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Phase 2a > Misc > Flashcards

Misc Flashcards

1
Q

What is amyloidosis?

A

group of conditions with extracellular deposition amyloid, can be localised or systemic leading to organ failure and death

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2
Q

How is amyloid formed?

A

from abnormally folded proteins that collect together and don’t break down as easily as normal proteins, causing a build up

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3
Q

How common is amyloidosis?

A

rare, only 600 cases per year in UK, mainly older people

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4
Q

Symptoms of amyloidosis?

A 
depend on which organs are affected:
kidneys - kidney failure, oedema, tiredness, weakness, loss of appetite
heart - heart failure, sob, oedema
bone marrow - multiple myeloma
foamy urine
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5
Q

Diagnosis of amyloidosis?

A

Congo red staining on biopsy of affected tissues (rectal biopsy if systemic), light chain assay, amyloid deposits stain red and show green fluorescence in polarized light, scintigraphy with 123I-labelled serum amyloid component, the protein coats amyloid deposits in your body highlighting the areas most affected

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6
Q

What is the most common form of amyloidosis and how does it occur?

A

AL - from misfolded monoclonal Ig light chains so plasma cells are producing too many defective light chain proteins

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7
Q

Where does AL most commonly affect?

A

kindeys, heart, liver, Gi tract, nervous system

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8
Q

What causes AA (secondary amyloidosis)?

A

increased levels of circulating serum amyloid A protein as a response to chronic infection and inflammation

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9
Q

Where does AA usually affect?

A

kidneys and liver

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10
Q

What causes ATTR?

A

amyloid originates from abnormal transthyretin protein in the liver (acquired or autosomal dominant)

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11
Q

Where does ATTR most commonly affect?

A

nervous system, heart and kidneys

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12
Q

Where does senile systemic amyloidosis result from?

A

TTR amyloid building up in the hearts of the elderly (could be caused by genetic or age)

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13
Q

What is localised amyloidosis made up of?

A

light chain proteins, but the plasma cell are in the affected tissue not the bone marrow unlike in AL

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14
Q

How does AL present?

A

cardiac failure, nephrotic syndrome, carpal tunnel syndrome, macroglossia

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15
Q

What disease is AL associated with?

A

myeloma, Waldernstroms macroglobulinaemia, non Hodgkin’s lymphoma

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16
Q

How does ATTR present?

A

neuropathy and cardiomyopathy

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17
Q

Treatment of AL?

A

prevent further light chain production, treat organ failure, diuretics, medications, chemo to damage abnormal bone marrow cells, inhibit production of abnormal proteins

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18
Q

Treatment of ATTR?

A

liver transplant

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19
Q

How does AA present?

A

proteinuria and hepatosplenomegaly (treat underlying cause)

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20
Q

Prognosis of amyloidosis?

A

1-2 year survival

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21
Q

What are breast lobules?

A

milk producing glands

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22
Q

What are breasts made up of?

A

lobules and ducts, surrounding by glandular, fibrous supporting tissue and fatty tissue

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23
Q

Where do fibro adenomas develop form?

A

a lobule and then the glandular tissue and ducts grow over the lobule and form a solid lump

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24
Q

How cancerous are fibro adenomas?

A

They are benign and don’t increase the risk of developing breast cancer

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25
Q

How do fibro adenomas feel?

A

solid, smooth, rubbery lump which moves easily under the skin, usually painless but can be tender, and are normally 1-3cm but can be giant if 5cm, can have more than one (they can change size and disappear or get bigger during pregnancy and in teenage years)

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26
Q

Who is most likely to acquire a fibro adenoma?

A

most in young women due to increased sensitivity to oestrogen

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27
Q

What is the triple breast examination?

A

breast examination, mammogram and fine needle aspiration/core biopsy

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28
Q

Who is more likely to have an US than a mammogram?

A

if you are under 40 as women’s breast tissue can be dense making the x ray less clear so harder to see breast conditions

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29
Q

Treatment of fibro adenoma?

A

vacuum assisted excision biopsy if it becomes bigger or painful, can leave a slight dent in the breast

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30
Q

What is cystic disease?

A

a benign condition where women have painful breast lumps

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31
Q

In who does cystic disease occur?

A

in >50% of those with fibro adenoma, leading to fibrocystic disease - leads to harder detection of breast cancer

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32
Q

What causes fibrocystic disease?

A

a higher sensitivity to hormones from the ovaries

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33
Q

Symptoms of fibrocystic disease?

A

swelling of breast lobules, tenderness and pain, thickening of fibrous tissue, lumps that can chnage size and are moveable, can be in one or both breasts, symptoms worse before period and resolve after menopause, pain under arms, green or dark brown nipple discharge

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34
Q

Treatment of fibrocytsic disease?

A

analgesics, supportive well fitting bra, warm and cold compresses, limit caffeine and fat intake

if severe pain - contraceptive pill to control hormones, FNA to remove fluid, surgical removal/lumpectomy

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35
Q

Breast cancer red flags?

A

new of different lumps, redness or puckering of the breast skin, discharge from nipple, indentation or flattening of nipple, size shape, armpit, dimpling, rash

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36
Q

What is intra ductal papilloma?

A

benign breast condition in women over 40 that develops naturally as the breast ages and changes

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37
Q

Symptoms of intra ductal papilloma?

A

wart like lump (in a duct, usually close to the nipple), discharge from nipple, not painful but discomfort, can be in one or both breasts

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38
Q

How cancerous are intra ductal papilloma?

A

they are benign and don’t increase cancer risk, unless they contain abnormal cells or there are multiple papillomas, there is a slight increased risk

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39
Q

Treatment of intra ductal papilloma?

A

vacuum excision, microdochetomy, total duct excision

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40
Q

Limitations of screening?

A

can give false protection, false positives and negatives, some cancers do not fit the screening criteria, cost to society

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41
Q

Principles of screening?

A

must be important disease, recognizable at an early stage, fully understood, have a suitable test which is accepted by society, findings should be continuous, an accepted treatment, facilities and treatment available, an agreed policy on who to treat, economically balanced, treatment for the early stage

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42
Q

Breast cancer investigations?

A

CXR, bone scan, liver USS, CT, MRI, PET CT, LFTs, Ca2+

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43
Q

Stages of breast cancer?

A

1 - confined to breast and mobile
2 - confined to breast, mobile but lymph node involvement
3 - fixed to muscle, lymph nodes matter, maybe fixed, skin involvement, larger than tumour
4 - complete fixation of tumour to chest wall, distant metastases

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44
Q

Sensitivity equation?

A

positive/all with disease

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45
Q

Specificity equation?

A

negative/all without disease

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46
Q

PPV equation?

A

positive with disease/all positive

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47
Q

How much more common is breast cancer in women than men?

A

200x

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48
Q

Risk factors for breast cancer?

A

alcohol, overweight, heavy smoking, HRT, contraceptive pill, family history, over expression of the HER2 gene or BRCA gene

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49
Q

Who is screened in breast cancer?

A

women every 3 years, 47-73 y/o for a mammo graph screening

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50
Q

Management of breast cancer?

A

surgery (mastectomy, lumpectomy, quadrentectomy), breast reconstruction, chemo, radiotherapy, ER blocker (tamoxifen), aromatase inhbitor (anastrozole), GnRH analogues (goserelin)

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51
Q

Prognosis of breast cancer?

A

96% 1 yr, 87% 5 yr, 78% 10 yr

5th highest survival rate of cancer or 10 years

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52
Q

What is the Nottingham Prognostic Index for breast cancer?

A

NPI = 0.2 x tumour size +histological grade + nodal status

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53
Q

What is lymph-edema?

A

swelling in one of more extremities caused by impaired flow of the lymphatic system so they are unable to carry excess lymph fluid away from tissues

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54
Q

Function of the lymph system?

A

collect excess lymph fluid with proteins, lipids and waste products form the tissues and then filter the waste products and contain lymphocytes and excess lymph fluid in the lymph vessels to return to the blood stream

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55
Q

Symptoms of lymph-edema?

A

mild - heaviness, tingling, tightness, warmth, shooting pains in affected extremity, swelling, decreased ability to feel and see veins and tendons, tightness of jewellery, redness of skin, asymmetrical appearance of extremities, tightness and reduced flexibility in joints, puffiness of skin

severe - more pronounced swelling, and other symptoms

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56
Q

Different types of lymph-edema?

A

Milroy disease - congenital anatomical abnormality of lymph vessel
lymph-edema praecox - most common primary lymph-edema occurring during puberty
Meige disease orlymph-edema tarda - >35yrs
secondary - blocked lymph system

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57
Q

Causes of lymph-edema?

A

breast cancer treatment with radiation, trauma, burns, radiation, infections, compression of lymph nodes from tumour, surgery, FILARIASIS

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58
Q

What is filariasis?

A

the most common cause of lymph-edema, with infestation of lymph codes with Wuchereria bancrofti which is spread by mosquitos leading to swelling, difficulty in fight infections and can cause permanent disability - common in the tropics

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59
Q

Investigations of lymph-edema?

A

CT/MRI to define lymph node architecture and identify tumors and other abnormalities
lymphoscintigraphy injects a tracer dye into lymph vessels and observing the flow using imaging technologies
Doppler US are sound wave tests to evaluate blood flow to identify blood clots which could be causing limb swellign

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60
Q

How can radiation cause lymph-edema?

A

causing scarring and inflammation of the lymph nodes

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61
Q

What us a lymphangiosarcoma?

A

a reddish lump on the skin which is aggressive and spreads rapidly which can increase lymph-edema risk

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62
Q

Treatment of lymphangiosarcoma?

A

amputation the affected limb, poor prognosis

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63
Q

Complications of lymph-edema?

A

cellulitis, lymphangitis, DVT, cosmetic issues, impaired functioning in affected area

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64
Q

How to reduce risk of lymph-edema?

A

keep affected limb raised above heart, avoid tight jewelry and clothes, do not heat it, avoid heavy lifting stay hydrated, skin hygiene, avoid insect bites and sunburns

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65
Q

Treatment of lymph-edema?

A

preventative measures, compression treatments, support groups, elastic sleeves and stockings, bandages, pneumatic compression devices, manual compression, exercises that light contract and stimulate the affected limb, surgical treatments to remove excess fluid, antibiotics for infection

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66
Q

What causes carbon monoxide and how does this cause poisonin?

A

incomplete combustion of carbon or carbon containing compounds e.g. tobacco smoke in an inadequate supply of oxygen which then competes with oxygen to form carboxyhaemoglobin instead of oxyhaemoglobin due to carbon monoxides high affinity for Hb and myoglobin

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67
Q

How does methylene chloride cause poisoning?

A

it is readily absorbed and metabolized to CO by the liver, leading to poisoning

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68
Q

How common is CO poisoning?

A

kills 50 people and injuries 200 people per year in UK

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69
Q

Symptoms of CO poisoning?

A

headache at COHb 10%, mental impairment, convulsions, cardiac arrest, tachypnoea, pink skin and coma at >50%

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70
Q

Investigations of CO poisoning?

A

direct spectrophotometric measurement of HbCO and ABG in blood gas analyser, HbCO oximeter, low O2 sat, ECG shows myocaridal ischemia or infarction, creatinine and troponin levels indicate myocardial damage, MRI, CXR, neuropsychological testing

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71
Q

Management of CO poisoning?

A

remove source, ABC, give O2, mannitol 1g/kg IV for cerebral ischemia, monitor ECG, neuropsychiatric testing, contact local health protection unit for enviromental testing and management

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72
Q

Prognosis of CO poisoning?

A

can recover spontaneously , no long term treatment

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73
Q

Symptoms of TCA overdose?

A

tachycardia, hypotension, fixed dilated pupils, convulsions, urinary retention, arrhythmia, decreased conscious level

74
Q

Management of TCA overdose?

A

diazepam for convulsions, IV sodium bicarbonate for tachycardia

75
Q

Symptoms of benzodiazepine overdose?

A

drowsiness, ataxia, dysarthria, respiratory depression, coma

76
Q

Treatment of benzodiazepine overdose?

A

IV flumazenil (CI for TCA for epilepsy)

77
Q

Symptoms of phenothiazine overdose?

A

hypotension, hypothermia, arrhythmia, respiratory depression, coma, convulsions, dystonic reactions

78
Q

Treatment of phenothiazine overdose?

A

symptomatic treatment e.g. diazepam for convulsions, benzatropine for dystonic reactions

79
Q

Symptoms of NSAID overdose?

A

coma, convulsions, metabolic acidosis, renal failure

80
Q

Treatment of NSAID overdose?

A

symptomatic and supportive

81
Q

Symptoms of BB overdose?

A

bradycarida, hypotension, come, convulsion, hypoglycaemia

82
Q

Treatment of BB overdose?

A

IV glucagon, inotropic action on heart, atropine IV

83
Q

What is the toxicity risk for severe liver damage based on paracetamol (acetaminophen) dose?

A

250mg/kg likely
>12g fatal

serious adverse affects occur at around 150mg/kg in adults

84
Q

paracetamol metabolism?

A

absorbed in stomach and small intestine, reaching peak plasma concentration in one house, then inactivated in the liver by glucuronide or sulphate and then excreted

85
Q

What happens in paracetamol overdose?

A

liver conjugations becomes inundated so paracetamol must be metabolised by an alternative pathway which forms NAPQI which must be inactivated by gluthatione to prevent harm

86
Q

What happens in paracetamol overdose if gluthatione stores are depleted to

A

NAPQI binds with sulfhydryl groups on liver cell membranes causing necrosis and to liver and kidney tubules

87
Q

What can cause depleted gluthatione stores?

A

induction of the P450 system through drugs (rifampicin, phenobarbital, phenytoin, carbamazepine), alcohol, genetic variation, HIV, malnutrition, under 5 years

88
Q

What is the most common form of poisoning in the UK?

A

paracetamol

89
Q

Symptoms of paracetamol poisoning?

A

asymptomatic, nausea, vomiting, hepatic necrosis with associated symptoms, encephalopathy, oliguria, hypoglucaemia, lactic acidosis

90
Q

Investigations of paracetamol poisoning?

A

find out dosages, formulation, concomitant tablets, time of overdose, suicide risk, any alcohol taken

paracetamol levels 4 hours post igestion, U+Es, creatinine to look for renal failure, normal LFTs but increased ALTs, capillary blood glucose for hypoglycaemia, PT, ABG for acidosis

91
Q

Management of paracetamol overdose?

A

IV acetylecysteine in 5% dextrose as a glutathione precursor and reduce the adverse affects (stop if anaphylactic reactions occur), methionine is alternative, gstric lavage, transplant, liver unit

if longer after overdose, toxbase

92
Q

When should you discontinue treatment for paracetamol overdose?

A

bass on nomogram

93
Q

When should you have a liver transplant for paracetamol induced acute liver failure?

A

arterial pH 3 after adequate fluid resuscitations

OR if all 3 occur in 24hrs

creatinine >300umol/L
PT>100 seconds
grade III/IV encephalopathy

94
Q

Prognosis of paracetamol overdose?

A
95
Q

What dose causes aspirin poisoning?

A

125mg/kg is mild toxitty, 250mg/kg is moderate toxicity and 500mg/kg is severe and potentially fatal

96
Q

How does aspirin cause poisoning?

A

uncoupling of oxidative phosphorylation leading to anaerobic metabolism and lactate and heat production

97
Q

Symptoms of aspirin poisoning?

A

mild - nausea, vomiting, tinitus
moderate - hyperventilation and confusion
severe - hallucinations, seizures, coma, cerebral oedema, pulmonary oedema

nausea, vomiting, tinnitus, lethargy, dizziness, dehydration, hyperthermia, hyperventilation, respiratory alkalosis, metabolic acidosis, seizures, fever, confusion, hallucinations, sweating, rapid pulse

98
Q

Investigations for salicylate/aspirin poisoning?

A

plasma salicylate concentrations 2-4 hours post ingestion as it takes this long for concentration to peak, then another 2 hours post measurement and repeated every 3 hours until concentrations are falling

renal function and electrolyes, FBC, coagulation studies, urinary pH, blood glucose, plasma potassium every 3 hours, respiratory alkalosis, metabolic acidosis, high pH, CXR

99
Q

Acid base staging of salicylate poisoning?

A

1 = pH>7.4, urine pH>6, resp alk, increased urine HCO3

2 = pH>7.4, urine pH7.4, urine pH

100
Q

Management of salicylate poisoning?

A

oral activated charcoal if >125mg/kg 500mg/kg

101
Q

What are organophosphate pesticides and how to they poison?

A

odourless liquids in sprays that inhibits ACh esterase so ACh accumulated at nerve synapses and neuro muscular junctions, stimulating muscuranic and nicotinic receptors and the CNS

102
Q

Symptoms of pesticide poisoning?

A

pinpoint pupils, conjunctival injection, pain and blurred vision, headache, nausea, mild muscle weakness, localised muscle twitching, dizziness, disorientation, agitation, SOB, sweating, flushing, seizures, drooling, bronchospasm, twitching, coma

103
Q

Investigations of pesticide poisoning?

A

decontaminate patient, obtain samples, plasma cholinesterase level to screen for exposure

RBC cholinesterase correlate with severity and prognosis

mixed cholinesterase determines if sufficient pralidoxime has been given

104
Q

Management of pesticide poisoning?

A

wear gloves, removed soiled clothes, wash skin, take blood

atroping IV 2mg/10minutes until full atropinisation

pralidoxime 30mg/kg IVI, diazepam IV

ABC, control haemorrhage , ABGs, UandEs, glucose, monitor ECG, EEG

105
Q

What is atropinisation?

A

skin dry, pulse >70, pupils dilated

106
Q

Complications of pesticide poisoning?

A

resp failure, poor conc and memory and PTSD

107
Q

What is HIV?

A

human immunodeficiency virus, an RNA retrovirus of the lentiviruses genus which causes AIDS

108
Q

How is HIV transmitted?

A

heterosexual sex in africa, homosexual sex in uk, shared contaminated needles, contaminated blood transfusions, vertical transmission through placenta and breast milk

109
Q

Risk factors for HIV?

A

increase in sexual partners, sexual contact with those from a high prevalence, occupation due to needles, having other STIs

110
Q

Epidemiology of HIV?

A

falling deaths but increased infection and prevalence, high cost from treatment, social care, lost working days, benefits claimed, associated costs, 25% are undiagnosed, and 1/6 are >55

111
Q

What is the HIV point of care test?

A

a fingerprick blood test

112
Q

Advantages and disadvantages of the HIV point of care test?

A

D - lower sensitivity and specificity and gives false positives and negatives, missed window periods

A -convenient, increased access, reduces transmission, early diagnosis, non specialist clinics

113
Q

The law on HIV?

A

illegal to transmit the infection if you know you are at risk

114
Q

Prevention of HIV?

A

circumcision, screen blood products, reduce needle excnahge, post exposure prophylaxis, sex education, reduce partner exchange, use condom, highly active antiretroviral therapy, PEP, screening, avoid ulcers, remove Langerhan cells

115
Q

What is involved in HIV screening?

A

> 99% detectable post 12 weeks

4th gen with IgM and P24 antigen is

116
Q

Symptoms of HIV?

A

fever, arthralgia, myalgia, lethargy, lymphadenopathy, sore throat, mucosal ulcer, maculopapular rash, head ache, photophobia, myelopathy, neuropathy

117
Q

What are the two types of HIV-1?

A 
type M (main) - more prevalent in Europe, America and sub sahara afric
type 0 (outlying) - mainly in cameroon
118
Q

Where does HIV-2 mainly occur?

A

confined to west africa

119
Q

Pathophysiology of HIV?

A

infects CD4+T cells binding to its receptor and co receptor sites which interact with protein complexes gp120 and gp41 in the viral envelope

the gp120 receptor complex promotes binding to the coreceptor, inducing a change in gp120 so gp41 can unfold and insert its hydrophobic end into the cell membrane

gp41 folds back on its self to bring the virus towards CD4 to fuse membranes

viral nucelocapsid enters the host cell and releases 2 viral RNA strands and 3 replication strands (reverse transcriptase, integrase and protease)

reverse transcriptase causes revers transcription on viral RNA then transcribed into a double helix which is integrated into the host DNA using integrase to now be manufactured into new virons

protease cleaves longer proteins into smaller ones to create an infectious viral

the 2 viral RNA strands and the replication enzyme comes together and surrounded by core proteins forming the capsid and leave the cell to mature and infect other cells

leads to a gradual CD4 decline

120
Q

What causes asymptomatic or generalised lymphadenopathy with CD4 decline?

A

in west and central africa, with enlarged lymph nodes involving 2 or more non contagious sites other than the inguinal nodes

121
Q

What is the CD4 count for type C1, C2 and C3 HIV?

A

1 - >500
2 - 200-499
3 -

122
Q

When does CD4 count cause immunodepression?

A
123
Q

Investigations for HIV?

A

HLA-B 5701 status, lymphocyte subsets

ELISA in 6-8 weeks, western blot, immunofluorescence assay, nuclei acid testing

virology screen

serologic testing algorithm for recent HIV serovconversions (STARHS) to identify recent activation

viral p24 antigen, isolation of virus in culture, detect IgG antibodies to envelope components

124
Q

What is screened in a virology screen for HIV?

A

HIV antibody, HIV viral load, HIV genotype, hepatitis serology, CMV antibody, syphilis screen

125
Q

Treatment of HIV?

A

educate, transmission reduction, advice, contact tracing, psychological support

highly active antiretroviral therapy (HAART)
2xNRTI + 1xNNRTI or
2xNRTI + 1xPI or 1xII

(non nucloside reverse transcriptase inhibitor, nucleoside reverse transcriptase inhibitor, protease inhibitor, integrase inhibitor)

126
Q

What are the co receptor sites in M and T tropic strains of HIV?

A 
M = CCR5
T = CXCR4
127
Q

Example of a protease inhibitor?

A

indinavir

128
Q

Example of integrase inhibitor?

A

raltegravir

129
Q

Complications of HIV?

A

increased risk of opportunistic infections e.g. toxoplasmosis, CMV. PJP, cryptococcal meningitis, aspergillosis

increased risk of malignancies e.g. Kaposis sarcoma, NHL, cervical, anal

AIDS (5-10yrs post)

130
Q

Symptoms of AIDS?

A

candiasis of bronchi, trachea, lungs and oesophagus, lymphoma, pneumocytosis pneumonia, leucocenphalopathy, meningitis, CNS mass lesions, cervical cancer, TB

131
Q

What is the treatment of HIV based on?

A

awareness, delivery, clinical services, cost, adherence, efficacy, co morbidities, side effects, 2ndline, combined formulants, paediatric formulants, ease of use

132
Q

What is the difference between HIV-1 and -2?

A

they are closely related retroviruses, capable of reverse transcriptase and made up of 9 genes causing genetic variation

133
Q

What are the 9 genes that code for the HIV genome?

A

Tat - viral replication and increased host transcription factor production
Rev - binds to RNA to allow export form nucleus and regulate RNA splicing
Nef - increase infectivity
Gag - encodes structural proteins
Pol - encodes enzymes
Env - encodes envelope proteins
Vif - host restriction factor to block replication and mediate degradation

134
Q

Which three genes help encoding in HIV?

A

Gag, Pol, Env

135
Q

What are the different types of tropic medicine?

A

neoplastic disease, chronic illness, blood dyscrasias, nutritional, envonoming

136
Q

Examples of vector borne tropical diseases?

A

dengue, viruses, malaria, protozoa, trypanosomes, leishmaniasis, filaria, trachoma, bacteria, typhus, rickettsia, helminthiases

137
Q

Examples of soil/water borne tropical diseases?

A

hookworm, ascaris, buruli ulcer

138
Q

Examples of faecal oral tropical diseases?

A

amoebae, giardia, thyphoid, bacteria

139
Q

Examples of sexual tropical diseases?

A

HIV and STIs

140
Q

Examples of airborne tropical diseases?

A

measles, meningitis, pneumonias, TB

141
Q

Symptoms of Dengue fever?

A

fever, headache, severe musculo skeletal pains (back break fever), fever temporarily drops, rash

142
Q

How is Dengue fever transmitted?

A

aedes mosquito - in south america and central africa

143
Q

Examples of arthropod borne viruses?

A

dengue fever, yellow fever, japanese encephalitis, west nile, o’nyong nyong, chikunggunya

144
Q

Examples of human to human directly transmissable haemorrhagic viruses?

A

lassa fever, ebola, marburg, CCHF

have a high case fatality and need a high level barrier nursing of cases advised

145
Q

What can sand flies (phlebotomus sp) cause, how does it present and what is the treatment?

A

causes a fever, biopsy shows amastigotes, shows the leishmania species, and treated with sodium stibogluconate

146
Q

What is African Trypanosomiasis?

A

the sleep sickness, causing strange behaviour and hard to rouse

transmitted via the tryspansoma bruceii tsetse fly

it is a transient parasitaemia, with lymph gland invasion and chronic meningoencephalitis

147
Q

Treatment of the African Trypanosomiasis?

A

IV suramin (urea derivative) and melarsoprol (trivalent arsenic compound), need CSF to diagnose if no symptoms

148
Q

Symptoms of the Chagas disease?

A

initial lesion, oedema, transient toxaemia, long latent period, cardiomegaly, CCF, arrhythmia, megooesopghagus, megacolon, destructon of enteric nerve plexus

no treatment

149
Q

Tropical infections with short (

A

arboviral infections (dengue), enteric bacterial infections, paratyphoid, plague, typhus, haemorrhagic fevers

150
Q

Tropical infections with long (>21 day) incubation period?

A

viral hepatitis, TB, HIV, schistosomiasis, amoebic liver abscess, visceral leishmaniasis, filariasis

151
Q

Symptoms of typhoid?

A

fever, relative bradycardia, abdominal pains, dry cough, constipation, lymphadenopathy, headache, splenomegaly, rose spots

152
Q

Symptoms of an amoebic liver abscess?

A

fever, jaundice, RUQ pain

153
Q

What are sarcomas?

A

rare (1%) tumours of the mesenchymal tissue and should be managed through specialist care (50 different types)

154
Q

What does a biopsy show in a high grade sarcoma?

A

pleomorphic spindled cells arranged in long fasicles

increased mitosis, with necrosis, deep margin

155
Q

What does a biopsy show in low grade sarcoma?

A

well differentiated liposarcoma, most of which is lipid like

low mitosis, no necrosis, mostly covered by a pseudocapsule but can have focal capsular breach and tumour present at one margin

156
Q

How can sarcoma recurrence be reduced?

A

radiotherapy, usually fractioned

treat the same place each time (RT tattoo)

157
Q

Side effects of radiotherapy?

A

depends upon the area treated

early - tiredness, skin inflammation, hair loss

late - lymph-edema, joint stiffening, pathological fracture

158
Q

When should radiotherapy be used for sarcoma treatment?

A

for high grade tumours, >5cm with positive surgical margins, reduces distant recurrances but no overall survival effect

159
Q

What is used in adjuvant chemotherapy?

A

doxorubicin and ifosfamide

160
Q

What does a biopsy show in Ewing’s sarcoma?

A

round cell tumour, CD99+, EWSR1 rearrangement

161
Q

Where does Ewings sarcoma usually affect?

A

the pelvis or femur

162
Q

In who is Ewing’s sarcoma most common?

A

young males 10-20

163
Q

Treatment of Ewing’s sarcome?

A

surgery, chemo, radiotherapy

164
Q

Side effects of chemo?

A

early - anaemia, thrombocytopenia, neutropenia, mouth ulcers, thrush, N+V, constipation, neurotoxcity, peripheral neuropathy, encephalopathy, haemorrhagic cystitis, hair loss, tiredness

late - cardiotoxcity, nephrotoxicity, neurotoxicity, osteopenia, fertility, secondary malignancies

165
Q

Aims of advanced stage sarcoma treatment?

A

downstage with pre op RT and chemo to make the lesion operable

or

palliative for symptomatic lesions, with surgery an radiotherapy, typically systemic treatment with cytotoxic chemo or targeted agents

166
Q

What is used in palliative chemo?

A

single agent doxorubicin

167
Q

Treatment of GI sarcomas?

A

insensitive to traditional chemo agents so used activating mutation in KIT or PDGRF or oral agent imatinib targets KIT and PDGFR

168
Q

Side effects of imantinib?

A

nausea, vomiting, diarrhea, fluid retention, skin rash, tiredness

169
Q

Risk factors for sarcoma?

A

age (10-20), radiation, previous cancer, family history, exposure to chemical, infections, lowered immunity, arm or leg swelling, body weight, injury, smoking

170
Q

Symptoms of sarcoma?

A

painless less that becomes painful, big, getting bigger, deep in body tissues,

171
Q

Diagnosis of sarcoma?

A

core needle biopsy with US assistance, mri, ct, xray, fine needle aspiration, PET scan, cytogenetic tests for more specific diagnosis

172
Q

What 3 things is a sarcoma grade based on?

A

differentiation - differentiated or abnormal

mitotic count

necrosis

173
Q

What are the 3 main types of worm and where do they affect in the body?

A

nematodes (roundworms)- intestine, larva migrains, tissue
trematodes (flukes) - blood, liver, lung, intestinal
cestodes (tapeworms) - invasive and non invasive in the gut from meat

174
Q

How are tapeworms detected?

A

detection of eggs in the stool microscopy (taenia saginata), serology (taenia solium and echinococcus granulosus), imaging of cysts with US, CT and MRI

175
Q

Symptoms and treatment of tapeworms?

A

taenia saginata - abdo pain and malabsorption (praziquantel)

taenia solium - disseminated disease in skin and skeletal muscle and brain causing fits and focal signs (albendazole)

echinococcus granulosus - cyst develop in liver lung and brain causing anaphlatic reactions (surgical excision and albendazole)

176
Q

Treatment of hookworm and threadworm?

A

Mebendazole

177
Q

Diagnosis of roundworms?

A

detection of eggs in faeces, serology, larvae in fresh stool (strongyloides stercoralis)

178
Q

Treatment of round worm?

A

Levamisole

179
Q

Symptoms of round worms?

A

LOCAL DERMATITIS at site of skin pentration, diarrhea, malabsorption, disseminated disease, nausea, epigastirc pain, iron deficient anaemia, prutitus ani (threadworm)

180
Q

How do fluke worms infect?

A

the schistosoma species have parasite eggs realeased in urine or faeces and hatch on contact with water, infecting fresh water snails who penetrate human skin (swimmer’s itch), they migrate to the pelvic veins and bladder causing haematuria, hydronephrosis and renal failure, treat with praziquantel

Phase 2a (15 decks)

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