all Flashcards

(224 cards)

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
what % compensated cirrhotics have varices at diagnosis
 40% of compensated cirrhotics have varices at diagnosis
26
o An ascitic fluid WCC of >250m3 is considered evidence of?..
spontaneous bacterial peritonitis
27
treat spontaneous bacterial peritonitis with?
with IV cefotaxime or ciprofloxacin
28
hepatic encepholopathy is caused when
o Acute liver failure o Portosystemic shunting without cirrhosis o Cirrhosis (chronic liver failure)
29
prevent kidney failure in spontaneous bacterial peritonitis
1.5g/kg 20% salt poor albumin on day 1 | 1g/kg 20% salt poor albumin on day 3
30
micronodular nature of onset and cause
slow onset over many years caused by alcohol
31
macronodular nature of onset and cause
faster onset most common cause is hep C or B | other causes include WILSON! and alpha1 antitrypsin deficiency
32
purpose of liver biopsy
identify if there is neoplasm stage it and determine nature rule out other underlying path
33
Tissue matching? marrow? kidney? liver? importance?
marrow - essential kidney - importnat Liver - fuck it off
34
whats primary biliary cholangitis?
autoimmune liver disease, more common in women, raised bilirubin, raise ALP
35
paracetamol to liver?
necrosis
36
fatty liver vs steatohepatitis??
```  Fatty liver shows no: o Ballooning degeneration o Mallory bodies o Neutrophils but steatohepatitis shows:  Ballooned cells  Mallory bodies  Neutrophils ```
37
mortality rate of alcoholic liver disease acutely?
60%
38
mortality of non-alcoholic cirrhosis acutely?
0%
39
 Pathology of alcoholic hepatitis and non-alcoholic steatohepatitis is identical but differs in severity of:
Ballooned cells Mallory bodies Neutrophils
40
number one cause of CKD?
diabetes
41
number 2 cause of CKD
glomerulonephritis
42
CKD diagnosis
Two eGFRs of less than 60ml/min/1.73m2 over a period of 90 days or more
43
number 3 cause of CKD
hypertension
44
what percentage of gluconeogenesis takes place in kidney.
25%
45
kidney is the only place what hormone is destroyed?
insulin - persistent insulin causes hypocalcemia
46
which part of kidney highly vulnerable to hypoxia?
medulla
47
ace inhibitors and ARBs in ckd protective or damaging?
protective, reduce renal hypertension, reducing proteinuria
48
when there is AKI what is the physiological response in the kidney and what does it lead to?
shunt to healthy remaining nephrons which maintains GFR but unforunatley results in renal hypertension, further damage and proteinuria
49
what do you give to someone for high BP if they are under 55
Ace or ARB to protectkidney function
50
what do you give to someone for high BP if they are over 55 and why
Ca chan Blocker because if they already have atherosclerotic disease narrowing affarent and you give ace or ARB you will cause ischemia
51
what do you give to someone for high BP if they have CKD and/or proteinuria what other group do you give this to?
Ace or ARB
52
Effects of CKD
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
53
what can hemodyalisis do for the patient at what can it not do?
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
54
problem with peritoneal dialysis
may reach equilibrium as there is no semipermeable membrane between the dyalisate and blood
55
polycystic kidney disease inheritance type?
autosomal recessive and dominant versions. dominant more common
56
polycystic is mutation in which genes?
PKD1 and 2
57
what stage should you be thinking transplant?
transplant as an option as soon a gfr reaches 20 and then within 6 months of dialysis.
58
Eligibility for kidney transplant?
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?
59
what is best donation type? what are the others?
live is best, in terms of cadaveric: Brainstem death is better than CV Death
60
muskuloskeletal disability proportions
1 in 4 have either disability or severe disability 42% had no problems 30% aches and pains
61
leading cause of absence from work
neck, upper limb and back
62
radiological features of osteoarthritis
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
63
why do the hips tilit
lack of strength in abductors from long sustained osteoarthritis
64
how many knee hip replacements and why
o 100,00 hip/knee replacement operations annually in the UK mainly for osteo
65
% of people over 60 who have osteo
more than half
66
why is obesity important in osteoarthritis
plays a hormonal role as well as a load role
67
when to use secondary care for OA?
primary care fails to manage pain or in doubt ab Dx
68
when to exercise in OA
at all stages of disease regardless of pain or severity
69
pharmacological line in OA
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)
70
most important part of collagen lost in oa from cartilage
aggrecan
71
weird places to get stem cells
 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
72
when scaffolding joints with stem cells and grafts what is the type of choice
 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
73
what is aggrecan really? what makes it so key
its a proteoglycan, need to bind to water electrostatically
74
collagen for bone collagen for catilage
bone 1 90% cartilage 2 45-50%
75
osteoclast lineage
monocytic-macrophage lineage
76
osteoclast lifespan
o Live for around 3-4 weeks
77
how is brone break down cellularly modulated
Osteoblasts produce osteoprotegerin OPG binds to RANKL and stops osteoclasts. • Balance between RANKL and OPG expression by osteogenic cells regulates osteoclastogenesis.
78
denosumab?
an antibody to osteoprotegerin used to treat osteoperosis
79
which bones grow by intramembranous ossification?
Skull bone, clavicle, pelvis – flat bones
80
cortical bone?
also known as compact, most bon is this, hard bone
81
trabecular bone?
spongey, cancelous bone makes up areas like joint, less of this
82
o Adult skeleton completely remodelled every...?
10yrs
83
how many bone modelling units active at one time?
o 1 million BMUs operating at any one time.
84
order of drugs to treat osteoporosis
 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
85
what T scores mean what disease?
• Osteoporosis is defined as T score
86
what are T scores?
density of bone compared to the mean average. 0 is a healthy young adult mean
87
FRAX score
online tool used to identify fracture risk, very sensitive but still some false pos/neg
88
who should have dexa?
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
89
can we use hrt for better bone mineral density?
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
90
why cant use raloxifene for early menopause? | what type of drug is it?
early menopause causes worse vasodilatory symptoms | oestrogen receptor modulator (like tamoxifen)
91
how to take bisphosphonate
low intestinal absorption, take first thing in the morning on completely empty stomach, don’t eat or drink anything for half an hour.
92
teriparatide?
synthetic parathyroid hormone, shown to increase bone mass more than break down, once daily subcut for 24 months in most severe cases
93
FETUS AND FRACTURES?
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
how does having a facture influence risk of future fractures in osteoporosis?
massively inc. risk, especially with spinal as changes mechanics
95
• Which component of cartilage provides compressive strength
proteoglycans
96
in terms of bone what does BMU stand for and what is it composed of
bone multicellular unit of osteoclasts AND blasts
97
• What attracts osteoblast precursors to site left by osteoclasts
factors left by bone matrix
98
• Mechanoreceptor of bone?
osteocyte
99
• Community acquired infection?
less than 48hours after admission
100
hospital aquired infection
greater than 48hours after admission develops
101
findings lumb punc in meningitis
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
nitrofurantoin uses?
great for community UTIs that trimethoprim cant handle but no good at pyelonephritis as cant get to higher urinary tract
103
most common cause organism of uti?
e.coli
104
diagnosis of sarcopenia made with?
bioimpedence or DEXA, bioimpedence not possible if ulcers or fluid collections
105
• Beta lactams cidal or static, narrow or broad?
broad, cidal
106
• Glycopeptides, type and names of two?
vancomycin and teicoplanin, narrow spec
107
vancomycin mode of giving
oral for C dif as not absorbed but iv for all else. must consider renal impairment
108
if it begins with C probs caused the c dif
lol
109
treat c dif
 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
• Infection control principles in infectious diarrhoea (eg norovirus and c.diff)
 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
• 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?
norovirus PCR as in the uk and norovirus common
112
• 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
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
how many hiv particles form per day?
a billion HIV particles each day
114
hiv key receptors
GP 120 and GP 41 binding to CD4 molecule which is key receptor
115
CD4 levels in HIV
``` 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
how long do you need to wait for hiv tests?
o Antibody and antigen (4th generation) tests shorten the window period but still repeat in 3 months if risk exposure
117
what is seroconversion illness?
glandular fever type symptoms you get with first HIV infection
118
result of attacking marrow with anti-cancer drugs
neutropenic sepsis
119
neutropenic sepsis key treatment
iv tazocin within 1 hour will reduce mortality by 15%
120
illness straight after HIV infection
seroconversion illness
121
proportion of hiv who get seroconversion illness
60-70%
122
in the UK the most common hiv opportunistic infection
caused by yeast like fungus Pneumocystis pneumonia
123
common neuro presentation of hiv
toxoplasma gondii, from cat faeces. more common in places where raw meet consumed
124
kaposis sarcoma, what causes it?
infection by herpes virus 8 and in hiv
125
worldwide the most common hiv opportunistic infection is
TB
126
is TB from hiv treated differently from normal TB?
nope
127
what enzymes break down lung in tB and what does it form?
metalloproteinases forming cavities
128
• Which of the following is an HIV related opportunistic infection?
qawd
129
when treating Pneumocystis pneumonia, what must you do?
abx is co-trimoxazole. give high dose steroid alongside abx to prevent inflammation damaging the lung.
130
PCP on x-ray shows what sign?
ground glass
131
neutropenic sepsis
WCC
132
treatment for hiv
``` HAART 2x NRTI (AZT, lamivudine, tenofovir, abacavir) backbone of regime then NNRTI or Intergrase inhibitor or PI like darunavir ```
133
nnrti problems?
liver toxicity | psychiatric problems
134
HIV pill burden?
used to be big issue, more combo drugs now
135
when to commence HAART for HIV?
ALL PEOPLE LIVING WITH HIV
136
lifespan of hiv individual if adheres to HAART?
65+
137
why sequence exons
• 85% of disease causing mutations are within exons as they most change protein
138
if denovo exome sequencing who do you sequence?
child, mum, dad
139
consanguinous families?
 Distantly related concordantly affected individuals
140
what kind of words do we use to make sure everyone uses the same language about symptoms for exoming purposes?
 Human phenotype ontology
141
o Segregation analyses ?
when a parent had a disease causing gene but didnt affect them due to protective factors, child inherits
142
database for exoming
clinvar
143
chemicals in burns and what they do
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
what happens to electrolytes in burns?
plasma sodium falls, this is an oedema | plasma potassium rises slightly from cell lysis
145
in 1990 what proportion of people with 50% burns survived
50% and it goes up 1% a year
146
jackson
 Central zone of eschar: coagulation/necrosis zone of hyperaemia zone of stasis
147
describe erethyyma burn
``` 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
describe partial thickness
``` • 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
types of partial thickness
superficial - most skin appendages maintained | deep
150
describe full thick
``` • 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
short way to id burn thickness
o Is the burn painful? NO -> full thickness o If yes are there any blisters? NO -> erythema o If yes then partial thickness
152
erythema and resus
dont count eretheyma or you'll over resus
153
what do you resus burns with?
crystalloid as colloid makes worse
154
• Who to resuscitate in burns?
o Adults >15% BSA o Childrens >10% BSA o ? Oral resuscitation for smaller burns
155
how to resus burns
``` 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
dark urine in burns?
 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
surgery in burns?
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
fluid output and haematocrit % in burns
```  Monitor fluids: • Adults: 0.5-1ml/kg/hr • Children: 1-2ml/kg/hr  Haematocrit: • Adults: 40-44% • Children: 36-40% ```
159
bones and electricity
maximum electricity goes through long bones, as they get superheated heat muscles around them and get compartment syndrome
160
nutrition costs hosp
75% food 25% specialised nutrition - big percentage for what it is
161
how does temperature of body effect energy expenditure
1% inc = 13% inc
162
malnourished people electrolytes
K+ reduced, Na+ raised
163
• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity
reductive adaptation
164
reductive adaptation
• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity
165
Oedema in malnourished associated with what?
hypoalbuminemia, salt and water retention, cellular dysfunction
166
what guides us for nutrition
• WHO 10 steps Management of severe malnutrition
167
what proportion of hosp admissions are at risk of malnutrition
25-34%
168
est. cost malnutrition
19.6bil pound
169
must score step 1
BMI • BMI >20 = 0 • BMI 18.5 -20 = 1 • BMI
170
must step 2
 Step 2: Unplanned weight loss | • Wt loss 10% = 2
171
must step 3
 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
what to do must
* 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
confirm NG tube position
measure pH of secretions should be less than 5.5 if PPI then use xray
174
intestinal failure
 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
type of feed used in crohns and not uc
enteral
176
elemental feed?
predigested feed, useful in crohns for single nutrient absorption Elemental feeding causes remission, with positive impact of growth
177
who is palliative care for?
people suffering from life threatening illness and their familise, psychologoical, social, physical needs, impecable pain management
178
how many people die of cancer around the world?
o Annually, 5 million people die of cancer around the world.
179
at southampton how many people will be in last year of life?
o 1 in 3 will be in their last year of life
180
how many will die this admission?
o 1 in 10 will die during this admission
181
pain ladder
 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
commonest life-threatening occurence in someone with cancer
hypercalcemia
183
vomiting centre receptors
o 5HT3, D2, mAChR, H1
184
outside the bbb sickness centre?
CTZ
185
cyclizine mechanism?
anticholinergic and antihistamine
186
• Levomepromazine mechanism?
broad spec antiemetic (5HT,D2,AChR,H2)
187
• Metoclopramide
o DA antagonist, 5HT4 agonist, central 5ht3 antagonist, prokinetic
188
body temperature and energy
Every 1-degree rise in body temperature increases 13% of energy expenditure.
189
supply of which electrolytes is needed for malnourished, reductively adapted patients
o Administration of additional sodium is potentially toxic | o Administration of additional potassium is essential
190
patients who weigh less on discharge percentage?
70%
191
replaced aggressively in crohns?
vitamin D
192
treatment for crohns not ulcerative colitis?
enteral nutrition - same results if not better than steroids, useful for those who would be likely to have steroids long term
193
how many people in a study to discover very rare ADR?
30000
194
how many people in study to work out common ADR?
5000
195
What information do you need to help you fill out the Yellow Card as helpfully as possible?
 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
most common travellers complaint
Gi disease
197
2nd most common travellers complaint
fever
198
3rd most common travellers complaint
derm
199
A patient returning from Africa is most likely to return with what illness?
febrile
200
What is haem converted to before it becomes unconjugated bilirubin?
biliverdin
201
. What proportion of patient’s varicies bleed within 2 years of diagnosis?
25%
202
granulomas in liver?
weird infections and primary biliary cirrhosis, and hepatitis C
203
Which conditions is anti-smooth muscle Ab (SMA for?
AICAH (comes out smoothly)
204
At what GFR would a patient be reviewed for transplantation
less than 20 gfr
205
radiotherapy on localised disease
20-50%
206
brachytherapy?
form of radiotherapy
207
chemosensitive cancers
Choriocarcinoma Testicular cancer Leukaemia Some lymphomas e.g. Hodgkin
208
woman lifetime risk of breast cancer?
1 in 8
209
mans lifetime risk breast cancer
1 in 868
210
. Approximately how many new breast cancer cases are there annually in the UK?
50000
211
% of breast cancers HR positive
70%
212
tamoxifen qualities?
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
criteria for infective endocarditis?
modified Dukes
214
ECG abnormalities associated with aortic valve endocarditis?
prolonged PR interval
215
negative culture IE what to do with abx?
If a negative culture returns, antibiotic therapy may need to be stopped for 7-10 days before cultures become positive
216
. Which pathogens likely to result in a culture negative infective endocarditis?
a. Haemophilus b. Aggregatibacter c. Cardiobacterium d. Eikenella e. k
217
chronic/subacute presentation of NVE abx?
amoxicillin 2g IV/4 hours
218
prosthetic valve endocarditis
vanco, gent, rifampicin
219
sepsis and multiple resistance
vanc and meropenam
220
resistance, penicillin allergy
vanc and gent
221
emboli in IE
• 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
people admitted delirium will die, and how many will die if developing as inpatient
o ¼ people admitted delirium will die, and ¾ will die if developing as inpatient
223
oral steroid associations in regnancy
pre-eclampsia, pre-term and low birth weight infants
224
worst asthma in pregnancy cymptoms
week 24-6