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1
Q

dengue is what type of infection

A

virus carried by mosquito

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2
Q

complications of malaria inc.

A 
	Cerebral malaria
	AKI
	Pulmonary oedema (ARDS)
	Metabolic acidosis (more common in children)
	Hypoglycaemia (more common in children
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3
Q

cases malaria uk

A

1500

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4
Q

vivax treat 1st line

A

choloroquine and primaquine for liver stage

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5
Q

treat falciparum

A

co-artem (artesunate/halofantrine)

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6
Q

vivax vs falciparum time to present

A

months vs a few weeks/days

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7
Q

• Where are most cases of falciparum acquired

A

W. africa

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8
Q

What proportion of cases with imported malaria had taken prophylaxis:

A

82% did not. 18% who did didn’t take it properly

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9
Q

treat ebola

A

iv zmapp

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10
Q
  • What proportion was caused by falciparum of imported cases in UK:
  • What proportion was caused by vivax:
A

75%

15%

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11
Q

ebola pathogen type and family

A

Virus of family Filoviradae

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12
Q

likely carrier animal for ebola

A

fruit bat

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13
Q

fatality of ebola?

A

50%

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14
Q

arabian with lung disease

percentage of cases from saudi

A

• Middle eastern respiratory syndrome (MERS)

o >85% cases Saudi Arabia

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15
Q

arabian with lung disease pathogen likely to be:

A

coronovirus

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16
Q

swine flu h and N type?

 Global mortality estimates:

A

novel form of H1N1

150,000-575000

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17
Q

avian flu h and n type

A

many circulating strains

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18
Q

bird flu treatment?

transfer human to human?

A

 Neuraminidase inhibitors (oseltamivir/Tamiflu) recommended for treatment

no

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19
Q

cholestasis blood panel

A

ALP high but this could be due to pregnancy or liver disease of any time or bone growth.
GGT high could be alcohol
total bilirubin raised
direct bilirubin (conjugated) will go up as the liver is functioning and has conjugated the bilirubin
if it was pre or sometimes intrahepatic direct would be normal but indirect would be high.

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20
Q

o Metabolism in hepatocytes

A

phase 1 cytochrome p450

phase 2 conjugation

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21
Q

albumin per day

A

200 mg/kg/day

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22
Q

what clinical sign means that the individual has become decompensated?

A

the presence of ascites +/- varicies

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23
Q

normal portal pressure?
risk of varices at?
risk of bleed at?

A

5mmhg
10mmhg
12mmhg

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24
Q

When varices form what chemicals released?

A

VEgF, superoxide, NADPH

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25
Q

what % compensated cirrhotics have varices at diagnosis

A

 40% of compensated cirrhotics have varices at diagnosis

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26
Q

o An ascitic fluid WCC of >250m3 is considered evidence of?..

A

spontaneous bacterial peritonitis

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27
Q

treat spontaneous bacterial peritonitis with?

A

with IV cefotaxime or ciprofloxacin

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28
Q

hepatic encepholopathy is caused when

A

o Acute liver failure
o Portosystemic shunting without cirrhosis
o Cirrhosis (chronic liver failure)

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29
Q

prevent kidney failure in spontaneous bacterial peritonitis

A

1.5g/kg 20% salt poor albumin on day 1

1g/kg 20% salt poor albumin on day 3

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30
Q

micronodular nature of onset and cause

A

slow onset over many years caused by alcohol

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31
Q

macronodular nature of onset and cause

A

faster onset most common cause is hep C or B

other causes include WILSON! and alpha1 antitrypsin deficiency

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32
Q

purpose of liver biopsy

A

identify if there is neoplasm
stage it and determine nature
rule out other underlying path

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33
Q

Tissue matching? marrow? kidney? liver? importance?

A

marrow - essential
kidney - importnat
Liver - fuck it off

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34
Q

whats primary biliary cholangitis?

A

autoimmune liver disease, more common in women, raised bilirubin, raise ALP

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35
Q

paracetamol to liver?

A

necrosis

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36
Q

fatty liver vs steatohepatitis??

A 
	Fatty liver shows no:
o	Ballooning degeneration
o	Mallory bodies
o	Neutrophils
but steatohepatitis shows:
	Ballooned cells
	Mallory bodies
	Neutrophils
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37
Q

mortality rate of alcoholic liver disease acutely?

A

60%

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38
Q

mortality of non-alcoholic cirrhosis acutely?

A

0%

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39
Q

 Pathology of alcoholic hepatitis and non-alcoholic steatohepatitis is identical but differs in severity of:

A

Ballooned cells
Mallory bodies
Neutrophils

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40
Q

number one cause of CKD?

A

diabetes

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41
Q

number 2 cause of CKD

A

glomerulonephritis

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42
Q

CKD diagnosis

A

Two eGFRs of less than 60ml/min/1.73m2 over a period of 90 days or more

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43
Q

number 3 cause of CKD

A

hypertension

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44
Q

what percentage of gluconeogenesis takes place in kidney.

A

25%

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45
Q

kidney is the only place what hormone is destroyed?

A

insulin - persistent insulin causes hypocalcemia

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46
Q

which part of kidney highly vulnerable to hypoxia?

A

medulla

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47
Q

ace inhibitors and ARBs in ckd protective or damaging?

A

protective, reduce renal hypertension, reducing proteinuria

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48
Q

when there is AKI what is the physiological response in the kidney and what does it lead to?

A

shunt to healthy remaining nephrons which maintains GFR but unforunatley results in renal hypertension, further damage and proteinuria

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49
Q

what do you give to someone for high BP if they are under 55

A

Ace or ARB to protectkidney function

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50
Q

what do you give to someone for high BP if they are over 55 and why

A

Ca chan Blocker because if they already have atherosclerotic disease narrowing affarent and you give ace or ARB you will cause ischemia

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51
Q

what do you give to someone for high BP if they have CKD and/or proteinuria what other group do you give this to?

A

Ace or ARB

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52
Q

Effects of CKD

A

Retained nitrogenous waste, water and salt (oliguria) bloods will show inc. urea/creatinine
Hyperphosphatemia
Impaired ubule function
Polyuria - if it’s primarily tubular disease rather than glomerular
Acidosis and hyperkalemia (when pH goes down potassium goes up K+ opposes h+)
Hormonal function
Anemia - starts as dietary (asked to have low protein diet) with occult loss and then becomes anemia of chronic disease treat with parenteral iron, recombinant EPO and hypoxia induced factor stabilisers
Vitamin D deficiency and hyperparathyroidism

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53
Q

what can hemodyalisis do for the patient at what can it not do?

A

it can: balance electrolytes, deal with acid/base imbalances, remove waste products
it can’t: treat CVD risk, might make it worse and cant fix hormonal imbalances

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54
Q

problem with peritoneal dialysis

A

may reach equilibrium as there is no semipermeable membrane between the dyalisate and blood

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55
Q

polycystic kidney disease inheritance type?

A

autosomal recessive and dominant versions. dominant more common

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56
Q

polycystic is mutation in which genes?

A

PKD1 and 2

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57
Q

what stage should you be thinking transplant?

A

transplant as an option as soon a gfr reaches 20 and then within 6 months of dialysis.

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58
Q

Eligibility for kidney transplant?

A

progressive, irreversible end stage renal failure,
no current infection or malignancy and some history of malignancy is unacceptable

extensive compliance proof,

life expectancy with transplant
BMI,

is there good enough vascularity and in the case of polycystic is there space or do we have to remove?

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59
Q

what is best donation type? what are the others?

A

live is best, in terms of cadaveric: Brainstem death is better than CV Death

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60
Q

muskuloskeletal disability proportions

A

1 in 4 have either disability or severe disability
42% had no problems
30% aches and pains

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61
Q

leading cause of absence from work

A

neck, upper limb and back

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62
Q

radiological features of osteoarthritis

A

o Joint space narrowing
o Sclerosis: whiteness, denser and whiter nearer to the joint
o Sub-chondral cysts: cystic changes in subchondrum around the joint.
o Osteophytes

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63
Q

why do the hips tilit

A

lack of strength in abductors from long sustained osteoarthritis

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64
Q

how many knee hip replacements and why

A

o 100,00 hip/knee replacement operations annually in the UK mainly for osteo

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65
Q

% of people over 60 who have osteo

A

more than half

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66
Q

why is obesity important in osteoarthritis

A

plays a hormonal role as well as a load role

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67
Q

when to use secondary care for OA?

A

primary care fails to manage pain or in doubt ab Dx

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68
Q

when to exercise in OA

A

at all stages of disease regardless of pain or severity

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69
Q

pharmacological line in OA

A

oral paracetamol and local ibu (safest)
 then add opioid analgesics or an oral COX-2 inhibitors or NSAID with PPI (indigestion, addiction, cognitive function side effects)
 Topical capsaicin for knee or hand OA (active ingredient of red hot chilis, sting when first applied, but done for 4 times a day regularly, deplete substance P and reduces pain and go down from 4x a day to 2x a day, warn not to touch eyes, have to rub it on and wash it off fingers afterwards)
 Intra-articular corticosteroid injections when pain moderate or severe (short term relief)

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70
Q

most important part of collagen lost in oa from cartilage

A

aggrecan

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71
Q

weird places to get stem cells

A

 Induced pluripotent cells – iPS (taking skin cells and reprogramming them to make any tissue in the body)
 Adult-derived skeletal stem cells (from bone marrow)
 Trab bone – periosteal cells
 Placental/umbilical cord blood/AFS
 Fetal derived populations

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72
Q

when scaffolding joints with stem cells and grafts what is the type of choice

A

 Autograft – graft of choice but amounts limited (only so much bone you can take out
 Bone banked allograft attempts to bridge shortfall (expensive and issues

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73
Q

what is aggrecan really? what makes it so key

A

its a proteoglycan, need to bind to water electrostatically

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74
Q

collagen for bone collagen for catilage

A

bone 1 90% cartilage 2 45-50%

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75
Q

osteoclast lineage

A

monocytic-macrophage lineage

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76
Q

osteoclast lifespan

A

o Live for around 3-4 weeks

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77
Q

how is brone break down cellularly modulated

A

Osteoblasts produce osteoprotegerin OPG binds to RANKL and stops osteoclasts.
• Balance between RANKL and OPG expression by osteogenic cells regulates osteoclastogenesis.

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78
Q

denosumab?

A

an antibody to osteoprotegerin used to treat osteoperosis

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79
Q

which bones grow by intramembranous ossification?

A

Skull bone, clavicle, pelvis – flat bones

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80
Q

cortical bone?

A

also known as compact, most bon is this, hard bone

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81
Q

trabecular bone?

A

spongey, cancelous bone makes up areas like joint, less of this

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82
Q

o Adult skeleton completely remodelled every…?

A

10yrs

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83
Q

how many bone modelling units active at one time?

A

o 1 million BMUs operating at any one time.

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84
Q

order of drugs to treat osteoporosis

A

 Bisphopshonates (alendronate, risedronate, zoledronic acid, etidronate, ibandronate): first port of call for patient, alendronate widely prescribed and been around for more than 40 years
 Raloxifene – selective estrogen receptor modulator (SERM): ability to drive bone formation and inhibit osteoclasts
 Strontum ranelate (protelos/protos)
 Teriparatide (recombinant PTH); one of few agents that stimulate bone formation. Relatively expensive, in right patient or right situation, eg last port of call
 Denosumab (monoclonal antibody – RANKL inhibitor): because we know what RANKL does have new tool in armoury

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85
Q

what T scores mean what disease?

A

• Osteoporosis is defined as T score

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86
Q

what are T scores?

A

density of bone compared to the mean average. 0 is a healthy young adult mean

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87
Q

FRAX score

A

online tool used to identify fracture risk, very sensitive but still some false pos/neg

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88
Q

who should have dexa?

A

o Prior low-trauma (osteoporotic) fracture
o Height loss, kyphosis on examination
o Vertebral deformity on spine x-ray (barium enema or IVP)
o Family history of fracture (maternal hip fracture)
o Steroids (especially > 3 months and/or >7.5mg/day)
o Hypogonadism/low body mass index/prolonged amenorrhoea/early menopause
o Heavy smokers/excess alcohol/malabsorption
o FRAX score

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89
Q

can we use hrt for better bone mineral density?

A

Women with HRT higher risk of CHD, stroke, breast cancer and VTE, lower risk of colorectal cancer and hip fracture.
o Overall net loss more than net gaini

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90
Q

why cant use raloxifene for early menopause?

what type of drug is it?

A

early menopause causes worse vasodilatory symptoms

oestrogen receptor modulator (like tamoxifen)

91
Q

how to take bisphosphonate

A

low intestinal absorption, take first thing in the morning on completely empty stomach, don’t eat or drink anything for half an hour.

92
Q

teriparatide?

A

synthetic parathyroid hormone, shown to increase bone mass more than break down, once daily subcut for 24 months in most severe cases

93
Q

FETUS AND FRACTURES?

A

o Birthweight and weight in infancy predict adult bone mass
o babies of mother who don’t smoke are already advantaged in terms of skeletal strength at birth
o Growth in infancy and childhood predicts future risk of hip fracture

94
Q

how does having a facture influence risk of future fractures in osteoporosis?

A

massively inc. risk, especially with spinal as changes mechanics

95
Q

• Which component of cartilage provides compressive strength

A

proteoglycans

96
Q

in terms of bone what does BMU stand for and what is it composed of

A

bone multicellular unit of osteoclasts AND blasts

97
Q

• What attracts osteoblast precursors to site left by osteoclasts

A

factors left by bone matrix

98
Q

• Mechanoreceptor of bone?

A

osteocyte

99
Q

• Community acquired infection?

A

less than 48hours after admission

100
Q

hospital aquired infection

A

greater than 48hours after admission develops

101
Q

findings lumb punc in meningitis

A

usually clear but sometimes cloudy if bacterial, clear in viral and clear if normal, WCC usually over 100 and over 90% of this neurophilic, 40% gluc or less
• Opening pressure can be raised or can be normal

102
Q

nitrofurantoin uses?

A

great for community UTIs that trimethoprim cant handle but no good at pyelonephritis as cant get to higher urinary tract

103
Q

most common cause organism of uti?

A

e.coli

104
Q

diagnosis of sarcopenia made with?

A

bioimpedence or DEXA, bioimpedence not possible if ulcers or fluid collections

105
Q

• Beta lactams cidal or static, narrow or broad?

A

broad, cidal

106
Q

• Glycopeptides, type and names of two?

A

vancomycin and teicoplanin, narrow spec

107
Q

vancomycin mode of giving

A

oral for C dif as not absorbed but iv for all else. must consider renal impairment

108
Q

if it begins with C probs caused the c dif

A

lol

109
Q

treat c dif

A

 Fluid rehydration as needed
 Avoid antiperistalsis agents (eg loperamide)
 Consider stopping PPIs (proton pump inhibitors)
 Mild CDI: metronidazole
 Recurrent/severe CDI: vancomycin (oral) (more potent, cell wall inhibitors, given IV as not absorbed from the gut, if you ask patient to swallow it stays in the gut and is not absorbed, also much more expensive)

faecal transplant (fashionable and very effective, stool from another person, down NJ tube into jejunum and can improve condition considerably.

110
Q

• Infection control principles in infectious diarrhoea (eg norovirus and c.diff)

A

 Avoid moving these patients around the hospital to prevent the spread
 Personal protective equipment (PPE): gloves and apron
 Hand washing
 Consider patients infectious until asymptomatic for 48 hours

111
Q

• A usually healthy 36 year old inmate from the local prison is admitted to hospital with fever and diarrhoea. What is the most important microbiology test to request on stool?

A

norovirus PCR as in the uk and norovirus common

112
Q

• A 25-year-old woman is admitted for appendicitis and has an uncomplicated appendicectomy. She is found to be MRSA positive on swab culture screening. Which is the least appropriate management option?

o Start IV vancomycin
o Move her to a side room
o Move her to a side room on a different ward
o Healthcare workers to use gloves and aprons with her
o Start chlorhexidine gluconate washes and mupirocin nasally

A

Start IV vancomycin CORRECT – least appropriate management because she doesn’t need it, as wound is clean, what she doesn’t have is active disease at the site. Isolate give washes and mupirocin nasally

113
Q

how many hiv particles form per day?

A

a billion HIV particles each day

114
Q

hiv key receptors

A

GP 120 and GP 41 binding to CD4 molecule which is key receptor

115
Q

CD4 levels in HIV

A 
o	>500 Normal
o	350-500 (most people ok)
o	200-350 TB, oral thrush, shingles, 
o	100-200 PCP, kaposis sarcoma, toxoplasma (unusual opportunistic infections)
o
116
Q

how long do you need to wait for hiv tests?

A

o Antibody and antigen (4th generation) tests shorten the window period but still repeat in 3 months if risk exposure

117
Q

what is seroconversion illness?

A

glandular fever type symptoms you get with first HIV infection

118
Q

result of attacking marrow with anti-cancer drugs

A

neutropenic sepsis

119
Q

neutropenic sepsis key treatment

A

iv tazocin within 1 hour will reduce mortality by 15%

120
Q

illness straight after HIV infection

A

seroconversion illness

121
Q

proportion of hiv who get seroconversion illness

A

60-70%

122
Q

in the UK the most common hiv opportunistic infection

A

caused by yeast like fungus Pneumocystis pneumonia

123
Q

common neuro presentation of hiv

A

toxoplasma gondii, from cat faeces. more common in places where raw meet consumed

124
Q

kaposis sarcoma, what causes it?

A

infection by herpes virus 8 and in hiv

125
Q

worldwide the most common hiv opportunistic infection is

A

TB

126
Q

is TB from hiv treated differently from normal TB?

A

nope

127
Q

what enzymes break down lung in tB and what does it form?

A

metalloproteinases forming cavities

128
Q

• Which of the following is an HIV related opportunistic infection?

A

qawd

129
Q

when treating Pneumocystis pneumonia, what must you do?

A

abx is co-trimoxazole. give high dose steroid alongside abx to prevent inflammation damaging the lung.

130
Q

PCP on x-ray shows what sign?

A

ground glass

131
Q

neutropenic sepsis

A

WCC

132
Q

treatment for hiv

A 
HAART
2x NRTI (AZT, lamivudine, tenofovir, abacavir) backbone of regime
then NNRTI or
Intergrase inhibitor or 
PI like darunavir
133
Q

nnrti problems?

A

liver toxicity

psychiatric problems

134
Q

HIV pill burden?

A

used to be big issue, more combo drugs now

135
Q

when to commence HAART for HIV?

A

ALL PEOPLE LIVING WITH HIV

136
Q

lifespan of hiv individual if adheres to HAART?

A

65+

137
Q

why sequence exons

A

• 85% of disease causing mutations are within exons as they most change protein

138
Q

if denovo exome sequencing who do you sequence?

A

child, mum, dad

139
Q

consanguinous families?

A

 Distantly related concordantly affected individuals

140
Q

what kind of words do we use to make sure everyone uses the same language about symptoms for exoming purposes?

A

 Human phenotype ontology

141
Q

o Segregation analyses ?

A

when a parent had a disease causing gene but didnt affect them due to protective factors, child inherits

142
Q

database for exoming

A

clinvar

143
Q

chemicals in burns and what they do

A

histamine - local vasodilation, inc flow, mast cell release
thromboxane - vasoconstriction in undamaged local tissue
prostaglandins - attraction of neutrophils and macrophs
o Oxygen free radicals
produced by neuts and macrophs, damage endothelium causing leak
ctecholamines - do the same as thromboxane

144
Q

what happens to electrolytes in burns?

A

plasma sodium falls, this is an oedema

plasma potassium rises slightly from cell lysis

145
Q

in 1990 what proportion of people with 50% burns survived

A

50% and it goes up 1% a year

146
Q

jackson

A

 Central zone of eschar: coagulation/necrosis
zone of hyperaemia
zone of stasis

147
Q

describe erethyyma burn

A 
o	Erythema:
	Red
	Painful
	Blanches when pressed
	Do not count erythema as a part of burns body surface area for resuscitation. Will result in over resuscitation of the patient. 
	Commonest cause is sunburn
148
Q

describe partial thickness

A 
•	Partial thickness
o	Blistered: fluid damage/expansion below epidermis. 
o	Red
o	Painful
o	Tissue paper appearance
o	Wet
o	Loss of skin integrity
o	Swelling
o	Fluid loss
o	Specific causes: bath scald
149
Q

types of partial thickness

A

superficial - most skin appendages maintained

deep

150
Q

describe full thick

A 
•	Full thickness
o	Painless (although not all burns are uniform)
o	Thick and leathery
o	No blisters
o	Dry
o	Dark red, brown, black or white
o	No blanching
o	Swelling in limbs
o	Specific causes: flame
151
Q

short way to id burn thickness

A

o Is the burn painful? NO -> full thickness
o If yes are there any blisters? NO -> erythema
o If yes then partial thickness

152
Q

erythema and resus

A

dont count eretheyma or you’ll over resus

153
Q

what do you resus burns with?

A

crystalloid as colloid makes worse

154
Q

• Who to resuscitate in burns?

A

o Adults >15% BSA
o Childrens >10% BSA
o ? Oral resuscitation for smaller burns

155
Q

how to resus burns

A 
o	4ml/kg/% burn in the 1st 24 hours
	Half in first 8 hours (from the time of burns)
	Remainder in the next 16 hours
use parkland formula
give enough to sustain urine output 
monitor
156
Q

dark urine in burns?

A

 Myoglobinuria: lysis of sarcomeres of muscle, loss of muscle protein and precipitates in renal tubules, in order to flush it out, make sure greater volume given. Look at colour of urine and make sure it goes lighter.

157
Q

surgery in burns?

A

escharotomy, • Sudden decompression of underlying bloody areas and bleeds like crazy. Need good diathermy control and pack the area with alginate dressings for haemostasis. Calculated guarded emergency procedure

158
Q

fluid output and haematocrit % in burns

A 
	Monitor fluids:
•	Adults: 0.5-1ml/kg/hr
•	Children: 1-2ml/kg/hr
	Haematocrit:
•	Adults: 40-44%
•	Children: 36-40%
159
Q

bones and electricity

A

maximum electricity goes through long bones, as they get superheated heat muscles around them and get compartment syndrome

160
Q

nutrition costs hosp

A

75% food 25% specialised nutrition - big percentage for what it is

161
Q

how does temperature of body effect energy expenditure

A

1% inc = 13% inc

162
Q

malnourished people electrolytes

A

K+ reduced, Na+ raised

163
Q

• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity

A

reductive adaptation

164
Q

reductive adaptation

A

• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity

165
Q

Oedema in malnourished associated with what?

A

hypoalbuminemia, salt and water retention, cellular dysfunction

166
Q

what guides us for nutrition

A

• WHO 10 steps Management of severe malnutrition

167
Q

what proportion of hosp admissions are at risk of malnutrition

A

25-34%

168
Q

est. cost malnutrition

A

19.6bil pound

169
Q

must score step 1

A

BMI
• BMI >20 = 0
• BMI 18.5 -20 = 1
• BMI

170
Q

must step 2

A

 Step 2: Unplanned weight loss

• Wt loss 10% = 2

171
Q

must step 3

A

 Step 3: Acute disease score give a point for acute illness and 2 points if no oral intake for next five or last 5 days

172
Q

what to do must

A
  • Low risk – routine clinical care
  • Medium risk – observe and monitor
  • High risk – treat and refer (instant referral to dietician and put on care plan)
173
Q

confirm NG tube position

A

measure pH of secretions should be less than 5.5 if PPI then use xray

174
Q

intestinal failure

A

 Type 1: self-limiting
 Type 2: prolonged PN support (weeks/months), GI surgery complications (Entero-cutaneous fistulae) (PN feeding at home for up to a year)
 Type 3: chronic IF (long term parenteral nutrition – years). Short bowel, ischaemia, IBD, dysmotility

175
Q

type of feed used in crohns and not uc

A

enteral

176
Q

elemental feed?

A

predigested feed, useful in crohns for single nutrient absorption

Elemental feeding causes remission, with positive impact of growth

177
Q

who is palliative care for?

A

people suffering from life threatening illness and their familise, psychologoical, social, physical needs, impecable pain management

178
Q

how many people die of cancer around the world?

A

o Annually, 5 million people die of cancer around the world.

179
Q

at southampton how many people will be in last year of life?

A

o 1 in 3 will be in their last year of life

180
Q

how many will die this admission?

A

o 1 in 10 will die during this admission

181
Q

pain ladder

A

 1: Non-opioid +/- adjuvant (paracetamol)
 Pain persisting or increasing
 2: Opioid for mild to moderate pain +/- non opioid +/- adjuvant (weak opioids; codeine dihydrocodeine and tramadol)
 Pain persisting or increasing
 3: Opioid for moderate to severe pain +/- non-opioid +/- adjuvant (morphine, oxycodone, diamorphine, fentanyl)

182
Q

commonest life-threatening occurence in someone with cancer

A

hypercalcemia

183
Q

vomiting centre receptors

A

o 5HT3, D2, mAChR, H1

184
Q

outside the bbb sickness centre?

A

CTZ

185
Q

cyclizine mechanism?

A

anticholinergic and antihistamine

186
Q

• Levomepromazine mechanism?

A

broad spec antiemetic (5HT,D2,AChR,H2)

187
Q

• Metoclopramide

A

o DA antagonist, 5HT4 agonist, central 5ht3 antagonist, prokinetic

188
Q

body temperature and energy

A

Every 1-degree rise in body temperature increases 13% of energy expenditure.

189
Q

supply of which electrolytes is needed for malnourished, reductively adapted patients

A

o Administration of additional sodium is potentially toxic

o Administration of additional potassium is essential

190
Q

patients who weigh less on discharge percentage?

A

70%

191
Q

replaced aggressively in crohns?

A

vitamin D

192
Q

treatment for crohns not ulcerative colitis?

A

enteral nutrition - same results if not better than steroids, useful for those who would be likely to have steroids long term

193
Q

how many people in a study to discover very rare ADR?

A

30000

194
Q

how many people in study to work out common ADR?

A

5000

195
Q

What information do you need to help you fill out the Yellow Card as helpfully as possible?

A

 At least one piece of patient information, which can be any of: age, sex, weight, initials, height or a local identification number
 Name(s) of suspect drug(s) thought to have caused the ADR
 Brief description of the ADR
 Contact details of the reporter

196
Q

most common travellers complaint

A

Gi disease

197
Q

2nd most common travellers complaint

A

fever

198
Q

3rd most common travellers complaint

A

derm

199
Q

A patient returning from Africa is most likely to return with what illness?

A

febrile

200
Q

What is haem converted to before it becomes unconjugated bilirubin?

A

biliverdin

201
Q

. What proportion of patient’s varicies bleed within 2 years of diagnosis?

A

25%

202
Q

granulomas in liver?

A

weird infections and primary biliary cirrhosis, and hepatitis C

203
Q

Which conditions is anti-smooth muscle Ab (SMA for?

A

AICAH (comes out smoothly)

204
Q

At what GFR would a patient be reviewed for transplantation

A

less than 20 gfr

205
Q

radiotherapy on localised disease

A

20-50%

206
Q

brachytherapy?

A

form of radiotherapy

207
Q

chemosensitive cancers

A

Choriocarcinoma
Testicular cancer
Leukaemia
Some lymphomas e.g. Hodgkin

208
Q

woman lifetime risk of breast cancer?

A

1 in 8

209
Q

mans lifetime risk breast cancer

A

1 in 868

210
Q

. Approximately how many new breast cancer cases are there annually in the UK?

A

50000

211
Q

% of breast cancers HR positive

A

70%

212
Q

tamoxifen qualities?

A

Is a competitive antagonist of ERs in breast tissue

d. Is a weak agonist of ERs in endometrial tissue
e. Has equal efficacy in pre and post menopausal women
a. Menstrual disturbance
b. Hot flushes
c. Altered libido
e. Small increase in risk of thromboembolism

213
Q

criteria for infective endocarditis?

A

modified Dukes

214
Q

ECG abnormalities associated with aortic valve endocarditis?

A

prolonged PR interval

215
Q

negative culture IE what to do with abx?

A

If a negative culture returns, antibiotic therapy may need to be stopped for 7-10 days before cultures become positive

216
Q

. Which pathogens likely to result in a culture negative infective endocarditis?

A

a. Haemophilus
b. Aggregatibacter
c. Cardiobacterium
d. Eikenella
e. k

217
Q

chronic/subacute presentation of NVE abx?

A

amoxicillin 2g IV/4 hours

218
Q

prosthetic valve endocarditis

A

vanco, gent, rifampicin

219
Q

sepsis and multiple resistance

A

vanc and meropenam

220
Q

resistance, penicillin allergy

A

vanc and gent

221
Q

emboli in IE

A

• 20-50% of all patients
• Reduces to 6-21% after antibiotics
o Greatest in first few days of antibiotics
o Decreases after 2 weeks of antibiotics
depends on size and mobility of vegetations

222
Q

people admitted delirium will die, and how many will die if developing as inpatient

A

o ¼ people admitted delirium will die, and ¾ will die if developing as inpatient

223
Q

oral steroid associations in regnancy

A

pre-eclampsia, pre-term and low birth weight infants

224
Q

worst asthma in pregnancy cymptoms

A

week 24-6

SBOM (2 decks)

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