Exam Flashcards

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1
Q

Describe Neutrophils

A

First line defenders
Move rapidly to site of infection in large numbers
Most abundant but die fighting
Become phagocytic on exposure to infectious material

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2
Q

Describe Macrophages

A

Develop from monocytes, chief phagocytic cells, robust cells

Free and fixed

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3
Q

Describe Eosinophils

A

Mildly phagocytic

Defence against parasites and regulation of vascular mediators

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4
Q

Describe Natural Killer Cells

A

Function = recognise and eliminate cells infected with viruses and eliminating cancer cells

Non-phagocytic large granular lymphocytes

Attack cells that lack “self” cell-surface receptors

Induce apoptosis in cancer cells and virus-infected cells

Secrete potent chemicals that enhance inflammatory response

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5
Q

Purpose of Interleukins

A

Produced by macrophages and lymphocytes in response to a pathogen or stimulation by other products of inflammation

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6
Q

Purpose of Interferons

A

Protect against viral infections

Released by viral infected cells and protect neighbouring cells; activate NK cells and macrophages.

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7
Q

What line of defence is innate immunity?

A

1 and 2

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8
Q

What line of defence is adaptive immunity?

A

3

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9
Q

Outline innate immunity

A

Natural resistance

Epithelial barriers
Mucous membranes
Phagocytes
NKC
Chemical mediators (cytokines)
Inflammation
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10
Q

Outline adaptive immunity

A
Gained after birth
Involves memory
Specific ID of pathogens
Recognition of self and non self
Lag between exposure and response

Antigens
Immune cells (lymphocytes, antigen presenting cells, effector cells)
Humoral response
Cell-mediated response

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11
Q

Outline primary response

A

Initial exposure
Has latent period or lag phase when B cell differentiation occurs
After 5-7 days an IgM antibody for specific antigen is detected
An IgG response equal or slightly less follows IgM response

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12
Q

Outline secondary response

A

More rapid
Larger amounts of antibodies are produced from memory cells
Mature T cells already present
IgM produced in similar quantities to primary response byt IgG is significantly higher

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13
Q

What is an allergy?

A

Exaggerated hypersensitivity response to environmental antigens

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14
Q

What is hypersensitivity?

A

Exaggerated or inappropriate immunologic response to an antigen that results in disease or damage to the host

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15
Q

What is autoimmunity?

A

Body defences are misdirected against the body’s tissues

Autoimmune disease occurs when autoantibodies and cytotoxic T cells start to damage the persons own tissue

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16
Q

What is immunodeficiency?

A

Body defences are insufficient to protect the host

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17
Q

Categories of transplant rejection

A

Hyperacute
Acute
Chronic

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18
Q

Outline Hyperacute transplant rejection

A

Immediate and rare

Pre-existing antibody to the antigens of the graft

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19
Q

Outline Acute transplant rejection

A

Takes days to months
Cell-mediated immune response against unmatched HLA antigens
Biopsy demonstrates infiltration of lymphocytes and macrophages characteristic of type IV reactions.

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20
Q

Outline Chronic transplant rejection

A

Months or years after period of normal function
Slow, progressive organ failure
Inflammatory damage as a result of a weak cell-mediated reaction against minor HLAs

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21
Q

What is Systemic lupus erythematosus

A

Chronic multisystem inflammatory disease

Autoantibodies against: nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc.

Deposition of circulating immune complexes containing antibody against host DNA

Excessive levels of autoantibodies react with circulating antigens and form immune complexes, causes reactions in kidneys, brain, heart, spleen, lungs, GI tract, peritoneum and skin.

More common in females (10:1), esp 20-40 yrs

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22
Q

CM of Systemic lupus erythematosus

A
Arthralgias or arthritis (90% of individuals)
Vasculitis and rash (70–80%)
Renal disease (40–50%)
Haematologic changes (50%)
Cardiovascular disease (30–50%)
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23
Q

Tx of Systemic lupus erythematosus

A

No cure (as for most autoimmune diseases)
Aim to treat symptoms and suppress the autoimmune response
NSAIDS
Corticosteroids for serious active disease
Immunosuppressive drugs, e.g. methotrexate
Avoid UV exposure to reduce “flares”
Potential Rx with stem cell treatments

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24
Q

Why doesn’t the body clear the HIV virus totally?

A

It has a high replication rate - main reason for lack to total clearance

Provirus can be hidden where it is not detectable by the immune system

High mutation rate - antigens to antibodies and CD8s have mutated so cannot recognise and destroy.

Mutation is continual.

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25
Q

Define drug abuse

A

using a drug in a fashion inconsistent with medical or social norms

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26
Q

Define drug addiction

A

chronic, relapsing brain disease process characterized by compulsive seeking and use of a specific psychoactive substance despite harmful consequences

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27
Q

Define drug tolerance

A

regular drug doses elicit a smaller response than initially, requiring higher and higher doses to elicit desired effects

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28
Q

Define psychological dependence

A

an intense, subjective need for a particular drug

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29
Q

Define physical dependence

A

a state where an abstinence syndrome will occur if drug use is discontinued

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30
Q

Define withdrawal syndrome

A

S&S that occur in physically dependent people when they discontinue drug use

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31
Q

Define cross tolerance

A

tolerance to one drug confers tolerance to another drug, usually same group

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32
Q

Define cross dependence

A

same for dependence

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33
Q

Diagnostic criteria for substance use disorder

A

Maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by 2 or more of the following, occurring within a 12 month period:

  • Recurrent use resulting in failure to fulfill role obligations - - Recurrent use in situations where physically hazardous
  • Continued use despite problems
  • Tolerance
  • Withdrawal
  • Taken in larger amounts and longer than intended
  • Persistent desire and unsuccessful quitting/controlling
  • Time spent on activities relating to substance abuse
  • Giving up other activities
  • Continued despite knowing harmful effects
  • Craving
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34
Q

Substance abuse involves which drugs

A

Schedule 8 or 9

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35
Q

What are schedule 8 drugs

A

Controlled drugs

Available for use but require restriction to reduce misuse or dependence

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36
Q

What are schedule 9 drugs

A

Prohibited substances

Substances which may be abused or misused

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37
Q

Neurobiology of Addiction

A

Voluntary users can become compulsive users as a result of molecular changes in the brain

Reward circuit is activated
Major transmitter is dopamine: regardless of what initiates the reward pathway, the end is the same

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38
Q

Factors that Contribute to Drug Abuse

A
Reinforcing properties of the drug
Physical dependence
Psychological dependence
Social factors
Drug availability
Vulnerability of the individual
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39
Q

Therapeutic use of alcohol

A

Antidote for antifreeze and methanol poisoning
Antiseptic (alcowipes)
Nerve blocks

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40
Q

Benefits from moderate consumption of alcohol

A

Prolongs life
Reduces risk of dementia, diabetes and cardiovascular disorders
Contributes to the joy of living

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41
Q

Cognitive effects of alcohol

A

Acute effects

  • General depression of CNS function
  • Enhances GABA-mediated inhibition
  • Dose-dependent
  • Activation of the reward circuit
  • Binds with 5-HT3 receptors

Chronic effects

  • Encephalopathy
  • Effect on sleep
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42
Q

Physical effects of alcohol

A
  • Cardiovascular system
  • ↓respiration
  • Liver damage
  • Stomach
  • Kidney
  • Pancreas
  • ↓blood glucose levels by inhibiting hepatic glucose output → risk for hypoglycaemia, masks signs (diabetics!)
  • Sexual function
  • Cancer: breast and colorectal cancer
  • Pregnancy and lactation
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43
Q

What is Fatty Liver

A

Large amounts of fat accumulate in hepatocytes (steatosis)
Liver enlarges and becomes yellow
Damage reversible once alcohol is discontinued

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44
Q

What is Alcoholic Hepatitis

A

Often due to binge drinking
Inflammation and necrosis
Stimulates irreversible fibrosis

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45
Q

What is cirrhosis

A
Irreversible fibrosis of the liver 
Fat deposits, ↑connective tissue
Loss of liver function
 - Loss of hepatocytes
 - Obstruction of biliary duct system

Cessation of alcohol reverses the fatty deposits but not the fibrosis or hepatocyte damage

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46
Q

CM of ALD

A
Tenderness/pain in Rt upper quadrant
Portal hypertension
Coagulation disturbance
Hepatic encephalopathy
Jaundice, pruritus 
Feminisation
Weight loss, anorexia
Weakness
Diarrhoea, nausea
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47
Q

DX of ALD

A

History (social, work)
Questionnaires (AUDIT) and DSM-5 criteria
S & S
Liver US or biopsy

Bloods

  • liver enzymes (ALT, AST, γ-GT)s and bilirubin
  • serum albumin
  • prothrombin time
  • U & Es, FBC
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48
Q

TX alcohol use disorder

A

Reduce or stop alcohol intake (CBT, drugs)
Reduce portal hypertension (beta blockers)
Varices (balloon tamponade, vasopressin)
Bleeding (administration of clotting factors)
Ascites (diuretics, abdominal paracentesis)
Dietary intake (low protein, high carbohydrate, vitamin supplements)
Correct electrolyte and fluid imbalance and hypoglycaemia
Transplant in severe cirrhosis?

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49
Q

Drugs which facilitate alcohol withdrawal

A

Benzodiazepines

  • Diazepam (drug of choice, tapered dosage over 6 days)
  • Oxazepam, lorazepam (in severe liver disease)

Adjuncts to benzodiazepines

  • Antipsychotics (haloperidol)
  • Antiepileptics (carbamazepine)
  • Antiemetics (metoclopramide)
  • Thiamine (IM/IV and oral) and multivitamins
  • Beta blockers (atenolol, propanolol)
  • Review/cease drugs that ↑seizure risk (SSRIs)
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50
Q

Drugs used to Maintain Abstinence

A

Acamprosate (Campral)

  • Structure similar to GABA
  • Administered orally
  • Adverse effects (diarrhoea, rash, nausea)

Naltrexone

  • Pure opioid antagonist
  • Administered orally, implants are being tested
  • Adverse effects (nausea, headache, anxiety, sedation)
  • Hepatotoxic

Disulfiram (Antabuse)

  • Causes irreversible inhibition of aldehyde dehydrogenase
  • Acetaldehyde syndrome (nausea, flushing, vomiting, headache, palpitations, chest pain)
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51
Q

Effects of Nicotine

A

Cardiovascular effects

  • SNS and adrenal gland
  • Arrhythmias
  • Tachycardia
  • Vasoconstriction

GI effects

  • PNS, vomiting
  • ↑gastric acid and motility

CNS effects

  • Pregnancy and lactation
  • Low birth weight
  • Pre-term labour
  • SIDS?

Up-regulation of receptors

  • Tolerance
  • Dependence

Acute poisoning

  • 40mg can be fatal
  • No specific antidote – activated charcoal can be given
  • Monitor for respiratory depression and supportive treatment

Chronic toxicity from smoking

  • Cancers
  • Cardiovascular diseases
  • COPD
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52
Q

Symptoms of withdrawal from nicotine

A
Craving 
Irritability, restlesness
Frustration, anger
Anxiety
Sleep disturbances
Difficulty concentrating
↓heart rate
↑appetite, weight gain
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53
Q

“5 As” Model for treatment of tobacco addiction

A

Ask (screen all patients for tobacco use)
Advise tobacco users to quit
Assess willingness to make a quit attempt
Assist with quitting (offer medication and provide or refer to counseling)
Arrange follow-up contacts, beginning within the first week after the quit date

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54
Q

TX of tobacco addiction

A

Nicotine replacement therapy

  • Chewing gum
  • Lozenges and sublingual tablets
  • Transdermal patches
  • Mouth spray
  • Inhaler

Other non-nicotine drug treatments

  • Bupropion (Zyban)
  • Varenicline (Chantix)
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55
Q

What is nicotine replacement therapy

A

High dose and combination therapy safe for heavy smokers
Smoking rate or serum cotinine
Assess adequacy of nicotine replacement by patient response or percent replacement
More complete nicotine replacement improves withdrawal symptom relief
Adverse effects usually minor and transient
Withdrawal symptoms
Nicotine overdose (tachycardia, palpitations, arrythmias)

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56
Q

Adverse reactions to NRT

A
Indigestion
Irritation of mouth and throat
Sinusitis
Irritation of mouth and throat
Take care if patient has dentures
Local site reactions 
Insomnia, dizziness, agitation, lack of concentration
Fever, rash, nausea, dry mouth
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57
Q

What is nociception

A

perception of pain

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58
Q

What are neuromodulators

A

substances that alter pain transmission

Located in pathways of nervous system
Triggered by tissue injury and or inflammation

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59
Q

What is the endorphin response

A

Endorphins interact with the opiate receptors in the brain to reduce our perception of pain and act similarly to drugs such as morphine and codeine

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60
Q

What are opioid receptors

A

3 main classes of opioid receptors have been identified:
Mu (μ)
Kappa (К)
Delta (δ)

Analgesic drugs stimulate μ receptors with some action on К

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61
Q

Classic triad of acute toxicity

A

Respiratory depression
Coma
Pinpoint pupils

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62
Q

Immediate effects of heroin

A

Lower abdominal sensation similar to sexual orgasm

Euphoria

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63
Q

Long term effects of heroin

A
Intense sadness 
Irregular periods and infertility 
No sex drive
Constipation 
Damaged heart, lungs, liver and brain 
Vein damage 
Skin, heart and lung infections from injecting 
Tolerance and dependence on heroin 
Financial, work or social problems
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64
Q

Effects of first time heroin use

A

nausea
vomiting
dysphoria

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65
Q

Routes of administration of heroin

A

High lipid solubility
IV route preferred, but also smoking, nasal inhalation
Overdose

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66
Q

Signs of heroin overdose

A
Cognitive (sleepy, LOC)
Urinary retention
Itchiness
Arrhythmias
↓resps
Death

Rx: Naloxone, ventilation

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67
Q

Heroin withdrawal symptoms

A

Cravings for heroin
Restlessness, irritability, depression, crying
Diarrhoea, vomiting
↑HR

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68
Q

Why is Pethidine the choice of health professionals

A

Highly effective in oral route

Minimal effect on smooth muscle: fewer problems with constipation and urinary retention

Don’t get tell-tale signs of repeated injections

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69
Q

Routes of administration of oxycodone

A

Abusers crush tablet, snort powder or dissolve in water for IV

Controlled-release drug
Entire dose absorbed immediately with high risk of death

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70
Q

Immediate effects of oxycodone

A

Euphoria
Dental problems
Mood swings

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71
Q

Signs of oxycodone overdose

A

respiratory depression
arrhythmias
LOC

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72
Q

Treatment of acute toxicity / overdose

A

Naloxone

  • pure opioid antagonist used to counter the effects of opioid, especially in overdose
  • extremely high affinity for μ-opioid receptors in CNS
  • reverse depression of CNS, respiratory system, and hypotension
  • Naloxone may be combined with other opioids so when taken orally the opioid has effect but if misused the naloxone blocks the effect of the opioid

Naltrexone - structurally similar but has increased affinity for κ-opioid receptors over naloxone, can be administered orally, and has a longer duration of action.

Nalmefene - opioid receptor antagonist used in management of alcohol dependence.

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73
Q

Methods of opioid detoxification

A

Methadone:
Substitute methadone for dependent opioid to prevent abstinence syndrome as has cross-dependence.
Gradually reduce doses
Abstinence syndrome is mild (moderate influenza)
10 days

Clonidine:
Used for physically dependent person on opioids
Suppresses symptoms of abstinence (nausea, vomiting, diarrhoea, muscle aches, restlessness, anxiety and insomnia)
Doesn’t diminish opioid craving

Rapid and ultra-rapid withdrawal:
Given opioid antagonist to precipitate immediate withdrawal and accelerate withdrawal process
Done under GA or heavily sedated

Social/family support
Counselling
Rehabilitation

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74
Q

Long-term opioid addiction management

A

Three groups of medications:

1) opioid agonists
2) opioid agonist-antagonists
3) opioid antagonists

Methadone (opioid agonist)
Maintenance and suppressive therapy
Aim = avoid withdrawal symptoms, prevent addiction

Buprenorphine (opioid agonist-antagonist)
Maintenance therapy and detox facilitation
Aim = alleviate cravings, reduce drug use

Naltrexone (opioid antagonist)
Discourages renewed opioid abuse by blocking euphoria and other effects

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75
Q

Effects of barbiturates

A

Depressant effects are dose-dependent
Mild sedation to sleep to coma and death
Subjective effects similar to those of alcohol

76
Q

Signs of immunodeficiency

A

Unusual or recurrent infection
T cell deficiency
B cell and phagocyte deficiency
Compliment deficiency

77
Q

Types of immunodeficiency

A

Primary (congenital)

  • rare
  • genetic defect

Secondary (acquired)

  • more common
  • caused by other conditions (malnutrition, trauma, infection, AIDs, etc)
78
Q

What is type 1 hypersensitivity

A

IgE mediated release of histamine

FIRST EXPOSURE

  • allergen delivered to naive ThC in lymph node via antigen presenting cell
  • ThC binds to antigen becoming primed in response to interleukins
  • ThC release IL-4 causing B cell to produce IgE specific to antigen
  • IgE binds to surface of mast cell

SUBSEQUENT EXPOSURE
- mast cell binds to antigen signalling mast cell to degranulate and release mediators generating allergic reaction

79
Q

CM of type 1 hypersensitivity

A
Bronchial constriction
Oedema
Vasodilation and increased permeability of blood vessels
Gastric acid production increases
Urticaria
Low blood pressure
80
Q

TX of type 1 hypersensitivity

A

Antihistamines
Clinical desensitisation
Adrenaline

81
Q

What is type 2 hypersensitivity

A

Antibody-mediated destruction of cells
Antibody binds to tissue specific antigen

Self-reactive B cell is activated and produces IgM and IgG
Antigen binds to cell producing antigen antibody complex

COMPLEMENT SYSTEM

  • small proteins work via enzymatic cascade to fight infection
  • protein attracts neutrophils causing degranulation

MEMBRANE ATTACK COMPLEX

  • insets into cell membrane allowing passage of fluid and molecules
  • causes cell lysis

IgE ANTIBODY BINDS TO CELL
- causes phagocytes to target cell

NKC

ANTIBODY-MEDIATED CELLULAR DYSFUNCTION
- block receptors on cell

82
Q

What is type 3 hypersensitivity

A

Mediated by immune complexes
Similar process to type 2 hypersensitivity but occurs with soluble antigens

Immune complex able to travel further in body and moves to basement layer of blood vessel

COMPLEMENT SYSTEM

  • small proteins work via enzymatic cascade to fight infection
  • protein attracts neutrophils causing degranulation

Neutrophil degranulares causing vasculitis and oedema

83
Q

What is type 4 hypersensitivity

A

T cell mediated
Delayed reactions

  • antigen taken to lymph node by APC
  • ThC recognised antigen and binds
  • APC releases IL-12 causing ThC to mature into effector cell
  • ThC release substances causing ThC to proliferate and attract macrophages which create more ThC
  • macrophages release proinflammatory cytokines causing leaky endothelial barriers allowing more immune cells into area causing inflammation
  • KTC directly destroy cell
  • cell presents antigen from inside cell
  • T cell recognises and binds to molecule
  • release perforin (perforate cell) and granzymes (cause apoptosis)
84
Q

Size of bacteria

A

0.5 to 5 um

85
Q

Shape of bacteria

A

COCCI
spherical cells occuring singularly, in pairs, clusters or chains

BACILLI
rod shaped cell with flagella for movement

SPIRILLA
twisted cell

VIBRIO
curved rod (comma)
86
Q

Structure of bacteria

A

Rigid cell wall
Single circular chromosome of DNA
Plasmids

87
Q

Purpose of plasmids

A

Carry non-essential information (eg resistance)

88
Q

Reproduction of bacteria

A

asexually through binary fission

89
Q

Bacteria are what kind of organism

A

Prokaryotic

90
Q

Size of virus

A

12 - 350 nm

91
Q

Shape of virus

A

Icosahedral (20 sides)
Helical
Bullet

92
Q

Structure of virus

A

Sphere of protein containing RNA/DNA

Essential components = nucleic acid, capsid, envelope

93
Q

Replication of virus

A

Replicate inside host cell

Use metabolic machinery of cell

94
Q

What are antibacterials

A
  • damage construction, structure, synthesis or function of cell wall
  • interfere with protein synthesis by inhibiting ribosomes
  • interfere with bacterial DNA
  • interfere with metabolic processes
95
Q

What are antivirals

A
  • work against viral life cycle
  • inhibit entry
  • inhibit synthesis
  • inhibit release
96
Q

What are antifungals

A
  • inhibit synthesis

- inhibit function of membrane

97
Q

What is antibiotic resistance

A

Developed resistance of bacteria by gaining genes that protect them from antibiotics

Genes arise through mutation or are acquired from other bacteria

98
Q

What is antiviral resistance

A

Developed resistance of viruses

Virus replication is prone to errors resulting in a large number of variants. As the virus replicates and mutations occur, the genome changes resulting in resistance.

99
Q

Causes of obesity

A

LIFESTYLE

  • poor diet
  • physical inactivity
  • stress
  • smoking
  • socioeconomic

GENETIC

  • 300 genes affect obesity
  • account for 30%

METABOLIC

  • increased cortisol
  • polycystic ovarian syndrome
  • hypothyroidism
100
Q

Opioid reward pathway

A

Mesolimbic dopamine neurons release dopamine in response to numerous stimuli

Drug abuse bypasses natural neurotransmitters and acts directly on mesolimbic pathways

Amygdala is involved with connections to both ends of mesocortical dopamine pathway. Connections from ventral segmental area to the cause it to develop changes to remember the rewards of drug abuse.

Amygdala connects to the nucleus accumbens (involved in memory) and is triggered by substance abuse stimuli.
Repeated exposure creates pathological learning, hijacks entire reward system and addiction develops.

101
Q

Outline alcohol metabolism

A

Metabolized in liver and stomach.

Alcohol is converted to acetaldehyde by alcohol dehydrogenase (slow)

Acetaldehyde is rapidly converted to acetic acid (byproduct NADH)

NADH buildup causes acidosis from lactic acid build-up and hypoglycemia from lack of glucose synthesis. It can also lead to weight gain, fatty liver, and heart attack.

Summary:
Enzyme catalyzes conversion of alcohol to acetaldehyde and hydrogen
H goes to make NADH, acetaldehyde loses another H. metabolized to acetate, released into blood stream,
The excess of NADH is thought to contribute to the liver damage that comes with excess alcohol.

102
Q

Effects of acute alcohol overdose

A

Vomiting
Coma
Pronounced hypotension
Respiratory depression

103
Q

Stages of ALD

A

Alcohol consumption
Fatty liver - steatosis
Alcoholic hepatitis - steatohepatitis
Alcohol cirrhosis

104
Q

Outline Fatty Liver/Steatosis

A

Large amounts of fat accumulate in hepatocytes (steatosis)

Liver enlarges and becomes yellow
Damage reversible once alcohol is discontinued

105
Q

Outline Alcoholic Hepatitis/Fibrosis

A

Often due to binge drinking
Inflammation and necrosis
Stimulates irreversible fibrosis

106
Q

Outline cirrhosis

A
Irreversible fibrosis of the liver 
Fat deposits - increased connective tissue
Loss of liver function
 - Loss of hepatocytes
 - Obstruction of biliary duct system

Cessation of alcohol reverses the fatty deposits but not the fibrosis or hepatocyte damage

107
Q

Symptoms of ALD

A
Tenderness/pain in Rt upper quadrant
Portal hypertension
Coagulation disturbance
Hepatic encephalopathy
Jaundice, pruritus 
Feminisation
Weight loss, anorexia
Weakness
Diarrhoea, nausea
Neurological issues
108
Q

DX of ALD

A

History
Questionnaires (AUDIT) and DSM-5 criteria
Symptoms
Liver ultrasound or biopsy

Bloods

  • liver enzymes (ALT, AST, γ-GT)s and bilirubin
  • serum albumin
  • prothrombin time
  • U & Es, FBC
109
Q

Symptoms of mild alcohol withdrawal

A
Anxiety
Agitation
Tremor
Nausea
Tachycardia
Hypertension
Disturbed sleep
Fever
110
Q

Symptoms of severe alcohol withdrawal

A

Vomiting
Hyperventilation
Extreme agitation

Disorientation
Confusion
Paranoia
Delirium tremens

111
Q

Types of Nicotine replacement therapy

A
Chewing gum 
Lozenges and sublingual tablets
Transdermal patches
Mouth spray 
Inhaler
112
Q

Complications of obesity

A

CARDIOVASCULAR

  • dyslipidaemia
  • coagulation issues
  • increased thrombus formation
  • atherosclerosis

RESPIRATORY

  • impaired respiratory function
  • increased sleep apnoea

CANCER
- increased risk of reproductive, digestive, kidney, gallbladder and colon cancer

GALLBLADDER AND LIVER

  • 3-4x greater risk of gallstones
  • steatohepatitis
  • osteoarthritis

MORTALITY
- 12x increase in the 25-35 year age group

113
Q

DX of obesity

A

BMI (kg/m^2)
Waist circumference
Body fat composition

114
Q

Calculation for BMI

A

kg/m^2

115
Q

Purpose of adipose cells

A

Produce cytokines that regulate:

  • food intake
  • lipid storage
  • metabolism
  • insulin sensitivity
  • female reproduction

Influence on

  • immune system
  • homeostasis
  • blood pressure
  • angiogenesis
116
Q

TX of obesity

A
Motivation and support
Behavioural modification
Dietary factors
Physical activity
Orlistat (inhibit pancreatic lipase)
Gastric Banding
Gastric bypass
Sleeve gastrectomy
117
Q

Stages of stress

A

ALARM
arousal of body defences
fight or flight

RESISTANCE AND ADAPTION
hormones exhance fight or flight mentality until the body has adapted

EXHAUSTION
progressive breakdown of compensatory mechanisms
onset of disease

118
Q

What happens in the alarm phase of a stress reaction

A

arousal of body defences

fight or flight

119
Q

What happens in the resistance and adaptation phase of a stress reaction

A

hormones exhance fight or flight mentality until the body has adapted

120
Q

What happens in the exhaustion phase of a stress reaction

A

progressive breakdown of compensatory mechanisms

onset of disease

121
Q

Response to stress

A
SNS
Hypothalamic pituitary adrenal axis
Increase CO and RR
Increase BP
Increase BGL and lipid levels
Altered immune response
122
Q

How does stress link to inflammation and chronic disease

A

Chronic stress causes increased proinflammatory cytokines

Common in:

  • CVD
  • metabolic syndrome
  • type two diabetes
  • cancer
  • aging
  • etc
123
Q

What is metabolic syndrome

A

Abdominal obesity + two of:

  • elevated triglycerides
  • low HDL cholesterol
  • hypertension
  • elevated plasma glucose
124
Q

TX of metabolic syndrome

A

Decreased risk of CHD

Prevent progression of type two diabetes

125
Q

What is cancer

A

the uncontrolled proliferation of cells

126
Q

Types of cancer

A
Carcinomas
Sarcomas
Ademoma
Adenocarcinoma
Terato-
127
Q

What is a Carcinomas

A

Cancer of the endothelial and epithelial tissue

128
Q

What is a Sarcomas

A

Cancer of the connective tissue

129
Q

What is a Ademoma

A

Cancer of the glandular or ductal epithelium

Benign

130
Q

What is a Adenocarcinoma

A

Carcinoma from glandular or ductal epithelium

131
Q

What is a Terato- cancer

A

Cancer of the germ cells

132
Q

Characteristics of benign cancer

A
Grow slowly
Well defines capsule
Non-invasive
Well differentiated
Low mitotic index
Does not metastasise
133
Q

Characteristics of malignant cancer

A
Grows rapidly
Not encapsulated
Invasive
Poorly differentiated
High mitotic index
Spreads (metastasises)
134
Q

Factors increasing the risk of cancer

A
DIET
high fat, low fibre, meat, aflotaxin, etc
links to cancers of the:
 - bowel
 - stomach
 - prostate
 - breast
 - pancreas 

OBESITY
links with BMI
increased fatty acid leading to hyperinsulinaemia and insulin resistance

ALCOHOL AND CIGARETTE USE
increases risk of developing cancer of the:
 - pharynx
 - larynx
 - oesophagus
 - liver
 - lungs
 - mouth

UV RADIATION
increases risk of basal and squamous cell carcinoma and melanoma
promotes skin inflammation and cytokine

OCCUPATIONAL HAZARD
increased risk of cancer of the:
 - respiratory tract
 - lungs
 - bladder
examples
 - asbestos
 - fumes
 - ionising radiation
 - air pollution
135
Q

What is autonomy

A

Cancer cells independent from normal cellular controls

Does not act like normal cells

136
Q

What is anaplasia

A

Loss of differentiation
Increased nucleus size due to rapid replication
Normal function of cell is lost

No defines shape, size or growth

137
Q

What is angiogenesis

A

Development of new blood vessels

Needed for cancer to enlarge

138
Q

What is metastasis

A

Spread of cancer to distant tissues and organs

139
Q

How do you stage tumours

A

Using TNM staging

Tumour, nodes, metastases

140
Q

Outline the tumour section of TNM staging

A

(size and location)

0 = organ free of cancer
1 = lesion less than 2cm
2 = lesion between 2-5cm
3 = skin or chest wall involves by invasion
141
Q

Outline the nodes section of TNM staging

A

(quantity involved)

0 = no axillary nodes involved
1 = mobile nodes involved
2 = fixed nodes involved
142
Q

Outline the metastases section of TNM staging

A

(extent)

0 = no metastases
1 = demonstatable metastases
2 = suspected metasteses
143
Q

What is a stage 1 cancer

A

Cancer confined to organ

144
Q

What is a stage 2 cancer

A

Cancer locally invasive

145
Q

What is a stage 3 cancer

A

Cancer spread to nearby structures

146
Q

What is a stage 4 cancer

A

Cancer metastasised to distant parts

147
Q

Risks associated with colorectal cancer

A

Older
Family history
Diet (increased fat, sugar, decreased vitamin A, C, K)

148
Q

CM of colorectal cancer

A
Bleeding
Altered bowel habits
Diarrhoea
Constipation
Urgency
Incomplete emptying
Pain
149
Q

DX of colorectal cancer

A

Digital rectal exam
Faecal blood test
Xray
Cononoscopy

150
Q

Risks associated with melanoma

A

Fair skin
Family history
Freckles and moles
3+ blistering sunburns before age 30

151
Q

CM of melanoma

A
Asymmetry
Irregular boarders
Different colours
Diameter change
Evolution
152
Q

DX of melanoma

A

Self exam
Biopsy
TNM staging

153
Q

TX of melanoma

A

Excision

154
Q

Risks associated with cervical cancer

A

Cigarette smoking

HPV

155
Q

CM of cervical cancer

A

Often none

156
Q

Risks associated with lung cancer

A

Smoking
Asbestos
Family history

157
Q

CM of lung cancer

A
Chronic cough
SOB
Wheezing
Haemoptysis
Pain
Hoarseness
Difficulty swallowing
Dyspnoea
Pleural effusion
Atelectasis
158
Q

DX of lung cancer

A
History
Examination
Xray
Bronchoscopy
Lung biopsy
Lymph node biopsy
CT
MRI
PET
159
Q

TX of lung cancer

A
Radiotherapy
Chemotherapy
Surgery
 - lobectomy
 - pneumonectomy
160
Q

CM of liver cancer

A
Weakness
Anorexia
Weight loss
Fatigue
Bloating
Abdomen pain
Ascites
Jaundice
Increase liver size
161
Q

DX of liver cancer

A

Ultrasound
CT
Biopsy
Symptoms

162
Q

TX of liver cancer

A

Hepatectomy
Chemotherapy
Radiotherapy
Transplant

163
Q

Risks associated with testicular cancer

A

Aged 15-35
Cryptorchidism
Genetics

164
Q

CM of testicular cancer

A

Enlargement of testes
No pain initially
Dull heaviness in groin
Abdominal, groin, or testicular pain

165
Q

DX of testicular cancer

A

Physical exa,
Ultrasound
CT
Cancer markers

166
Q

Staging of testicular cancer

A

1 - tumour confined to testes
2 - tumour spread to lymph nodes
3 - metastases to other organs

167
Q

TX of testicular cancer

A

Orchidectomy
Radiotherapy
Chemotherapy

168
Q

Risks associated with leukaemia

A
History
Genetics
Radiation
Smoking
Drugs that suppress bone marrow
Infections
169
Q

CM of leukaemia

A
Accumulation of blast cells
Bone marrow crowding and suppression
Anaemia
Decreased platelets
Decreased neutrophils
Bone erosion
Pain
Headaches
Lymph, spleen and liver enlargement
170
Q

DX of leukaemia

A

Blood and bone marrow exam

171
Q

TX of leukaemia

A

Chemotherapy

Bone marrow or stem cell transplant

172
Q

Outline antibody mediated immunity

A

B CELLS

1) Unspecialised B cell is activated by an antigen which is presented by direct exposure or via APC
2) B cell differentiate and proliferate to form clone cells
3) Most form plasma cells which secrete specific antibodies (immunoglobulins) capable of attaching to antigens
4) Others form memory cells stores in lymph nodes. They spread to body tissues to allow a faster response next time.

173
Q

Outline cell mediated immunity

A

T CELLS

1) Unspecialised T cell is sensitised by an antigen which is presented by on a macrophage or B cell
2) T cell differentiates and proliferates to form clone T cells
3) Most become killer or helper T cells and migrate to areas high in antigens
4) Some become memory T cells which initiate faster response next time
5) some become suppressor T cells which act when immune activity becomes excessive or infection is dealt with. Release substances inhibiting B and T cell activity

174
Q

Transmission of HIV

A
Blood, semen, vaginal secretions
Sexual contact
IV drug use
Blood products
Mother to infant
175
Q

Progression of HIV

A
  • Patient is infected with HIV
  • HIV binds to CD4 cell and injects RNA
  • Infected cell migrates to the lymph nodes and spleen
  • Initial spike in HIV replication as many immune cells
  • Acute HIV syndrome (3 weeks) causing flu-like symptoms
  • Immune response initiated (increase in antibodies) allowing for partial control of virus
  • Viral replication increases causing decrease in ThC

200-500 ThC = swollen lymph nodes, yeast infection
Less than 500 ThC = AIDs, fatigue, fever, decreased weight, diarrhea

176
Q

AIDs defining characteristics

A

Recurrent pneumonia
Pneumocystis pneumonia
Fungal infection
Tumours : kapasi sarcoma, primary lymphoma

177
Q

DX of HIV

A

ANTIBODY TEST
detect antibodies against HIV
only effective 3-17 weeks post infection

ANTIGEN ANTIBODY TEST
detect HIV and antibody

RNA/DNA TEST
detect viral RNA or copies of DNA

178
Q

Management of HIV

A
Baseline evaluation
ThC count
Prophylaxis and early treatment
Reverse transcriptase inhibitors
Protease inhibitors

Highly active anti-retrovirus treatment

  • slow HIV replication
  • help immune system recover
179
Q

Prevention of HIV

A

Largely education based

  • safe sex
  • clean needles
  • etc

PrEP = pre-exposure prophylaxis

180
Q

Types of antiretrovirals

A

Nucleoside analogue reverse transcriptase
Non nucleoside inhibitor
Protease inhibitor
Integrase inhibitor

181
Q

Effect of nucleoside analogue reverse transcriptase

A

Block transcription of viral RNA to DNA

When NRTIs are ceased, viral replication resumes

182
Q

Effect of non nucleoside inhibitor

A

Bind to reverse transcriptase, altering the enzyme and making it ineffective

183
Q

Effect of protease inhibitor

A

Inhibits HIV protease
HIV protease ‘trims’ proteins into the required sections
PI disrupts this and therefore the ability of HIV to replicate

184
Q

Effect of integrase inhibitor

A

Viral DNA is transported to nucleus and incorporates into host DNA by viral integrase
Integrase inhibitor blocks this process

185
Q

What are carcinogens

A

Substances which transform normal cells into tumours

186
Q

Causes of cancer

A

GENETICS

  • allow perforation
  • disable apoptosis
  • damage tumour suppressor genes

TELOMERES

  • protective cap on chromosome
  • become smaller with each replication
  • cancer repairs their telomeres (immortal)

ONCOGENES

  • mutant genes
  • non-mutant state = direct protein synthesis and cell growth
  • mutant state = promote cell proliferation and cancer

BACTERIAL

  • Helicobacter pylori
  • alters gastric epithelial cell cycle
  • mutates DNA
  • alters growth factors

VIRAL

  • alter cellular DNA
  • HPV
  • Hep B and C
187
Q

How does cancer escape the immune system

A

Lack tumour-specific antigens (not recognised as foreign)
Weakly immunogenic (poor immune response)
Genetically unstable (ineffective immune response)
Replicate quickly (immune system overwhelmed)
Secrete immunosuppressive molecules or enzymes
Surround self with collagen or fibrin (become invisible)
Shed their antigens (block antibodies and T cells)