all Flashcards
dengue is what type of infection
virus carried by mosquito
complications of malaria inc.
Cerebral malaria AKI Pulmonary oedema (ARDS) Metabolic acidosis (more common in children) Hypoglycaemia (more common in children
cases malaria uk
1500
vivax treat 1st line
choloroquine and primaquine for liver stage
treat falciparum
co-artem (artesunate/halofantrine)
vivax vs falciparum time to present
months vs a few weeks/days
• Where are most cases of falciparum acquired
W. africa
What proportion of cases with imported malaria had taken prophylaxis:
82% did not. 18% who did didn’t take it properly
treat ebola
iv zmapp
- What proportion was caused by falciparum of imported cases in UK:
- What proportion was caused by vivax:
75%
15%
ebola pathogen type and family
Virus of family Filoviradae
likely carrier animal for ebola
fruit bat
fatality of ebola?
50%
arabian with lung disease
percentage of cases from saudi
• Middle eastern respiratory syndrome (MERS)
o >85% cases Saudi Arabia
arabian with lung disease pathogen likely to be:
coronovirus
swine flu h and N type?
Global mortality estimates:
novel form of H1N1
150,000-575000
avian flu h and n type
many circulating strains
bird flu treatment?
transfer human to human?
Neuraminidase inhibitors (oseltamivir/Tamiflu) recommended for treatment
no
cholestasis blood panel
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.
o Metabolism in hepatocytes
phase 1 cytochrome p450
phase 2 conjugation
albumin per day
200 mg/kg/day
what clinical sign means that the individual has become decompensated?
the presence of ascites +/- varicies
normal portal pressure?
risk of varices at?
risk of bleed at?
5mmhg
10mmhg
12mmhg
When varices form what chemicals released?
VEgF, superoxide, NADPH
what % compensated cirrhotics have varices at diagnosis
40% of compensated cirrhotics have varices at diagnosis
o An ascitic fluid WCC of >250m3 is considered evidence of?..
spontaneous bacterial peritonitis
treat spontaneous bacterial peritonitis with?
with IV cefotaxime or ciprofloxacin
hepatic encepholopathy is caused when
o Acute liver failure
o Portosystemic shunting without cirrhosis
o Cirrhosis (chronic liver failure)
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
micronodular nature of onset and cause
slow onset over many years caused by alcohol
macronodular nature of onset and cause
faster onset most common cause is hep C or B
other causes include WILSON! and alpha1 antitrypsin deficiency
purpose of liver biopsy
identify if there is neoplasm
stage it and determine nature
rule out other underlying path
Tissue matching? marrow? kidney? liver? importance?
marrow - essential
kidney - importnat
Liver - fuck it off
whats primary biliary cholangitis?
autoimmune liver disease, more common in women, raised bilirubin, raise ALP
paracetamol to liver?
necrosis
fatty liver vs steatohepatitis??
Fatty liver shows no: o Ballooning degeneration o Mallory bodies o Neutrophils but steatohepatitis shows: Ballooned cells Mallory bodies Neutrophils
mortality rate of alcoholic liver disease acutely?
60%
mortality of non-alcoholic cirrhosis acutely?
0%
Pathology of alcoholic hepatitis and non-alcoholic steatohepatitis is identical but differs in severity of:
Ballooned cells
Mallory bodies
Neutrophils
number one cause of CKD?
diabetes
number 2 cause of CKD
glomerulonephritis
CKD diagnosis
Two eGFRs of less than 60ml/min/1.73m2 over a period of 90 days or more
number 3 cause of CKD
hypertension
what percentage of gluconeogenesis takes place in kidney.
25%
kidney is the only place what hormone is destroyed?
insulin - persistent insulin causes hypocalcemia
which part of kidney highly vulnerable to hypoxia?
medulla
ace inhibitors and ARBs in ckd protective or damaging?
protective, reduce renal hypertension, reducing proteinuria
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
what do you give to someone for high BP if they are under 55
Ace or ARB to protectkidney function
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
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
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
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
problem with peritoneal dialysis
may reach equilibrium as there is no semipermeable membrane between the dyalisate and blood
polycystic kidney disease inheritance type?
autosomal recessive and dominant versions. dominant more common
polycystic is mutation in which genes?
PKD1 and 2
what stage should you be thinking transplant?
transplant as an option as soon a gfr reaches 20 and then within 6 months of dialysis.
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?
what is best donation type? what are the others?
live is best, in terms of cadaveric: Brainstem death is better than CV Death
muskuloskeletal disability proportions
1 in 4 have either disability or severe disability
42% had no problems
30% aches and pains
leading cause of absence from work
neck, upper limb and back
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
why do the hips tilit
lack of strength in abductors from long sustained osteoarthritis
how many knee hip replacements and why
o 100,00 hip/knee replacement operations annually in the UK mainly for osteo
% of people over 60 who have osteo
more than half
why is obesity important in osteoarthritis
plays a hormonal role as well as a load role
when to use secondary care for OA?
primary care fails to manage pain or in doubt ab Dx
when to exercise in OA
at all stages of disease regardless of pain or severity
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)
most important part of collagen lost in oa from cartilage
aggrecan
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
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
what is aggrecan really? what makes it so key
its a proteoglycan, need to bind to water electrostatically
collagen for bone collagen for catilage
bone 1 90% cartilage 2 45-50%
osteoclast lineage
monocytic-macrophage lineage
osteoclast lifespan
o Live for around 3-4 weeks
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.
denosumab?
an antibody to osteoprotegerin used to treat osteoperosis
which bones grow by intramembranous ossification?
Skull bone, clavicle, pelvis – flat bones
cortical bone?
also known as compact, most bon is this, hard bone
trabecular bone?
spongey, cancelous bone makes up areas like joint, less of this
o Adult skeleton completely remodelled every…?
10yrs
how many bone modelling units active at one time?
o 1 million BMUs operating at any one time.
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
what T scores mean what disease?
• Osteoporosis is defined as T score
what are T scores?
density of bone compared to the mean average. 0 is a healthy young adult mean
FRAX score
online tool used to identify fracture risk, very sensitive but still some false pos/neg
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
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
why cant use raloxifene for early menopause?
what type of drug is it?
early menopause causes worse vasodilatory symptoms
oestrogen receptor modulator (like tamoxifen)
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.
teriparatide?
synthetic parathyroid hormone, shown to increase bone mass more than break down, once daily subcut for 24 months in most severe cases
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
how does having a facture influence risk of future fractures in osteoporosis?
massively inc. risk, especially with spinal as changes mechanics
• Which component of cartilage provides compressive strength
proteoglycans
in terms of bone what does BMU stand for and what is it composed of
bone multicellular unit of osteoclasts AND blasts
• What attracts osteoblast precursors to site left by osteoclasts
factors left by bone matrix
• Mechanoreceptor of bone?
osteocyte
• Community acquired infection?
less than 48hours after admission
hospital aquired infection
greater than 48hours after admission develops
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
nitrofurantoin uses?
great for community UTIs that trimethoprim cant handle but no good at pyelonephritis as cant get to higher urinary tract
most common cause organism of uti?
e.coli
diagnosis of sarcopenia made with?
bioimpedence or DEXA, bioimpedence not possible if ulcers or fluid collections
• Beta lactams cidal or static, narrow or broad?
broad, cidal
• Glycopeptides, type and names of two?
vancomycin and teicoplanin, narrow spec
vancomycin mode of giving
oral for C dif as not absorbed but iv for all else. must consider renal impairment
if it begins with C probs caused the c dif
lol
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.
• 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
• 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
• 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
how many hiv particles form per day?
a billion HIV particles each day
hiv key receptors
GP 120 and GP 41 binding to CD4 molecule which is key receptor
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
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
what is seroconversion illness?
glandular fever type symptoms you get with first HIV infection
result of attacking marrow with anti-cancer drugs
neutropenic sepsis
neutropenic sepsis key treatment
iv tazocin within 1 hour will reduce mortality by 15%
illness straight after HIV infection
seroconversion illness
proportion of hiv who get seroconversion illness
60-70%
in the UK the most common hiv opportunistic infection
caused by yeast like fungus Pneumocystis pneumonia
common neuro presentation of hiv
toxoplasma gondii, from cat faeces. more common in places where raw meet consumed
kaposis sarcoma, what causes it?
infection by herpes virus 8 and in hiv
worldwide the most common hiv opportunistic infection is
TB
is TB from hiv treated differently from normal TB?
nope
what enzymes break down lung in tB and what does it form?
metalloproteinases forming cavities
• Which of the following is an HIV related opportunistic infection?
qawd
when treating Pneumocystis pneumonia, what must you do?
abx is co-trimoxazole. give high dose steroid alongside abx to prevent inflammation damaging the lung.
PCP on x-ray shows what sign?
ground glass
neutropenic sepsis
WCC
treatment for hiv
HAART 2x NRTI (AZT, lamivudine, tenofovir, abacavir) backbone of regime then NNRTI or Intergrase inhibitor or PI like darunavir
nnrti problems?
liver toxicity
psychiatric problems
HIV pill burden?
used to be big issue, more combo drugs now
when to commence HAART for HIV?
ALL PEOPLE LIVING WITH HIV
lifespan of hiv individual if adheres to HAART?
65+
why sequence exons
• 85% of disease causing mutations are within exons as they most change protein
if denovo exome sequencing who do you sequence?
child, mum, dad
consanguinous families?
Distantly related concordantly affected individuals
what kind of words do we use to make sure everyone uses the same language about symptoms for exoming purposes?
Human phenotype ontology
o Segregation analyses ?
when a parent had a disease causing gene but didnt affect them due to protective factors, child inherits
database for exoming
clinvar
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
what happens to electrolytes in burns?
plasma sodium falls, this is an oedema
plasma potassium rises slightly from cell lysis
in 1990 what proportion of people with 50% burns survived
50% and it goes up 1% a year
jackson
Central zone of eschar: coagulation/necrosis
zone of hyperaemia
zone of stasis
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
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
types of partial thickness
superficial - most skin appendages maintained
deep
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
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
erythema and resus
dont count eretheyma or you’ll over resus
what do you resus burns with?
crystalloid as colloid makes worse
• Who to resuscitate in burns?
o Adults >15% BSA
o Childrens >10% BSA
o ? Oral resuscitation for smaller burns
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
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.
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
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%
bones and electricity
maximum electricity goes through long bones, as they get superheated heat muscles around them and get compartment syndrome
nutrition costs hosp
75% food 25% specialised nutrition - big percentage for what it is
how does temperature of body effect energy expenditure
1% inc = 13% inc
malnourished people electrolytes
K+ reduced, Na+ raised
• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity
reductive adaptation
reductive adaptation
• Reduced intake, structural and functional changes -> loss of reserve tissue and loss of functional capacity
Oedema in malnourished associated with what?
hypoalbuminemia, salt and water retention, cellular dysfunction
what guides us for nutrition
• WHO 10 steps Management of severe malnutrition
what proportion of hosp admissions are at risk of malnutrition
25-34%
est. cost malnutrition
19.6bil pound
must score step 1
BMI
• BMI >20 = 0
• BMI 18.5 -20 = 1
• BMI
must step 2
Step 2: Unplanned weight loss
• Wt loss 10% = 2
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
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)
confirm NG tube position
measure pH of secretions should be less than 5.5 if PPI then use xray
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
type of feed used in crohns and not uc
enteral
elemental feed?
predigested feed, useful in crohns for single nutrient absorption
Elemental feeding causes remission, with positive impact of growth
who is palliative care for?
people suffering from life threatening illness and their familise, psychologoical, social, physical needs, impecable pain management
how many people die of cancer around the world?
o Annually, 5 million people die of cancer around the world.
at southampton how many people will be in last year of life?
o 1 in 3 will be in their last year of life
how many will die this admission?
o 1 in 10 will die during this admission
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)
commonest life-threatening occurence in someone with cancer
hypercalcemia
vomiting centre receptors
o 5HT3, D2, mAChR, H1
outside the bbb sickness centre?
CTZ
cyclizine mechanism?
anticholinergic and antihistamine
• Levomepromazine mechanism?
broad spec antiemetic (5HT,D2,AChR,H2)
• Metoclopramide
o DA antagonist, 5HT4 agonist, central 5ht3 antagonist, prokinetic
body temperature and energy
Every 1-degree rise in body temperature increases 13% of energy expenditure.
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
patients who weigh less on discharge percentage?
70%
replaced aggressively in crohns?
vitamin D
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
how many people in a study to discover very rare ADR?
30000
how many people in study to work out common ADR?
5000
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
most common travellers complaint
Gi disease
2nd most common travellers complaint
fever
3rd most common travellers complaint
derm
A patient returning from Africa is most likely to return with what illness?
febrile
What is haem converted to before it becomes unconjugated bilirubin?
biliverdin
. What proportion of patient’s varicies bleed within 2 years of diagnosis?
25%
granulomas in liver?
weird infections and primary biliary cirrhosis, and hepatitis C
Which conditions is anti-smooth muscle Ab (SMA for?
AICAH (comes out smoothly)
At what GFR would a patient be reviewed for transplantation
less than 20 gfr
radiotherapy on localised disease
20-50%
brachytherapy?
form of radiotherapy
chemosensitive cancers
Choriocarcinoma
Testicular cancer
Leukaemia
Some lymphomas e.g. Hodgkin
woman lifetime risk of breast cancer?
1 in 8
mans lifetime risk breast cancer
1 in 868
. Approximately how many new breast cancer cases are there annually in the UK?
50000
% of breast cancers HR positive
70%
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
criteria for infective endocarditis?
modified Dukes
ECG abnormalities associated with aortic valve endocarditis?
prolonged PR interval
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
. Which pathogens likely to result in a culture negative infective endocarditis?
a. Haemophilus
b. Aggregatibacter
c. Cardiobacterium
d. Eikenella
e. k
chronic/subacute presentation of NVE abx?
amoxicillin 2g IV/4 hours
prosthetic valve endocarditis
vanco, gent, rifampicin
sepsis and multiple resistance
vanc and meropenam
resistance, penicillin allergy
vanc and gent
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
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
oral steroid associations in regnancy
pre-eclampsia, pre-term and low birth weight infants
worst asthma in pregnancy cymptoms
week 24-6
