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Year 2 > MISC: Notes > Flashcards

MISC: Notes Flashcards

1
Q

Define substance misuse

A
  1. Harmful use of any substance for non-medical purposes or effect
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2
Q

Name some illegal drug opiates

A
  1. HEROINE
  2. CODEINE
  3. TRAMADOL
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3
Q

Effects of illegal drug opiates

A

EUPHORIA

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4
Q

Effects of Depressants

A

Anxiolytic

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5
Q

Name some stimulant illegal drugs

A
  1. Amphetamines
  2. Cocaine
  3. Caffeine
  4. Crack
  5. Ecstacy
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6
Q

Effects of illegal drug stimulants

A

Increases alertness and alters mood

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7
Q

Effects of cannabis

A

Relaxation
Mild
Euphoria

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8
Q

Name two hallucinogens

A
  1. LSD

3. Magic mushrooms

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9
Q

Effects of hallucinogens

A
  1. Altered sensory perceptions
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10
Q

Name a illegal drug anaesthetic

A

KETAMINE

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11
Q

Effects of Ketamine

A

SEDATIVE

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12
Q

Harmful effects of drug misuse

A
  1. Mortality
  2. Morbidity
    - —–SOCIAL——-
  3. Crime
  4. Violence
  5. Criminal justice involvement
    - —-ECONOMIC—-
  6. Productivity
  7. Tax
    - ——PERSONAL—–
  8. Identity
  9. Stigma
  10. Relationships
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13
Q

What are the main theoretical models that lead to drug misuse

A
  1. Chronic recurrent illness
  2. Moral Model (Failure of morality)
  3. Socio-cultural model (health inequality)
  4. Behavioural model (A bad habit)
  5. Volitional Model (A failure of will)
  6. Genetic disorder
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14
Q

Define addiction

A
  1. A severe substance use disorder - involves compulsive use of a substance despite harmful consequences
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15
Q

Define psychological dependance

A

Feeling that life is impossible without drugs (fear, pain , shame)

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16
Q

Define physical dependance

A
  1. Body needs more and more of a drug for the same effect (tolerance) - withdrawal symptoms
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17
Q

What is dependence syndrome

A

3/6 or more in the past 12 months:

  1. Strong desire or compulsion to use
  2. Difficulties in controlling substance-taking behaviour
  3. Physiological withdrawal state when reduce use (or substitution to avoid withdrawal)
  4. Tolerance
  5. Progressive neglect of pleasures/interests, increased time spent using
  6. Persistent use despite evidence of harmful consequences
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18
Q

What is the Diagnostic and statistical manual or mental disorders (DSM-5)

A

Experience 2-3 (mild), 4-5 (moderate), 6+ (severe) in the past 12 months:

  1. Consuming more than originally planned
  2. Worrying about stopping failed efforts to control use
  3. Spending a large amount of time using substance
  4. Use results in failure to fulfil major role obligations
  5. Craving
  6. Continued use despite health problems caused
  7. Continued use despite negative relationship effects
  8. Repeated use in a dangerous situation (driving)
  9. Giving up or reducing activities
  10. Building up a tolerance to the alcohol or drug
  11. Withdrawal symptoms after stopping
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19
Q

Preventative factors for drug misuse

A
  1. Self control
  2. Parental minoring and support
  3. Positive relationships
  4. Neighbourhood resources
  5. Academic achievement
  6. School anti-drug policies
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20
Q

Risk factors for drug misuse

A
  1. Aggressive childhood behaviour
  2. Lack of parental support
  3. Poverty
  4. Drug experimentation
  5. Poor social skills
  6. Availability of drugs at school
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21
Q

Family risk factors for drug misuse

A
  1. Family substance use

2. Family conflict

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22
Q

Community risk factors for drug misuse

A
  1. Availability of drugs
  2. Community disorganisation
  3. Low neighbourhood attachment
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23
Q

School risk factors for drug misuse

A

Academic failure

Low school commitment

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24
Q

How is drug misuse managed

A
  1. Tailoring support to the drug they are addicted to
  2. GPs, harm recustion services, detox and recovery support (local services)
  3. Advice and counselling
  4. Community prescribing (substitution treatment, goal: stop patient using illicit drugs, enable a more stable life)
  5. DETOXIFICATION (relapse prevention and referral aftercare)
  6. Residential treatment
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25
Q

What advice will I give to drug misuser

A
  1. Support during subsitiution treatment
  2. Promote reduction in stimulant use
  3. Relapse prevention: planning strategies
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26
Q

How is opiate overdose treated

A

NALOXONE (opiate antagonist)

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27
Q

What is residential treatment of drug misuse

A
  1. For those who wish to attain/maintain abstinence
  2. Address underlying issues and learn coping mechanisms
  3. Work on finding employment
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28
Q

How long does residential treatment last

A

3-12 months

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29
Q

Formula for unit

A
  1. (Strength of drink x amount of liquid in ml) / 1000
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30
Q

What is considered binge drinking for women and men

A

Women > 6

Men > 8

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31
Q

What is the alcohol harm paradox

A
  1. Low SES (socio-economic groups) groups consume less alcohol than higher SES groups but these experience greater alcohol-related harm
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32
Q

Why is alcohol abuse more common these days

A

MORE AFFORDABLE and available

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33
Q

How does excess alcohol effect the CNS

A
  1. Peripheral neuritis (degeneration of the nervous system supplying the limbs)
  2. Marchiafava-Bignami disease
  3. Central pontine myelinolysis
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34
Q

Acute effects of excessive alcohol

A
  1. Accidents
  2. Respiratory depression
  3. Aspiration pneumonia
  4. Oesophagi’s/gastritis
  5. Mallory-weiss syndrome (gastric tears - haematamesis)
  6. Pancreatitis
  7. Cardiac arrhythmia
  8. Peripheral neuritis
  9. Myopathy
  10. Neurapraxia due to compression
  11. Hypoglycaemia
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35
Q

What is Marchiafava-Bignami disease

A
  1. CORPUS CALLOSUM demyelination and necrosis - atrophy

Clinical presentation:

  1. Consciousness
  2. Agression
  3. Seizures
  4. Hemiparesis
  5. Ataxia
  6. Apraxia
  7. Coma
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36
Q

Effects of alcohol withdrawal

A
  1. Activation syndrome
  2. Grand mal seizures
  3. Hallucination
  4. Delirium Tremens
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37
Q

What is activation syndrome

A

Tremulousness
Tachycardia
Agitation
High BP

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38
Q

What is Delirium tremens

A
  1. Tremors
  2. Agitation
  3. Confusion
  4. Sensitivity to light and sound
  5. SEIZURES
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39
Q

What is Fetal Alcohol Syndrome

A

RETARDATION of pre and post-natal growth

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40
Q

Clinical presentation of Fetal Alcohol Syndrome

A
  1. Craniofacial abnormalities
  2. Increase in the incidence of birthmarks and hernias
  3. Mental retardation, irritability, incoordination and hyperactivity
  4. Short palpebral fissure
  5. Epicanthic folds
  6. Thin upper lips
  7. Smooth philitrrum
  8. Microcephaly
  9. Upturned nose
  10. Hypoplastic jaw
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41
Q

Psychosocial effects of excessive alcohol consumption

A
  1. Relationships: Violence, Rape, depression
  2. Problems at work
  3. Criminality
  4. Social disintegration
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42
Q

How to reduce alcoholism

A
  1. Make alcohol less affordable
  2. Liscencing and import allowances
  3. Marketing (limit exposure)
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43
Q

Stereotypes of anorexic girls

A
  1. Female
  2. Underweight
  3. Young
  4. Manipulative
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44
Q

Define Anorexia Nervosa

A
  1. Restriction of energy intake relative to requirements leading to significantly low body weight in the context of age, sex, developmental trajectory and physical health (BMI < 17.5)
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45
Q

Clinical presentation of anorexia nervosa

A
  1. Fear of gaining weight or becoming fat

2. Visual perception in which one’s body weight or shape is experienced - denial of current low weight

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46
Q

Subtypes of anorexia nervosa

A
  1. Restricting

2. Binge-eating/purging

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47
Q

Define Bulimia Nervosa

A
  1. Eating in a discrete amount of time (in 2 hours)
  2. Sense a lack of control over eating during an episode

HAS PURGING PHASE

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48
Q

What is the purging phase

A

Recurrent inappropriate compensatory behaviour in order to prevent weight gain

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49
Q

What is binge-eating disorder

A
  1. Eating in a discrete period of time more than most people would eat during a smilier period
  2. Lack of control over eating during the episode
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50
Q

Characteristics of binge eating disorder

A
  1. Eating more rapidly than normal
  2. Eating until feeling uncomfortably full
  3. Eating large amounts of food when not feeling physically hungry
  4. Eating alone because embarrassed how much they re eating
  5. Feeling guilty after
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51
Q

What is OSFED

A

Other Specified Feeding and Eating Disorder - when patients do not meet full criteria for diagnosis

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52
Q

What is atypical anorexia nervosa

A

Despite weight loss, individual’s weight is in normal range

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53
Q

Name two OSFED syndromes

A
  1. Purging disorder

2. Night eating syndrome

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54
Q

What factors contribute to onset for Eating disorder

A
  1. Combination of low self-esteem and perfectionism leading to a need for control
  2. Triggers to using food as a means of self-control in this context

CORE MODEL

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55
Q

What stops eating disorders from getting better

A
  1. Enhances overvaluation of eating: shape and weight

2. Terror of losing control (body image disturbances re-appear)

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56
Q

Risk factors when looking at a patient with potential eating disorder

A
  1. Severe restriction of food/fluid
  2. Electrolyte imbalance
  3. Bone Deterioration
  4. Haematamesis from vomtiting
  5. Alcoholism
  6. Muscular weakness
  7. Breathing problems
  8. Ectopic beats, tachycardia, bradycardia and low BP
  9. Rapid weight loss
  10. Risky behaviours (suicide)
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57
Q

Treatment of eating disorders

A
  1. Doing therapies
  2. Diary keeping and weight monitoring

BULLIMIA: Cognitive Behaviour Therapy

ANOREXIA: Specialist Support Clinical Management or CBT

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58
Q

What is ‘nerd’ factor

A
  1. Structured treatments count beans (more evidence than should be)
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59
Q

What is the government’s alcohol strategy

A
  1. Minimum pricing
  2. Licensing
  3. Law
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60
Q

Risk factors for breast cancer

A
  1. AGE
  2. Lifestyle:
    Overweight
    Alcohol
    Smoking
    Occupational exposure (night shift work)
    Physical Inactivity
  3. Oestrogen exposure (HRT, Obesity, breastfeeding and menarche)
  4. Family History
  5. Genetics
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61
Q

What gene mutation increases chance of developing breast cancer

A
  1. BRCA1 + BRCA2
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62
Q

What condition is caused by BRCA1 + 2 specifically

A

Hereditary breast-ovarian cancer syndrome

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63
Q

What is hereditary breast-cancer syndrome

A

Higher risk of breast AND ovarian cancer in individuals

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64
Q

What conditions increase the risk of breast cancer

A
  1. Diabetes Mellitus

2 .SLE

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65
Q

Diagnosis of breast cancer

A
  1. BIOPSY
  2. FBC
  3. MAMMOGRAPHY (2 taken from the side and above breast ) >35
  4. Fine needle aspiration of lump (as it could be a cyst)
  5. Ultrasound + MRI <35
  6. History + Examination
    PUMB
    P - palpation
    U - Ultrasound
    M - Mammogram
    B - Biopsy
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66
Q

What colour would fluid collected from cysts and lump of a breast indicates breast cancer

A
  1. Blood fluid
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67
Q

Clinical presentation of breast cancer

A
  1. Lump that feels different to the rest of the tissue (detected by mammogram) or in axillary lymph nodes
  2. Thickening
  3. One breast is larger or smaller
  4. Change in nipple position or shape (becoming inverted)
  5. Dimpling
  6. Discharge
  7. Constant pain in part of the breast
  8. Paeu d’orange skin due to inflammation
  9. Paget’s disease of the breast
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68
Q

What is Paget’s disease of the breast

A

Skin changes resembling eczema (redness, discolouration and flaking)

Itchy, burns and pains later

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69
Q

What are phyllodes tumours

A

Tumours formed within the storm of the breast tissue

70
Q

What breast lump is common between the age of 15-30

A
  1. FIBROADENOMAS
71
Q

What are fibroadenomas

A

Benign breast tumours made of storm and epithelial tissues

72
Q

Role of breast lobules

A

Milk producing glands

73
Q

How can we detect fibroadenomas

A
  1. Painless

2. Firm or rubbery

74
Q

WHAT IS THE COMMON BREAST LUMP between 30 and 45

A

Fibrocystic change

75
Q

Common breast lump between 45-55

A

Breast cyst

76
Q

Post-menopausal breast lump

A

Cancer

77
Q

The prevalence of what breast lump decreases over time

A

Diffuse nodularity

78
Q

Four purposes of surgical interventions

A
  1. Cure
  2. Staging
  3. Minimise recurrence
  4. Information to tailor treatment
79
Q

Surgical intervention for breast cancer

A
  1. Selective Aillary surgery to treat lymphoedema
80
Q

Benefit of selective axillary surgery

A
  1. Staging accuracy
  2. Sentinel Node Biopsy
  3. Breast conservation surgery
  4. Therapeutic mammoplasty
  5. Local perforator flaps
  6. Prosthesis
  7. Risk reducing surgery
81
Q

Con of selective axillary surgery

A
  1. No survival benefit of clearance
82
Q

Where is the sentinel node located

A

Node on upper outer part of breast

83
Q

How does cancer spread in the lymph nodes

A
  1. Start as isolated tumour cells
  2. Form micro metastases
  3. Form macro metastases
84
Q

What size are lymph tumours that are micrometastatic

A

0.2 mm

85
Q

What size are lymph tumours that are macro static

A

2.0mm (these need clearance or can erupt the lymphatics)

86
Q

What is breast conservation surgery

A

Alternative to mastectomy:

Limits cosmetic damage caused by surgery

87
Q

Requirements needed for breast conservation surgery

A
  1. CLEAR MARGINS

2. Breast radiotherapy

88
Q

How do we localise and impalpable cancer

A
  1. Wires inserted into the breast

2. Iodine-125

89
Q

What is therapeutic mammoplasty

A
  1. Operation to remove cancer and reshape breast to leave normal breast shape
90
Q

What is local perforator flaps

A
  1. Subcutaneous fat or skin is remove from distant part of the body to reconstruct the excised part (Make boobs look a bit like moobs)
91
Q

What two types of breast reconstruction do we have

A

IMMEDIATE (at time of mastectomy)

DELAYED

92
Q

Outline the types of breast reconstruction

A
  1. Implant added
  • —-AUTOLOGOUS—–
    2. Pedicled flap (from abdo or lat areas - contains all layers of the skin including subcutaneous tissue and keeps all blood vessels intact)
    3. Free flap (Creating a vascularised flap of tissue - has re-attached blood supply - and adding it to the breast to increase volume) - Latissimus dorsi, abdo or gluteus maximus)
93
Q

When is surgery contraindicated

A

Locally advanced tumours or inflammation has occurred in the breast

94
Q

How is male breast cancer treated

A
  1. Mastectomy + Radiotherapy
95
Q

T assessment in breast cancer

A

T1 - Size < 2
T2 - Size 2-5
T3 - >5
T4 - Tumour extends to skin or chest wall

96
Q

N assessment in breast cancer

A

N0 - No lymph node metastasis
N1 - Metastasis to ipsilateral, moveable and axillary Lns
N2 - Metastasis to ipsilateral fixed axillary
N3 - Metastasis to infra claviclular and supraclavicular

97
Q

What is adjuvant therapy of early breast cancer

A
  1. Prevent or delay the subsequent appearance of metastatic disease
  2. Eradicate unapparent micromeastases which are thought to account for distant treatment failure following local treatment alone
98
Q

What is neo-adjuvant therapy of early breast cancer

A
  1. To downside a breast tumour to make breast conserving surgery possible
  2. Early systemic therapy in high risk patients
99
Q

What treatments are used for early breast cancer

A
  1. Radiotherapy
  2. Endocrine treatments
  3. Chemotherapy
  4. HER2 targeted treatments
  5. Novel targeted treatments
100
Q

When is radiotherapy done for breast cancer

A
  1. Lumpectomy

2. Post-mastectomy

101
Q

What treatment is given for early breast cancer

A
  1. Oncotype DX
  2. Oestrogen receptor
  3. Herceptin
102
Q

What is Oncotype DX

A

Predicts how likely cancer will come back following surgery

103
Q

What is the role of HER2

A

controls cell growth and repair

104
Q

Why is Herceptin given

A

It reduces the amount of HER2 in cancer cells topping them from growing

105
Q

Four aspects on deciding what early breast cancer patients need chemotherapy

A
  1. Biological consideration (HER2, Grade, genomics)
  2. Anatomical consideration (Node and size)
  3. Co-morbidity
  4. Patient Choice
106
Q

Chemotherapy treatment for breast cancer

A
  1. ANtracyclines (cause DNA crosslinks preventing replication)
  2. Taxens (prevent microtubule formation so cells can’t divide)
107
Q

Name two antracyclines

A

Doxorubicin

Epirubicin

108
Q

Name two Tameness

A

Docetaxel

Paclitaxel

109
Q

When is endocrine therapy given to breast cancer patients

A
  1. Those who have been taking tamoxifen for 2 - 5 years

2. Postmenopausal women with oestrogen-receptor positive invasive breast cancer

110
Q

What is endocrine therapy

A

Aromatase inhibitor

111
Q

What is aromatase inhibitor

A
  1. Catalyses process of oestrogen synthesis (blocks oestrogen production)
112
Q

What is Tamoxifen

A

SELETIVE OESTROGEN RECEPTOR MODULUATORY (blocks growth of cancer cells)

113
Q

How does Herceptin cause toxicity

A
  1. Inhibits HER2 cell survival pathway
  2. Congestive heart failure
  3. Endothelial dysfunction (increased activation of oxygen species and NO inhibition so impaired blood flow to myocytes)

HER2 increases NO and reduces effects of oxygen species

114
Q

Who needs radiotherapy after mastectomy

A
  1. > 5cm
  2. Positive resection margin
  3. Skin involvement
  4. 1 or more positive nodes
115
Q

Side-effects of radiotherapy in breast cancer

A
  1. Rib fracture
  2. Pain and skin changes
  3. Fatigue
  4. Lymphedema
116
Q

Define advanced breast cancer

A
  1. Has spread locally to the extent of inoperable (METASTATIC)

Non-curable

117
Q

How is advanced breast cancer diagnosed

A
  1. XRAY
  2. CT
  3. Bone scan

Assess ER and HER2 if still not clear

118
Q

Common sites of breast cancer metastases

A
  1. Bone
  2. Lymph nodes
  3. Liver
  4. Lung
  5. Brain
119
Q

What is given is ER positive breast cancer

A
  1. Aromatase inhibitor
  2. Tamoxifen
  3. CDK4/6 inhibitors
120
Q

ER weak chemotherapy treatment

A

First: Anthracyclines
Second: Taxene or carboplatin
Third: Capecitabine/Vinorelbine
Fourth: Eribulin

121
Q

Treatment for HER@+ breast cancer

A

HER2 Targeting therapy
First: Herceptin + pertuzumab with docetaxol
Second: TDM1 (perception bound to a chemotherapy agent)
Third: Herceptin + lapatinib

122
Q

Supportive therapy for advanced breast cancer

A
  1. Radiotherapy (stop bone, brain and skin metastases)
  2. Surgery (Bowel obstruction, brain metastases, fractures and RFA)
  3. Nursing (support)
123
Q

Radiotherapy for brain metastases

A

STEREOTACTIC

124
Q

NHS support for breast cancer patients

A
  1. Macmillan nurses
125
Q

Role of Key worker

A

Provide support throughout patient journey

126
Q

What size things does a key worker do for a breast cancer patient

A
  1. Empower them (information on treatments and prognosis)
  2. Connecting (build up rapport)
  3. Value patient’s unique charcaertistics
  4. Finding meaning - helping patient make sense of what is happening
  5. Preserving integrity
  6. Doing for (sorting out their benefits)
127
Q

Effects of chemotherapy treatment

A
  1. Infertility
  2. Altered body image
  3. Premature menopause
128
Q

What are breast cysts

A
  1. Palpable, fluid-filled rounded lumps not fixed to surrounding tissue
129
Q

How is breast cyst diagnosed

A

Aspiration (treated with aspiration)

130
Q

What are intrasductal papillomas

A

Benign, warty lesions behind the areola

131
Q

Chemotherapy in Breast Cancer

A
  1. Epirubicin

2. CMF (CYCLOPHOSPHAMIDE + METHOTREXATE + FLUOROURACIL)

132
Q

What is the name of the aromatase inhibitor given

A

ORAL ANASTROZOLE

133
Q

How is premenopausal and ER positive treated

A

ORAL GOSERELIN (GnRH analogues)

Ovarian ablation by surgery and radiotherapy (stops oestrogen synthesis)

134
Q

How is Radiotherapy to bony lesions treated

A

ORAL ALENDRONATE

135
Q

How is breast cancer prevented

A
  1. Promote awareness

2. Screening (2-view mammography) every 3 years

136
Q

Define lymphoedema

A
  1. Chronic non-pitting oedema due to lymphatic insufficiency
137
Q

What part of the body is affected by lymphoedema

A

Legs (they become huge)

138
Q

What causes primary lymphoedema

A

Milord’s disease

139
Q

What causes secondary lymphedema

A 
Filarial infections (worms that infect lymphatic system stopping drainage)
Malignancy 
Trauma
Radiotherapy 
Surgery
140
Q

How is lymphedema treated

A
  1. Compression stocking

2. Physical massage

141
Q

How is Filariasis treated

A

ORAL DIETHYLCARBAMAZINE

142
Q

How is recurrent cellulitis treated (worsens the lymph vessel damage)

A

ORAL PHENOXYMETHYLPENICILLIN

143
Q

Clinical presentation of CO

A
  1. Mistaken for viral
  2. Hypoxia but no cyanosis
  3. Vomiting, increased pulse and tachypnoea
  4. Headache, coma, convulsions and cardiac arrest
  5. Metabolic acidosis and hypertonia
144
Q

How is CO diagnosed

A
  1. O2 sats normal

2. ABG (need to look at saturated oxygen haemoglobin and COhb)

145
Q

How do we diagnose CO form ABG

A
  1. Venous COhb > 3% in non smokers are >10 in smokers

Normal: <5%

146
Q

How is CO treated

A
  1. Remove from CO source
  2. Give 100% O2 until COhb <10%
  3. Hyperbaric O2 treatment hastens CO elimination
  4. IV MANNITOL to reduce ICP
147
Q

How are withdrawal symptoms of opioids treated

A

METHADONE

148
Q

Clinical presentation of opiate overdose

A
  1. Pinpoint pupils
  2. Reduced resp rate
  3. Coma
  4. Hypothermia, hypoglycaemia and convulsions
149
Q

How is opiate overdose treated

A
  1. IV NALOXONE until breathing is adequate
150
Q

What insecticide commonly cause poisoning

A

ORGANOPHOSPHORUS insecticides

151
Q

How do OP insecticides cause poisoning

A

Inhibit ACh binding so they accumulate at peripheral cholinergic nerve endings and central

152
Q

Clinical presentation of OP insecticide poisoning

A 
SLUD
Salivation
Lacrimation 
Urination 
Diarrhoea

Anxiety and restless ness

Abdo colics
Chest tightness
Sweating
Small pupils, coma, resp distress and bradycardia

153
Q

How is Op insecticide poisoning diagnosed

A

Measure erythrocyte ACh activity

154
Q

How is OP insecticide poisoning treated

A
  1. Wear gloves and remove soiled clothes and wash skin
  2. IV ATROPINE every 10 mins until skin is dry, pulse > 70 and pupils dilated
  3. IV PRALIDOXIME to stop inhibition of ACh
155
Q

How does cocaine overdose damage the body

A
  1. Blocks dopamine reuptake
  2. Blocks noradrenaline uptake - tachycardia
  3. Blocks serotonin reuptake - hallucinations
156
Q

Clinical presentation of cocaine overdose

A
  1. Agitation
  2. Tachycardia
  3. Hypertension
  4. Sweating
  5. Hallucinations
  6. Convulsions
  7. Metabolic acidosis
  8. Hyperthermia
  9. Rhabdomyolysis
  10. Dissection of aorta, myocarditis, MI, dilated cardiomyopathy
157
Q

Treatment of cocaine overdose

A
  1. IV DIAZEPAM to control agitation
  2. IV GLYCERYL TRINITATE to lower BP
  3. VERAPAMIL

Beta-adrenoceptors contraindicated as they worsen hypertension

158
Q

What is amyloidosis

A
  1. Proteins are at risk of misfiling
  2. Causes proteolysis
  3. Proteins do not dissolve during proteolysis causing fragments to aggregate - oligomers
  4. Hydrophobic beta-pleated sheets not dissolved
  5. Oligomers aggregate together an make amyloid fibrils
159
Q

Clinical presentation of amyloidosis

A 
HEART and KIDNEY most commonly effected
1. Nephrotic syndrome
2. Proteinuria
3. Diastolic or systolic HF
4. EKG changes  (atrioventricular block or sinus node dysfunction)
5. Orthostatic hypotension 
------- LIVER and GI------
Raised AST and ALT
Raised alkaline phosphatase
Hepatomegaly 
Deposits on tips of intestinal villi causing diarrhoea

——–EYES—–
Racoon eyes due to deposition in blood vessels and reduced activity of factor X

———ENDO—
Enlarged tongue
Hypothyroidism

160
Q

How is amyloidosis diagnosed

A
  1. Biopsy of tissue with CONGO RED stain + polarised light = green
  2. Type of amyloid protein via protein electrophoresis
161
Q

Two types of amyloidosis

A

AL - common

AA

162
Q

How is amyloidosis treated

A
  1. HIGH DOSE MELPHALAN (chemotherapy) and DEXAMETHASONE
163
Q

Risk factors for erectile dysfunction

A
  1. Lack of exercise
  2. Obesity
  3. Smoking
  4. Hypercholesterolaemia
  5. Metabolic syndrome
164
Q

Clinical presentation of erectile dysfunction

A
  1. Pyronie’s disease (fibrous plaque in pens causing bent erection)
  2. Hypogonadism
  3. Prostatic enlargement
  4. GP and HR
165
Q

What conditions can cause erectile dysfunction

A
  1. Diabetes Mellitus
  2. MI
  3. Hypertension
  4. Renal Failure
  5. Trauma
  6. Prostatectomy
166
Q

How is erectile dysfunction diagnosed

A
  1. Fasting glucose
  2. Lipid profile
  3. Morning testosterone (if low, check FSH, LH and prolactin)
167
Q

Treatment of erectile dysfunction

A
  1. PDE5 inhibitors : Sildenafil
    Second: Alprostadil intracavernous injection or intraurethral
    Tertiary: Vacuum constriction devices (passive engorgement)
168
Q

Define priapism

A
  1. lasts 4 hours
169
Q

Why does priapism have to be corrected

A

Causes ischaemia and damage

170
Q

Treatment for priapism

A
  1. Aspirate with 19 gauge needle

2. Inject phenylphrenine

Year 2 (155 decks)

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