Core conditions Flashcards
What is bronchiolitis
inflammation of the small airways
reduction in lumen size due to mucous hypersecretion, bronchospasm, inflammatory exudate
Is bronchiolitis largely bacterial, viral or fungal?
Which pathogen accounts for 80% of cases
90% of children affected are aged?
viral
RSV (respiratory syncitial virus)
1-9 months old
Clinical features of bronchiolitis
- coryza initially
- end-inspiratory crackles
- dry cough
- wheeze
- breathing difficulties
- recessions (intercostal, subcostal, sternal)
- poor fedding
- nasal flaring
how is bronciolitis diagnosed?
clinically
measure pulse oximetry
blood gas
CXR if concerned about respiratory failure
after how long does the severity of bronchiolitis peak?
under what conditions would you admit someone with bronchiolitis? (2)
3/4/5 days
admit if needing:
- breathing support
- feeding support
Describe the management of bronchiolitis
supportive
- humidified oxygen— 2L nasal canula
- CPAP (Continuous positive airway pressure) - if ventilation required
- Feeding support- NG feeds or Iv fluids
What is Croup
most commonly caused b y what kind of virus
What is the difference between croup and bronhiolitis
viral laryngotracheobronchiolitis
parainfluenza viruses (rhinovirus, RSV, influenza)
croup targets the upper respiratory tract while bronchiolitis targets the lower respiratory tract
what is the standard age range for croup
6 months to 6 years (peak age 2)
clinical featrues of croup
coryza and fever
hoarseness
barking cough (worse at night)
stridor
variable SOB
management of croup
- observe
- oral or nebularised steroids
for a seveere upper airway obstruction (nebularised adrenaline and oxygen)
Acute epiglotitis is caused by which pathogen?
what is epiglotitis?
Why is epiglotits an emergency?
epiglotitis is caused by H. Influenzae B
intense swelling of the epiglottis and sepsis
presentation of epiglotitis
incidence is reduced by 99% due to what
- high grade fever
- unwell looking child
- drooling
- no cough
- soft stridor
universal vaccination
Constipation what is it
infrequent passing of dry, hardened stool
associated with straining, pain or bleeding
what numbers does the bristol stool chart range
type 1 on the Bristol stool chart
describe a poo at the highest stage
1—->7
1= hard rabbit droppings
stage 7- wet like gravy
clinical features of constipation
management for constipation
- infrequent bowel movements
- straining
- abdominal pain
- loss of appetite
encourage fluids
encourage healthy, fibre rich diet
toileting routine
what are the 4 types of laxative
- Bulk forming laxatives
- osmotic laxatives- magnesuim hydroxide
- disaccharides and alditols- lactulose
- Emollients (hydrating)- parafin oil, docusate sodium
- Stimulant laxatives- senna
Red flags in paeds. What is each suggestive of?
- failure to pass meconium in 24 hours of life
- faultering growth
- abnormal limb neurology/ deformity
- scaral dimple over natal cleft
- perianal bruising
- hirschrpung’s disease
- hypothyroidism, coeliac disease
- lumbrosacral pathology
- spina bifida occulta
- sexual abuse
Iron deifiency
presentation
causes
- fatigue
- slow feeding
- pica
- pallor
- inadequate intake– diet, growth spurt
- malabsorption- coeliac disease
- blood loss- menstruation, meckel’s diverticulum
investigation for iron deficiency
management of iron deficiency
FBC— Hb and MCV decreases,,,, look for microcytic cells
look for derceased serum ferritin
management
iron supplementation
dietary advice- iron rich foods, vitamin C
ITP- immune thrombocytic cytopaenia
which kind of cell is destroyed? How are they destroyed?
presentation of ITP
platelets are destroyed by autoantibodies
presentation
- usually children aged 2-10
- 1-2 weeks after viral infection
- petechiae, purpura, superficial bruising
- epistaxis (nose bleed)
- uncommon to get profuse bleeding
how is ITP diagnosed?
investigations
treatment of ITP
diagnosis of exclusion
investigations
- FBC- look for low platelets
- blood film
- bone marrow biopsy
treatment of ITP
Observation. Self resolves in 6-8 weeks
may need steroids or IV Ig
cystic fibrosis
inheritance pattern
what protein does it affect? what is that protein’s function? what happens without it
autosomal recessive condition
(therefore if Xx and Xx have 4 kids; 1 will be affected xx, 2 will be carriers Xx and one will be free of it XX)
it affects the CFTR protein (membrane chloride channel). It carries out sodium transportation. A dysfuncitonal channel will produce thickened, sticky secretions
Presentation of Cystic fibrosis in neonates and children
since introduction of the heel prick test, most cases are picked up via screening
neonates- meconium ileus
children- frequent infection, failure to thrive, wheeze, cough, steatorrhoea
Which conditions are commonly present with Cystic fibrosis?
- sinusitis
- pancreatitis
- diabetes
- fertility
investigations for CF
management in CF
- heel prick test
- sweat test- high chloride
- genetic testing for mutations (change in F508)
lifelong MDT aproach
- Resp: mucolytics, prophylactic antibiotics, chest physio, vaccines
- GI: annual OGTT, creon replacement
- Targeted: Ivacaftor/ lumacaftor
Coeliac disease pathophysiology
gliadin + glutenin =
presentation of coeliac disease
- gluten broken down to gliadin and glutenin. Gliadin causes damaging immune response in proximal small intestinal mucosa
- gliadin + glutenin = gluten
presentation of coeliac disease
classical presentation vvvv
- malabsorption at 8-24 after weaning
- faltyering growth and buttock wasting
- abdominal pain and distension
- abnormal stools
- dermatitis herpetiformis ( scalp, shoulders, buttocks, elbows and knees)
Non specific GI symptoms
Anaemia (iron and/or folate deficiency)
investigations for coeliac disease
management
1) bloods- serological screening tests
- Anti-tTG (immunoglobulin A tissue transaminase antibodies)
- EMA (endomysial antibodies)
2) biopsy- mucosal changes of the small intestine (villous atrophy, flattened villi, crypt hyperlasia, lymphocyte infiltration)
management for coeliac disease
gluten free diet under dietician supervision
What is meningitis?
Caused more by bacteria or viruses? Which one has more severe consequences?
Presentation?
- inflammation of the meninges
- most commonly viral but bacterial more severe
presentation
- fever
- headache
- vomitig/ poor feeding
- drowsiness
- photophobia
- hypotonia
- seizures
examination findings of meningitis
- purpuric rash (meningococcal disease)
- neck stiffness
- bulging fontanelle (division on superior aspect of infants skull)
- back arching
- Brudzinki + kernig sign positive
- shock
- Altered conscious level
- focal neurology
Common casuative agents of meningitis at different ages
bacterial
- neonates
- 1 mo-6 years
- >6 years
viral
Neonates
- group B streptococcus
- Listeria monocytogenes
- E. Coli
1 mo- 6 years
- Neisseria meningitides
- Streptococcus pneumoniae
- Haemophilus influenzae
Over 6 years
- Neisseria meningitides
- Streptococcus pneumoniae
Viral causes of meningitis
Enteroviruses, Epstein- barr virus (EBV), adenovirus, mumps
investigation for meningitis
- FBC, CRP
- coag + U and E’s
- LFTs
- Blood glucose
- Blood gas
- Blood cultures
- Viral PCR
- Lumbar puncture
- Appearance
- WBCs
- Protein content
- Glucose content
Of csf of someone with normal health, bacterial and viral infection
Normal
Appx: clear
WBCs: 0-5/mm3
Protein: 0.15-0.5g/L
Glucose: >50% of blood
Bacterial
Appx: turbid
WBCs: large increase in polymorphs
Protein: large increase
Glucose: large increase
Viral
Appx: clear
WBCs: increase lymphocytes
Protein: normal/ raised
Glucose: normal / decreased
management of meningitis
IV antibiotics- usually cephalosporin
Dexamethosone in bacterial infections over 3 months
supportive therapy- e.g,. fluids, oxygen
What is gastro-oesophageal reflux disease
if it causes significant problems whay is it called
involunatry passage of stomach contents into the oesophagus
common in infancy and is usually benign and self limiting
its called GORD if it causes dysfunction
presentation of infants and older chidlren with reflux disease
infants:
- recurrent vomiting or regurgitation after feeds
- discomfort lying flat after feeds
- usually well and normal growth
older children:
- heartburn
- epigastric pain
- vomiting
How is reflux disease diagnmosed?
relfux disease has a higher prevalence in children with
management
diagnosed clinically with no need for investigations
higher incidence in cerebral palsy or neurodevelopmental disease
management
- reassurance- usually resolves by age 1
- feeding assessment
- smaller, more frequent feeding
- feed thickeners
- alginate therapy (gaviscon)
- 4 week trial of PPI or H2 receptor antagonist
What is appendicitis
presentation
inflammation of the appendix
Presentation
Symptoms:
- abdominal pain (initially central and collicky, later localises to RIF)
- anorexia
- vomiting
Signs:
- Fever
- Pain aggravated by movement
- Tenderness and guarding in RIF (mcBurney’s point)
If unwell abnormal observations, high temperature—— perforation?
investigations for appendicits
Complications of appendicitis
Management
Investigations
- Full blood count- increase WCC
- CRP
- Ultrasound scan
Complications
- Perforation
- Sepsis
- Abscess
- Appendiceal mass
Management
- Monitor observations
- Analgesia
- Fluid rescusitation and IV antibiotics (if unwell/ concerns of perforation)
- Appendicectomy
What is pyloric stenosis?
When does presentation occur? What is the presentation?
More common in?
Hypertrophy of pyloric musclce causing gastric outlet obstruction
presentation
- projectile vomiting
- gradually increases in frequency and forcefulness
- hunger after vomiting
- weight loss
more common in
- males
- first born child
- those with family history
Assessment of pyloric stenosis
test feed
- Gastric peristalsis- wave moving from left to right
- Pyloric mass- olive shaoed mass in RUQ
Capillary blood gas
- Hypochloraemic metabolic potassium
- Low sodium and potassium
Ultrasound scan
Management of pyloric stenosis
- rehydration
- correct electrolyte imbalances
- Pylomyotomy
Pneumonia
presentation
examination
Pneumonia
Presentation
- Fever
- cough
- increased work of breathing
- tachypnoea
- lethargy
- poor feeding
Examination
- Tachypnoea
- coarse crackles
- reduced oxygen saturations
- nasal flaring
- recessions
pneumonia
investigations (3)
management (2)
admit if: (3)
investigations
CXR- may confirm diagnosis
NPA aspirate for viral PCR
Bloods generally unhelpful
Management
- antibiotics- amoxicillin or clarithromycin
- supportive care- oxygen, fluids
Admit if:
- Oxygen sats >92%
- Apnoeas/ grunting
- Unable to maintain fluid intake
Causative agents of pneumonia
- newborn
- infantsa nd young children
- children over 5
Newborn causative agents pneumonia:
Bacteria——- (group B strep) + (gram negative enterococci)
Viruses and young children:
Viruses——– (RSV, Adenovirus, Rhinovirus, Influenza)
Bacteria——- (strep pneumoniae, H. Influenzae, chlamydia trochamatis)
Children over 5 years:
Bacteria ——( mycoplasma pneumoniae, strep pneu., chlamydia pneu.)
Anaphylaxis what is it
Presentation
anaphylaxis is a severe life-threatening systemic hypersensitivity reaction
Presentation
- Sudden onset and rapidly progressing
- Angioedema
- stridor
- wheeze
- tachypnoea
- tachycardia
- shock
- vomiting
- urticaria (hives- red, itchy welts that result from a skin reaction)
- collapse
Anaphylaxis
acute management (7)
Acute anaphylaxis management
- ABCDE approach
- Adrenaline 1:10000
- Oxygen
- Nebulisers
- fluid bolus
- hydrocortisone
- chlorphenamine
What is otitis media
which age group is it most frequent in? Why compared to adults?
what usually precedes OM?
inflammation of the middle ear
most common in infants. this is becasue the eustachian tube is:
- shorter
- horizontal
- functions poorly
a URTI usually precedes OM
presentation of OM
On examination
common causative agents of OM: viral and bacterial
Presentation of OM
- fever
- ear pain
- hearing loss
- loss of appetite
- generally unwell
On examination
- erythema
- bulging tympanic membrane
- loss of light reflex
- perforation
- effusion
Common causative agents of OM:
- Viral- RSV, Rhinovirus
- Bacterial- strep pneumonia, haemophilus influenza, moraxella catarrhalis
Management of OM (3)
what is glue ear and how is it treated
management of OM
- reassurance usually self resolves in 3-5 days
- analgesia and fluids
- antibiotics usually not required- can be given if not resolving
glue ear
-“recurrent ear infections can lead to OM with effusions”
Hearing loss and resultant developmental delay
may be treated with grommets
Label which ones are normal, Acute otitis media and OM with effusions
Urinary tract infections
presentation- infants and children
UTI presentations
Infants
- fever
- vomiting
- lethargy
- poor feeding
- irritability
Older children
- fever
- dysuria
- increased frequency
- abdominal pain
- vomitinng
- incontinence
Initial investigations for a UTI (2)
if there is good clinical evidence and patient is under 3 months what should you do?
initial investigatiuons for UTI
- urinalysis (if nitrites present start abx, if only leukocytes send for culture)
- urine culture and sensitivity (E.coli and krebsiella)
- no need for further investigations unless concerns of sepsis
start antibiotics
antibiotics for UTI
- upper UTI, prophylaxis
- lower uti
- under months
Further investigationsn for uti (3)
upper UTI, prophylaxis- cefalexin ot Co-amoxiclav
lower UTI- trimeythoprim
under 3 months- IV antibiotics
further investigations for UTI-
- renal USS
- micturating cystorethrogram (MCUG)
- DMSA scan
wheeze
what is it
inspiratory?
what does it indicate?
what can cause a wheeze?
wheeze- high pitched whistling sound, musical like quality
usually heard on expiration
indicates a narrowed airway
what can cause a wheeze?
- asthma
- bronchiolitis
- viruses
- foreign body aspiration
- structural abnormalities
- congenital heart defects
- GOERD
Treatment for wheeze? (3)
age based approach to diagnosing cause of wheeze
what does absence of wheeze suggest in acute asthma?
treatment for wheeze
- 02 as needed
- SABA
- if the patient doesnt respond to SABA ask why
age based approach to diagnosing cause of wheeze
impending resp failure
Asthma-
diagnosis (4)
acute management
long term management
general management strategies
Diagnosis:
- Episodic symptoms
- Wheeze confirmed by HCA
- Diurnal variability
- Atopic history
- Nothing suggesting alternate diagnosis
Acute management
- Oxygen
- Salbutamol + ICS
- Ipatropium (anticholinergic)
- Call for help + cardiac monitoring
- Aminphylline + salbutamol + Mg Sulphate
Long term management
SABA reliever “blue” PRN up to 10 puffs per 4 hours
”+ ICS brown preventer- budesonide
”+ LABA (e.g., salmeterol). if this fails stop and increase ICS
”+ LTRA (leukotriene receptor antagonist) like monteleukast (at this stage you have SABA,ICS, LABA, LTRA)
General management strategies
- assess symptoms, measure lug function, check inhaler technique and adherence
- adjust dose to find minimum effective
- update self-management plan
- move up and down medication ladder as required
how do you differentiate between causes of wheeze?
Onest of symptoms
a) gradual onset of wheeze in late infancy or early childhood
1ai) regular daily wheeze symptoms?—-
1ai. )improves with salbutamol?
yes- asthma
no- bacterial bronchitis?
1aii) intermittent episodes- interval symptoms (e.g, regular cough/ wheeze at night or after exercise?
yes- improve w salbutamol? (y- asthma n-bacterial bronchitis)
no- recurrent viral induced wheeze
b) sudden onset of coryzal symptoms
1bi) yes- suspect viral lrti like bronchiolitis or viral penumonitis
1bii) no- think inhaled foreign body
how can you tell the difference between asthma and viral induced wheeze?
children w viral induced wheeze are well between flare ups while children with asthma are not
what is viral induced wheeze
when do children usually grow out of it
Wheezing due to viral-induced wheeze or acute viral-induced asthma is caused by narrowing of the airways due to mucus production and bronchoconstriction.
grow out of it by 6 when their immunity develops
common causative agents of V.I.W. (5)
presentation of VIW
- severe
- life threatening
- RSV
- Rhinovirus
- coronaviruses
- parainfluenza
- influenza
Presentation of VIW
- severe- SpO2 >92%
- Too breathless to feed or talk
- HR >125 ( over 5’s) or >140 (under 5’s)
- Use of accessory muscles
Life threatening
- silent chest
- poor respiratory effort
- altered consciousness
- agitation/ confusion
- exhaustion
- cyanosis
difference between bronchiolitis and VIW
age
- bronchiolitis- <12 months old
- VIW 1-5 years
what kind of disease is type 1 diabetes mellitus
what protein is lacking
presentation:
- Autoimmune endocrine disorder
- insulin lack
presentation:
- hyperglycaemia (frequent urination, increased thirst, blurred vision, fatigue, headache)
- Polydipsia (extreme thirst)
- polyuria (lots of weeing)
- polyphagia (extreme hunger)
- weight loss
- abdo pain (Diabetic ketoacidosis)
management of T1DM
What 2 things do you teach to a T1DM patient?
What is a BM range? and what should a normal range be?
management
- lifelong insulin replacement
- regular blood sugar checks
- screen for complications and compliance
Teach
- how to treat hypos
- sick day rules
Bm range” outdated” but refers to your blood glucose level.
Normal range 4-7
HYPOglycaemia symptoms
HYPERglycaemia symptoms
what is of concern in adolescent patients
HYPO symptoms
- Sweating
- Pallor
- Irritibility
- Hunger
- Lack of co-ordination
- Sleepiness
HYPER symptoms
- Dry mouth
- Increased thirst
- Weakness
- headache
- blurred vision
- frequent urination
compliance is an issue
Diabetic ketoacidosis
presentation
3 changes to blood in DKA
presentation
- dehydration
- shock
- abdominal pain
- drowsiness
- acidotic respirations
3 changes to blood in DKA
- ketonaemia
- hyperglycaemia
- acidaemia
diabetic ketoacidosis
treatment
complications of DKA
treatment
- ABCDEFG-appraoch Don’t Ever Forget Glucose
- Complex and requires 1:1 nursing + senior support
- combination of fluids, insulin and postassium
Complications
- hypokalaemia
- cerebral oedema
- hypoglycaemia
- VTE
how does insufficient insulin lead to ketoacidosis?
- insuficient insulin
- gluocse can’t enter cells
- need for alternative energy source
- muscle cells broken down to amino acids (gluconeogenesis)
- fat cell- glycerol (gluconeogenesis) and fatty acids (converted to ketones)
- increased glucagon converted to ketones
gastroenteritis
most common cause in developed countries and during which seasons
presentation
its important to assess
management
commonest casuative agent- rotavirus
presentation
- diarrhoea
- vomiting
- fever
- poor feeding
- shock
assess hydration
management
- oral rehydration or IV fluid replacement
gastroenteritis
most common viral causes
bacterial
protozoan
Investigations
viral
- rotavirus
- adenovirus
- norovirus
- astrovirus
bacterial
- Campylobavter
- shigella
- salmonella
- E.coli
Protozoa
- Giardia
- crytposporidium
Investigations:
- stool culture (if septic or blood in stools)
- U+E’s if IV fluids required
- Glucose
- Blood culture (if satrted on antibiotics)
Shock presentation
- reduced consciousness
- decreased Urinary output
- pale or mottled
- cool peripheries
- dry mucous membranes
- prolonged cap refill
- sunken eyes
- tachycardia
- hypotension
- tachypneoa
- what is Henoch- Schlonlein purpura
- what is it usually triggered by
- What does PPP stand for
immune mediated disorder causing inflammation of small blood vessels, IgA mediated vasculitis
usually triggered by a viral URTI
Painful Palpable Purpura
presentation of henoch-schonlein purpura
most commonly affects which aged children
presentation of henoch-schonlein purpura
- non-blanching rash (100%) found on the buttocks and extensor surfaces of legs and arms
- painful swollen joints
- abdominal pain
- haematauria
most commonly affects 2-10 year olds
- investigations to rule out other pathologies and measure extent of organ failure (4)*
- management*
- 2% Of HSP patients develop:*
investigations
- FBC
- CRP
- Blood cultures
- U+Es
Management of HSP
- Usually self resolves within 6 weeks
- simple analgesia
- steroids are sometimes used for joint pain
2% of HSP patients develop renal failure
4 go to causes of paediatric limp
- transient synovitis “irritible hip syndrome”
- septic arthritis
- Perthe’s disease
- Slipped capital femiral epiphysis
Transient synovitis “irritible hip syndrome”
- how common of a problem is it
- associated with what kind of infection
- sudden onset symptoms (2)
- pain at rest?
- affect on ROM?
- how long does it take to resolve?
- average age of affect
Transient synovitis “irritible hip syndrome”
- most common cause of hip pain in children
- associated with viral infection
- sudden onset hip pain or limp
- no pain at rest
- reduced ROM, internal rotation hurts
- resolves itself within 1 week
- age of affect- 2-12
septic arthritis
presentation
investigations
treatment
most common in what age group
presentation
- red
- hot
- painful joint
- reduced ROM
Investigations
- FBC, CRP, ESR
- blood cultures
- joint aspirate
- Xray
Treatment
- Antibiotics +/- surgical washout
Most common in the under 2s
Limp
- What is Perthe’s disease
- pathophysiology
- affects which group of people most
- management
Limp
Perthe’s disease-“avascular necrosis of capital femoral epiphysis”
Pathophysiology
- Occurs due to interruption of blood supply, followed by revascularisation and reossification over 18-36 months
Mainly affects boys + 5-10 year olds
Management- rest, physio, casts and sometimes surgery
Limp
- What is a slipped capital femoral epiphysis?
- most common at which ages
- commonly occurs during which process
- increased risk with…?
- which movements are restricted
- management
- should be treated promptly to prevent…?
- Slipped capital femoral epiphysis- “displacement of epiphysis of femoral head postero-inferiorly
- 10-15 years
- common during adolescent growth spurt
- increased risk in obese patients
- restricted abduction and internal rotation
- surgical management
- should be treated promptly to prevent avascular necrosis
Leukaemia is a cancer of which cells
how common is leukaemia
presentation (7)
white blood cells
most common cancer in children
presentation
- lethargy
- pallor
- generally unwell
- non-blanching rash
- frequent infections
- lymphaednopathy
- hepatosplenomegaly
leukaemia
investigations
peak age for incidence
80% of leukaemias in children are
investigations
- FBC
- Blood film
- bone marrow arpirate/ biopsy
- lumbar puncture
incidence peaks at age 2-3 years
ALL most common childhood leukaemia
inflammatory bowel disease
a quarter of IBD cases present at which stage of life
IBD includes 2 distinct diseases, what are they?
What are the differences between these 2
presentation
- childhood
- IBD= crohn’s + IBD
- Crohn’s disease- affects any part of the GI tract from mouth to anus. Diffuse pattern of affect. Transmural. Non-caseating granulomata
- Ulcerative colitis- confined to the colon. Continuous inflammation. Damage limited to mucosa. Mucosal inflammtaiton and crypt cell damage..
Presentation of IBD:
- Abdominal pain
- diarrhoea
- failure to thrive
- weight loss
- delayed puberty
- extra-intestinal manifestations: oral lesions, uveitis (looks like red eye), arthralgia, erythema nodosum
Investigations for IBD
management for Crohn’s
management for Ulcerative colitis
Investigations for IBD
- FBC
- CRP and ESR
- foecal elastase
- biopsy
management for Crohn’s
- nutritional therapy
- systemic steroids
- immunosupressants
- anti-TNF (infliximab)
management for Ulcerative colitis
- aminosalicylates
- topical or systemic steroids
- immunosupressants
Paediatric normal values- <1 year
HR/ min
RR/ min
Systolic BP
Paediatric normal values- <1 year
HR/ min- 110-160
RR/ min- 30-40
Systolic BP- 70-90
Paediatric normal values- 1-2 years
HR/ min
RR/ min
Systolic BP
Paediatric normal values- 1-2 years
HR/ min- 100-150
RR/ min- 25-35
Systolic BP- 80-95
Paediatric normal values- 2-5 years
HR/ min
RR/ min
Systolic BP
Paediatric normal values- 2-5 years
HR/ min- 95-140
RR/ min- 25-30
Systolic BP- 80-100
Paediatric normal values- 5-12 years
HR/ min
RR/ min
Systolic BP
Paediatric normal values- 5-12 years
HR/ min- 80-120
RR/ min- 20-25
Systolic BP- 90-110
Paediatric normal values- over 12 years
HR/ min
RR/ min
Systolic BP
Paediatric normal values- over 12 years
HR/ min- 60-100
RR/ min- 15-20
Systolic BP- 100-120
General trends in paediatric vital signs with increasing age
Heart rate
Respiratory rate
Systolic blood pressure
as age increases:
HR- decreases
Respiratory rate- decreases
Systolic blood pressure- increases
