilirubin formed is transported through blood (complexed with albumin) to the liver 4. then taken up via facilitated diffusion by the liver and conjugated with glucuronic acid
34
Describe the second stages of removal of RBCs and heme breakdown in the GIT:
5. conjugated bilirubin is actively secreted into bile and then the intestine 6. in the colon the part of the intestine, the glucuronic acid is removed by bacteria, the resulting bilirubin is converted to urobilinogen 7. some of the urobilinogen is reabsorbed from the gut and enters the portal blood 8. a portion of this urobilinogen participates in the enterohepatic urobilinogen cycle
35
Describe the third stages of removal of RBCs and heme breakdown in the kidney:
9. the remainder of the urobilinogen is transported by the blood to the kidney, where it is converted to yellow urobilin and excreted, giving urine its colour 10. urobilinogen which remains in the colon, is oxidised by intestinal bacteria to brown stercobilin
36
Name other immune cells involved in the immunological function of the liver:
NK cells B cells Dendritic cells Neutrophils/ monocytes
37
Describe liver disease:
Over 200 types Affects over 2 million people in the UK and is increasing
38
What are the main causes of increasing liver disease?
Alcohol Obesity Undiagnosed hepatitis infection Drug or other chemical toxicity
39
Name types of liver diseases:
Alcohol related LD Drug toxicity Hepatitis Non-alcoholic fatty LD (NAFLD) Cirrhosis (late stage, fibrosis/ scarring ) Cancer (late stage) Gall stones- stop bile secretion Cholangitis Hemochromatitis (Fe overload, inherited) Wilson's disease (Cu over load, inherited) Gilbert's disease (inability to metabolise bilirubin properly)
40
What is acute liver disease?
Usually self limiting Results in hepatocyte inflammation/ damage Occasionally severe resulting in liver failure Generally caused by drugs/ viruses
41
What is chronic liver disease?
Inflammation present for longer than 6 months Results in permeant damage with structural changes resulting in cirrhosis Most common cause is alcohol abuse
42
What does the progression to early fibrosis involve from the normal liver?
Reversible Inflammation Fatty liver Inflammatory damage Matrix deposition Parenchymal cell death Angiogenesis
43
What does the progression to cirrhosis involve from early fibrosis?
Not reversible Distrupted architechture Loss of function Aberrant hepatocyte region Leads to hepatoceulluar carcinoma Both needing a liver transplant
44
What is fatty liver?
A reversible condition where large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis (mainly due to obesity)
45
What is the fat composition in fatty liver?
Increase in TGs, LFTs and liver fat
46
What are the issues with Non-alcoholic fatty liver disease?
15-20% will develop from fatty liver NASH liver: steatosis ballooning inflammation fibrosis
47
Describe the normal liver pathophysiology:
Hepatocytes Sinusoidal endothelial cell- normal capillaries Kupffer cells (normal)- few Hepatic stellate cell- few Sinusoid lumen with normal resistance to blood flow
48
Describe the liver pathophysiology in an advanced fibrosis liver:
Lots of hepatic stellate cells- causing lots of fibrosis and ECM proteins Infiltrating lymphocytes Activated kupffer cells- phagocytose any dead cells Apoptotic hepatocytes Sinusoid lumen with increased resistance to blood flow
49
Name the different types of hepatitis':
A,B,C,D,E,G
50
Describe the route and symptoms of Hep A:
Faecal oral route Acute inflammation that generally resolves spontaneously Vaccine available to prevent
51
Describe the route and symptoms of Hep B:
Body fluids, mother to baby Acute infection that progresses to chronic inflammation, cirrhosis and cancer Vaccine available to prevent- normally in health care workers
52
Describe the route and symptoms of Hep C:
Body fluids, chronic and may progress to cirrhosis and cancer No vaccine
53
Describe the route and symptoms of Hep D:
Body fluids, requires concomitant infection with Hep B to survive
54
Describe the route and symptoms of Hep E:
Contaminated food and water Usually self limited
55
Describe the route and symptoms of Hep G:
Body fluids Chronic infection Similar to HCV
56
Describe how drugs can cause liver damage:
Hepatocytes become temporarily inflamed or permanently damaged by drugs/ medicines Some drugs require overdose to cause damage e.g paracetamol Other may cause damage even when appropriately prescribed e.g statins, Abs amoxicillin, tetracycline, MTX Some natural products e.g Kava Kava, high doses of vit A
57
Describe how alcohol can cause liver damage:
Most common cause of liver disease/ cirrhosis Directly toxic to liver cells Alcohol causes inflammation which progress to fatty liver and eventually fibrosis Fibrosis alters the structure and blood flow leading to back pressure in portal vein, leading to portal hypertension and eventual liver failure
58
How much alcohol needs to be consumed to cause liver damage?
More than 40g/d in men More than 20g/d in women
59
How many grams of alcohol is 1 unit?
9g
60
How many units are in wine, beer and spirits?
Small glass of wine= 1.5 units Standard glass of wine= 2.1 units Large glass of wine= 3 units Pint of beer= 2 units Single spirit= 1 unit
61
What could cholestasis be due to?
It is due to lack of bile in the GIT either due to: -hepatocytes -bile duct
62
How can the hepatocytes contribute to cholestasis?
Failure of bile production and secretion Causes include hepatitis from viruses, alcohol, drugs and pregnancy
63
How can the bile duct contribute to cholestasis?
Failure of outflow via able ducts due to obstruction Gall stones, carcinoma, cholangitis (progressive scarring of bile ducts)
64
What are the symptoms of acute liver disease?
Possibly asymptomatic Generalised malaise Anorexia Fever Jaundice (later)
65
What are the symptoms of chronic liver disease?
Fatigue/ weakness Loss of weight N&V Loss of appetite Cachexia- wasting of muscle in arms and legs Abdominal swelling Right upper quadrant abdominal pain and tenderness Jaundice Bleeding from gums/nose and easy bruising
66
What are the progressive symptoms of patients with cirrhosis as the liver fails?
Inability to metabolise waste as liver fails- toxins lead to bilirubin in the skin Failure to produce proteins require for body function e.g clotting Symptoms include easy bruising, gynecomastia, impotence, confusion, ascites, portal hypertension, oesophageal varicies
67
What are the signs and complications of liver disease?
Jaundice Skin changes Ascites Portal hypertension and oesophageal varicose Circulatory changes Hepatic encephalopathy Haematological changes Endocrine abnormliaties Renal failure
68
Describe what jaundice is:
Yellow discolouration of the skin and mucous membranes (sclera) Causes: -haemolysis, RBCs breakdown, bilirubin buildup (haemolytic jaundice) -hepatocellular damage (hepatic jaundice) -cholestasis (obstructive jaundice)
69
Describe portal hypertension and oesophageal varicies:
Oesophageal varicies are swollen veins in the oesophagus Blood flow decreases in liver when disease and therefore back pressure builds up in portal vein High HP pushes blood into surrounding BVs including thin walled veins in oesophagus clot to surface If pressure to high, they can rupture and bleed uncontrolled blooding leads to shock and death
70
Describe what ascites is:
Abnormal accumulation of fluid in the peritoneal cavity due to pressure inbalance between the circulation (high) and outside, in this case the peritoneal cavity (low)
71
What can ascites cause in liver disease?
Portal hypertension Low plasma albumin Salt and water retention by kidneys e.g secondary hyperaldosteronism
72
What is hepatic encephalopathy?
Neurological abnormality caused by build up of substances (mainly ammonia) normally metabolised by liver in blood and crosses BBB leading to neurological abnormalities due to ammonia and nitrogenous substances from gut by passing the liver Can be associated with cirrhosis, or acute liver failure or portal systemic bypass of liver
73
How is ammonia produced?
Breakdown of a.a. Bacteria in gut producing it Kidney excretes urea
74
What are the symptoms of hepatic encephalopathy?
Altered mental state Fetor hepaticus (musty breath) Asterixis (hand tremor) Drowsiness Confusion Coma
75
What can hepatic encephalopathy be precipitated by?
Dehydration Hypovolaema GI bleed CNS drugs Alcohol Increase in dietary protein Constipation
76
What is Wernicke encephalopathy?
Due to deficiency of thiamine, with decreased mental function Occurs in chronic alcohol abuse
77
What are the haematological changes in liver disease?
Anaemia Bleeding and bruising
78
What are the effects of anaemia in liver disease?
Effects on iron homeostasis Splenomegaly from portal hypertension Alcohol toxic to bone marrow Decrease in clotting factor
79
What is the effect of bleeding and bruising in liver disease due to?
Results in decrease in clotting factor synthesis
80
What are circulatory changes in liver disease?
Palma erythema- like dermatitis but without the dryness, just redness Spider naevi- clusters of little veins on skin surface Finger clubbing- due to changes in interstitial fluid
81
What are the skin changes in liver disease?
Pruritus- toxic substances not broken down so get out into the skin

MPharm Y3S2 (22 decks)

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