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Life Maintenance > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What are the cells of the liver and their roles (4)

A

Hepatocytes - secrete bile
Kupffer cells - fixed macrophages that clean blood
Liver endothelial cells
Stellate cells - fat storing

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2
Q

Describe the biliary system

A

Bile secreted by hepatocytes
Moves through series of channels (canaliculi)
Move into small ducts, large ducts (hepatic ducts)
Anastomose onto common bile duct (and then into cystic duct if being stored in gallbladder)

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3
Q

What elements form protective barrier of the liver?

A

Kupffer cells in sinusoids clear endotoxins that arrive from gut

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4
Q

What are the components of bile? Where does it come from?

A

water, electrolytes, organic molecules (bile acids, cholesterol, bilirubin, phospholipids)

Secreted in 2 stages: By hepatocytes (bile salts, cholesterol and other organics) and by epithelial cells lining bile ducts that release watery solution of Na+ and HCO3- )

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5
Q

Describe development of bile salts

A

Cholesterol is turned into cholic and chenodeoxycholic acid which are conjugated with glycine and taurine to make Na+ salts which are secreted into the intestines

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6
Q

What does bile do? (3)

A

Fat digestion in prep for absorption
Bile + pancreatic juice neutralises gastric acid (Which aids digestive enzymes)
Aids elimination of waste products from blood (such as bilirubin and cholesterol)

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7
Q

Bilirubin

A

Yellow pigment formed from breakdown of haemoglobin

Useless & toxic - needs to be excreted

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8
Q

Describe formation and elimination of bilirubin

A

Bilirubin results from breakdown of haemoglobin during phagocyte destruction of RBC

Carried to hepatocyte by albumin and conjugated with glucuronic acid for excretion

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9
Q

What is jaundice? Where is it seen?

A

Excessive free OR conjugated bilirubin in ECF

Yellow skin, mucus membranes, sclera

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10
Q

What are the three types of janudice?

A

Pre-hepatic (haemolytic) - excessive breakdown of RBC, excess unconjugated bilirubin
Hepatic - excess conjugated and/or unconjugated bilirubin, caused by cirrhosis, drugs, hepatitis A/B/C/E, Gilberts Syndrome
Post-hepatic (obstructive) - Excess conjugated bilirubin, obstruction to passage into duodenum, enter circulation and into urine, gallstones, carcinoma of pancreas/bile duct

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11
Q

What transporter is involved in transporting blood glucose across hepatocyte cell walls?

A

GLUT2

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12
Q

Describe process and purpose of fat metabolism in the liver (3)

A

Triglycerides oxidised to PRODUCE ENERGY
SYNTHESIS og lipoproteins, cholesterol and phospholipids
CONVERSION or excess carbs/proteins to FA and TG for storage

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13
Q

Quick overview of types of GLUT transporters (4 main ones - where are they located?)

A

GLUT1 - Placenta, muscle, adipose, brain, endothelium
GLUT2 - Pancreas B-cells, liver, small intestines, Rental PCT
GLUT3 - Neural, small intestine
GLUT4 - Muscle, heart, adipose tissue

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14
Q

What substances does liver metabolise / excrete that would otherwise be toxic to body? (4)

A

Bilirubin
Ammonia
Hormones (androgens, oestrogens, aldosterone, thyroxine)
Drugs and exogenous toxins

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15
Q

Describe process of liver metabolism of drugs / hormones

A 
PHASE 1 (red/ox) - In smooth ER, cytochrome P450 makes substrate into polar compound
PHASE 2 (conjugation) - Makes it more water soluble for elimination via gallbladders or kidneys
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16
Q

Describe detoxification process of Paracetamol

A

Metabolisation by 3 pathways
Glucoronidation (most common 45-55%)
Sulfation (20-30%)
N-hydroxylation & dehydration - Less than 15% but important as intermediate product NAPQI is toxic

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17
Q

Describe metabolism of alcohol

A

Ethanol to acetaldehyde (toxic) to acetate into circulation

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18
Q

Describe process of liver regeneration

A

Adult liver cells generally DO NOT undergo cell division
BUT if part of liver is removed, it will regenerate to previous mass
2 pathways involved - Growth factor mediated pathway (hepatocyte growth factor, transforming growth factor alpha)
Cytokine signalling pathway using IL-6 via TNFa

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19
Q

Describe the role of liver in storage (7)

A

Stellate cells store fat soluble vit D, K, E, A
Vitamin B12 storage sufficient for 2-3 years
Folate
Iron stored as ferritin

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20
Q

Describe liver function tests used, what they can show (6)

A

Bilirubin - conjugated or not? - jaundice, where, severity of liver disease
Aminotransferase (ALT - hepatocellular damage) and (AST - progression of disease)
ALP - Diagnosing cholestasis, biliary obstruction, hepatic infiltration
Albumin - severity of chronic liver disease
PT - severity of hepatic synthetic function

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21
Q

First pass metabolism

A

Concentration of a drug is reduced significantly once it passes through GIT and liver (before reaching systemic circulation). Significant in prescribing of oral medication

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22
Q

Zero vs first order kinetics

A

Zero order - a constant amount (eg. so many milligrams) of drug is eliminated per unit time
First order - a constant proportion (eg. a percentage) of drug is eliminated per unit time

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23
Q

Nature of alcohol metabolism in terms of kinetics

A

First order up to 10mg/dl

Zero order above that

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24
Q

Goal of metabolism of drugs

A

Making them more water soluble/polar for excretion (as body sees them as foreign)

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25
Q

Describe phase I of metabolism

A

More polar (and possible reactive site for conjugation)
Oxidation
Reduction
Hydrolysis (insertion of H2O)

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26
Q

Effects of phase 1 reactions

A

inactivate the drug
OR produce active metabolite
OR produce toxic metabolite

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27
Q

Describe phase II reactiond

A

Conjugation - coupling of drug with one of several polar endogenous molecules (inert and water-soluble for excretion)

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28
Q

Describe normal metabolism of paracetamol

A

Either conjugated with glucuronide, sulphate

OR NAPQI needs to be conjugated by GSH

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29
Q

Describe what occurs during paracetamol overdose

A

Paracetamol usually conjugated with glucuronide and sulphate but in overdose that is saturated
Metabolism to NAPQI which is toxic is only path left, you run out of the glutathione which conjugates the NAPQI so it is free to attack you

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30
Q

What do you prescribe in paracetamol overdose and how does it work?

A

N acetyl cysteine

Converted to glutathione which mops up excess NAPQI to be eliminated in urine

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31
Q

Cytochrome P450 - what is it and what phase of reactions is it involved in?

A

Large family of isoenzymes that oxidise drugs (Phase I metabolism)
Essentially the CYP enzymes catalyse the phase 1 reactions, where the liver is turning lipid-soluble toxins to water-soluble for excretion

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32
Q

Cytochrome P450 inhibitors - what do they do, one example

A

Enzyme inhibition REDUCES metabolism of other drugs given at the same time

Erythromycin reduces warfarin metabolism, increasing drug levels and anticoagulation

Erythromycin 
Ciprofloxacin 
Sodium Valproate 
Omeprazole 
Simvastatin 
Fluconazole/ketoconazole 
Isoniazid
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33
Q

Cytochrome P450 inducers (5) and what do they do

A

CRAPS (GP not at important as rarely used)
Carbamazepine, Rifampicin, Alcohol, Phenytoin, Greseofulvin, Phenobarbitone, Smoking
Enzyme inducers increase metabolism of other drugs given at the same time
This reduces drug levels and reduces efficacy

E.g. rifampicin increases metabolism of the contraceptive pill and co-prescription may increase the chance of pregnancy

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34
Q

How are drugs eliminated? (6)

A 
Renal
Faecal (via bile)
Lungs
Tears
Sweat
Breast milk
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35
Q

Describe how metabolism and elimination of a drug determine plasma half life

A

The half-life of a zero-order reaction decreases as the initial concentration of the reactant in the reaction decreases. The half-life of a first-order reaction is independent of concentration

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36
Q

Describe how and why drugs are metabolised by the liver

A

Phase I - metabolism
Metabolism makes drug more polar (water soluble) and may create a reactive site for conjugation (phase II)
Oxidation - loss of electron(s), majority of action by cytochrome p450 enzymes
Reduction - gain of electron(s)
Hydrolysis - insertion of H2O into drug by esterases or proteases

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37
Q

What three elements move through liver together?

A

Portal vein
Hepatic artery
bile ducts

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38
Q

Overview of acinar concept and significance of zones 1-3

A

The acinus is roughly divided into zones that correspond to distance from the arterial blood supply - those hepatocytes closest to the arterioles (zone 1 below) are the best oxygenated, while those farthest from the arterioles have the poorest supply of oxygen.

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39
Q

Describe roles and contents of space of disse

A

Ito (stellate) cells store vitamin A and can generate collagen

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40
Q

Clinical signs of liver damage

A

Jaundice
Malaise
Bruising
Early sign may be high INR (due to clotting factors)

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41
Q

LFT interpretation - common tests and what variations may indicate (6)

A

Total bilirubin - Conjugated v unconjugated - Jaundice, severity of liver disease
Alanine (ALT) - Diagnosis of hepatocellular damage
Aspartate (AST) - Follow progression of disease
Alkaline phosphatase (ALP) - Diagnosis of cholestasis, biliary obstruction, hepatic infiltration
Albumin - Severity of chronic liver disease
Prothrombin time - Severity of hepatic synthetic function (synthesis)

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42
Q

What does it mean if ALT is high but Alkaline phosphatase is normal?

A

Hepatocyte rather than biliary injury

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43
Q

Majors causes of liver disease (8)

A 
Fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Metabolic / genetic disorders
Bile duct diseases
Vascular disorders
Tumours and tumour-like lesions
Drugs and toxins
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44
Q

Steatosis

A

Fatty liver

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45
Q

HAV, HBV, HCV - how are they passed? Which is the worst?

A

A - oral/faecal, acute
B - bloodborne, 10% of adults will develop chronic, 90% of children
C - bloodborne, worst one - leads to cirrhosis and HCC

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46
Q

Process of acute hepatitis at lobular level

A

Acute viral hepatitis inflammation is SCATTERED throughout lobule / portal tract

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47
Q

What do ground glass hepatocytes mean?

A

Hep B infection

48
Q

At what point is fatty liver disease generally considered irreversible?

A

Fibrosis

49
Q

What is occurring in cirrhosis? Why is it so bad? How can you measure it?

A

Diffuse throughout liver
Fibrous septa
Inflammation at borders or within nodules
Doppler flow to measure speed, shunts

50
Q

What does a patient likely have if they have plasma cell clusters?

A

Autoimmune hepatitis

51
Q

Microscopic features of cirrhosis

A

Fat, Mallory’s hyaline, neutrophil polymorphs

52
Q

Long term complications of cirrhosis

A

Cirrhosis and chronic liver failure
Portal hypertension
Hepatocellular carcinoma

53
Q

In a non-cirrotic liver, what is the most likely cause of a tumour found?

A

Metastisis from another part of the body

54
Q

In a cirrotic liver, what is most likely cause of tumour found?

A

Primary hepatocellular carcinoma (HCC)

55
Q

In what case might you see HCC in a non-cirrhotic liver?

A

Childhood-acquired chronic viral hepatitis (HBV or HCV)

56
Q

Describe the endocrine system

A

Integrates body functions via secretion of biologically active substances in the body

57
Q

Describe a hormone

A

Substance that is released in one tissue and travels via the blood stream (usually) to have an action in a remote tissue

58
Q

Types of hormone (3)

A

Peptides - charged, largely negative
Steroid - fat soluble
Amino acid derivatives - variable

59
Q

What are thyroid hormones?

A

Nuclear, Amino acid derivative

60
Q

When looking at endocrine tests, where do you look first to judge function?

A

Peripheral hormones

61
Q

What is the role of the hypothalamus?

A

To translate stimuli into hormone reaction

62
Q

How does hormone response get switched off?

A

Negative feedback

63
Q

Describe the pituitary

A

Two lobes
Lies in Sella Turcica
Anterior pituitary is glandular (creates its own hormones), posterior is not

64
Q

Anterior pituitary hormones (5) and role

A 
ACTH - regulation of adrenal cortex
TSH- thyroid hormone regulation
GH - growth
LH/FSH - reproductive control
PRL - breast milk production
65
Q

Posterior pituitary hormones

A

ADH - water retention

Oxytocin - breast milk, labour, psych

66
Q

Three considerations with pituitary tumours

A

Hormone hypersecretion
Space occupying lesion
Hormone deficiency states

67
Q

Requirement of development of growth hormone

A

REM sleep

68
Q

Effects of growth hormone excess in children vs adults

A

Giantism in children

In adults, MANY

69
Q

Actions of cortisol (6)

A 
Increase plasma glucose levels
Increases lipolysis
Proteins are catabolised
Sodium and H2O retention
Anti-inflammatory
Increases gastric acid production
70
Q

Describe Cushing’s Syndrome

A

Caused by excess cortisol

Changes in protein / fat metabolism
Changes in sec hormones
Salt and water retention

71
Q

Describe positive feedback loop involved in breast feeding

A

Baby starts to feed
Receptor senses, control centre compares to normal
Adjustment in the SAME direction as initial event

72
Q

Vision changes in pituitary tumour

A

Vision closing in from the sides

73
Q

Which cranial nerve is most at risk of damage from pituitary tumour?

A

6 as it lies most medially

74
Q

Treatment of pituitary tumours

A

Surgery
Radiotherapy
Drugs

75
Q

Causes of pituitary failure

A 
Tumour (mostly benign)
Trauma
Infection
Inflammation
Apoplexy - sudden vascular bleed
Iatrogenic
76
Q

Describe pituitary failure and treatments

A 
Depends on the resulting effects of the pituitary failure
Thyroid - thyroxine
Sex steroids - testosterone / oestrogen
Reduced cortisol - hydrocortisone
Reduced GH - GH
77
Q

What is nutrition?

A

Understanding the effects of food on the human body in health and disease

78
Q

Macronutrients and their energy values

A

Fat - 9kcal/g
Alcohol - 7kcal/g
Protein - 4kcal/g
Carbs - 4kcal/g

79
Q

Micronutrients

A

Water soluble - B, C

Fat soluble - A, D, E, K

80
Q

Biomarker of iron

A

ferritin (marker of iron storage)

BUT will also increase during inflammation or infection

81
Q

Determinants of total energy expenditure

A

Basal metabolic rate
Diet induced thermogenesis
Activity
Stress (illness / inflammation / surgery)

82
Q

What affects nutrient requirements?

A

Age, gender, body size, physical activity, state of health, physiological status (pregnant? lactating?), growth

83
Q

DRV

A

Dietary reference values

1991 report, useful for group, not for individuals

84
Q

Types of DRV (4)

A

Estimated Average Requirement
Reference Nutrient Intake
Lower Reference Nutrient Intake
Safe Intake

85
Q

Marasmus

A

Long term lack of protein / calories

86
Q

Seropthalmia

A

Vitamin A deficiency, blindness

87
Q

Kwashiorkor

A

Sudden onset protein malnutrition

88
Q

Ricketts

A

Vitamin D and/or calcium deficiency

89
Q

Why do we develop nutritional deficiencies?

A 
Inadequate intake
Reduced absorption
Increased losses
Increases demand
Other conditions that prevent storage (liver cirrhosis)
90
Q

Signs/symptoms of vitamin A deficiency

A

Low blood levels (as liver stores have been depleted)
Increased risk of infection
Xeropthalmia (non-blinding, blinding)

91
Q

Terminal ileum uniquely responsible for absorbing…

A

Vitamin B12

92
Q

Malnutrition

A

Not just under-nutrition, also over-nutrition

Deficiencies

93
Q

Consequences of malnutrition (8)

A 
Immune system 
Impaired wound healing
Loss of muscle mass
Kidneys impaired - over or dehydration
Reduces fertility
Neuro issues - apathy, depression
Impaired temp regulation
Micronutrient deficiencies
94
Q

What does low albumin indicate?

A

Body is not absorbing enough protein

95
Q

What does low urea indicate?

A

Poor protein intake (urea formed when protein is breaking down)

96
Q

Why can albumin be normal in cases of starvation?

A

Long half life
Increases due to dehydration
Falls due to stress/infection
Poorly correlated with nutritional status (normal levels can be seen in severe anorexia)

97
Q

Outline metabolic response to startvation

A 
Adaptive process
BMR falls by 30%
Loss of mass in metabolic tissues (Liver/ GI tract)
Minimise loss of protein
Maintain glucose supply to tissues
98
Q

Outline metabolic response to injury, trauma, sepsis

A

Energy metabolised for defense / repair
First few hours - ebb - shock
First few days - catabolism, energy store breakdown
Weeks - Anabolism, building energy stores, focus on nutritional therapy should be restoring protein synthesis

99
Q

Functions of the liver (6)

A 
Storage
Filtration
Synthesis
Secretion
Metabolism
Detox
100
Q

Encephalopathy

A

Confusion as liver cannot breakdown ammonia xxx

101
Q

Risk factors for liver disease

A 
Alcohol
Drugs
IV drug use
Blood borne virus risks
Other recreational drugs
102
Q

Presentation of chronic vs acute liver disease

A

Acute may not present with any outward issues, may move into organ failure quite quickly
Chronic will present with distension, jaundice, muscling wasting

103
Q

What causes massive AST/ALT elevation?

A

Drugs / toxins - paracetamol
Viruses
Ischaemia
Autoimmune hepatitis

104
Q

Bud-Chiari syndrome

A

Thrombosis of hepatic veins

105
Q

What is acute liver failure?

A

Severe liver injury, possibly reversible
MUST include encephalopathy
WIthin 8 weeks of first symptom in absence of pre-existing liver condition

106
Q

Level of acute measurements in liver failure

A

Measured in time between jaundice and encephalopathy
Hyperacute
Acute
Subacute

107
Q

Patient presenting with hepatitis / jaundice - investigations to perform?

A

Ultrasound scan - is there an obstruction? or liver disease?
Viral hep screen
xxx

108
Q

Encephalopathy grading (4)

A

1 - slight diorientation
2- more drowsy / disorientated / respond to verbal stimuli
3 - Extreme agitation
4 - Coma

109
Q

What is causing increase in chronic liver disease?

A

Metabolic syndromes
Obesity
Alcohol
Viruses

110
Q

5 clinical stages of cirrhosis

A

No varices, varices, bleeding, ascites, ascites bleeding

not necessarily in this order

111
Q

At what level of portal hypertension do you begin to develop varices?

A

about 10mmHg

Bleeding more likely from 12mmHg

112
Q

Assessment of severity of chronic liver disease

A

Child Pugh score looks at Bilirubin, albumin, ascites, encephalopathy, INR to estimate 2 yr survival

113
Q

Describe the process that creates increased portal hypertension

A

Loop where splanchnic and peripheral vasodilation indicate to body that blood volume is low which drives Na and water retention (which creates portal hypertension)

114
Q

Compensated vs uncompensated liver disease

A

Compensated - cirrhosis with no other clinical complications

Decompensated - WITH xxx5 other things jaundice, ascites, encephalopathy, varices

115
Q

Outline the ‘public interest’ required to break confidentiality

A

Real / serious risk of physical harm to an identifiable individual

116
Q

Examples of shunts in portal hypertension

A

Left gastric with azygous - oesophageal varices
Retroperitoneal with mesenteric - bare area
Epigastric with paraumbilical veins - Caput medusa
Splenic / IMA with superior rectal - Lower rectal varices / haemorrhoids

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