SPOPs Pathophysiology Flashcards
Pre-Eclampsia Pathophysiology
defective spiral artery remodelling causing placental hpoperfusion
diseased placenta releases proinflammatory proteins into maternal circulation
inflammatory markers attack endothelial cells
systemic vasoconstriction and endothelial dysfunction
hypertension and end-organ damage
HELLP Pathophysiology
believed to be an immunological response caused when maternal cells come into contact with a genetically distinct fetus
Breech Delivery Pathophysiology
foetus has not turned into normal cephalic presentation
head emerges last and can become entrapped as cervix not fully dialated
can result in foetal asphyxiation and death
Primary PPH Pathophysiology
During pregnancy the maternal blood volume increases by approx 50%
greater increase in plasma volume relative to RBC’s, leading to a fall in haemoglobin concentration and haematocrit
estimated blood flow at term to the uterus is 500-800 ml/min (10-15% of cardiac output), with most traversing the placental bed
failure of the uterine myometrial fibres to contract and retract with resultant continuation of bleeding
Pathophysiology of post delivery uterine contractions.
uterine vessels supplying placental site traverse a weave of myometrial fibres which contract after birth resulting in myometrial retraction. This results in the uterine blood vessels becoming compressed and kinked, occluding blood flow.
Pathophysiology of Secondary PPH
infection resulting from retained piece of placenta or membrane, causing a failure of uterine contraction and retraction
Croup Pathophysiology
virus causes swelling of the larynx and trachea causing the airways to narrow and breathing to become more difficult
RSV Pathophysiology
starts as an upper respiratory infection, with familiar cold symptoms
has ability to quickly spread down from the nose and throat into the lower respiratory tract
it infects and causes inflammation in the tissues of the lungs (causing pneumonia) and the tiny bronchial air tubes (causing bronchiolitis)
Bronchiolitis Pathophysiology
inflammation of the lining of the epithelial cells of the bronchioles causing mucus production, inflammation and cellular necrosis
these cells can then obstruct the airway cause wheezing
Pathophysiology of Asthma
The smooth muscles of bronchials are exposed to an antigen
Mast cells within the lung degranulate, spilling their contents which initiates an inflammatory mediated response causing bronchial smooth muscle constriction, mucosal oedema and mucosal plugging from thick tenacious fluid
Pathophysiology of Sepsis
inflammatory stimulus (eg, a bacterial toxin) triggers production of proinflammatory mediators
mediators cause neutrophil–endothelial cell adhesion, activate the clotting mechanism
and generate microthrombi
microthrombi opposed by anti-inflammatory mediators, causing a negative feedback mechanism
arteries and arterioles dilate, decreasing peripheral arterial resistance and cardiac output increases (Initial stages of shock)
Pathophysiology of Septic Shock
sepsis not treated
cardiac output decreases, BP falls (with or without an increase in
peripheral resistance) causing typical features of shock
Vasoactive mediators cause blood flow to bypass capillary exchange vessels (a distributive defect)
Poor capillary flow from this shunting and capillary obstruction by microthrombi decreases oxygen delivery, impairing removal of carbon dioxide and waste products
Decreased perfusion causes dysfunction and sometimes failure of one or more organs, including the kidneys, lungs, liver, brain, and heart
Lanugo
fine hair
Vernix
white coating thought to protect skin whilst in tummy
Fertilisation Steps
200 - 500 million sperm enter vagina
acid in vaginal kills all but a few hundred
sperm travel through vagina, cervix, uterus and fallopian tube
sperm try to attach to the egg’s zona palucida
egg snaps shut to stop sperm entering
zygote froms from chromosomes and DNA
baby formed
Pronuclei
formed by fusion of egg and sperm
Cleavage
zygote divides into 2, 4 then 8 cells
Morula
zygote with 16 cells
Blastocyst
has embryoblast and trophoblast cells
Placental Formation
Blastocyst implants into uterine wall
trophoblast invade endometrial lining for baby to get nutrients
special glands secrete glucose
placenta starts at 8-12 weeks
Aim of Physiological Changes During Pregnancy
maximise nutrition and oxygen to the developing fetus and help the maternal system adjust to the extra stress and demands of pregnancy to:
support foetus
protect foetus
prepare uterus for lablour
protect mother from cardiovascular injury at delivery
Human Chorionic Gonadotrophin (HcG)
Detected in blood 9 days and in urine 10-12 days after fertilisation
Linked to maternal changes in first trimester
causes nausea and vomiting in first trimester
changes to smell, taste, saliva
Prevents degeneration of the corpus luteum and stimulates production of oestrogen and progesterone until placenta takes over
Oestrogen Function During Pregnancy
Produced by corpus luteum, until the placenta takes over
Stimulates growth of tissues including vascularisation of the uterus
Causes swelling and softening of connective tissues (cervix, nipples, ligaments) by increasing water content in extracellular mix
Increased fluid retention
Later in pregnancy can block insulin and affect glucose uptake
Progesterone Function During Pregnancy
Secreted by the corpus luteum until the placenta takes over
thickens and nourish the uterus walls
Uterotonic inhibitor – lowers smooth muscle excitability to prevent uterine contractions, not only in the uterus but, in the ureters, stomach, and intestines
Increases the sensitivity of the maternal chemoreceptors to carbon dioxide, stimulatingventilation at lower atrial pressures
inhibits lactation during pregnancy
Prolactin Function During Pregnancy
inhibits lactation during pregnancy
enlarges mammary glands and prepares them for milk production
produces breast milk
Relaxin Function During Pregnancy
inhibits uterus contraction to prevent premature birth
relaxes blood vessles, increasing blood flow to placenta and kidneys
relaxes joints of the pelvis
softens and lengthens cervix during birth
Oxytoxin Function During Pregnancy
stimulates contraction of uterus muscles during labour
triggers production of prostaglandins to increase contractions
can be used to induce labour
Uterus Changes During Pregnancy
uterus leaves the pelvis and ascends into the abdominal cavity
uterus can grow up to 5 times its normal size
abdominal contents become displaced
fundus increases in size until 38 weeks and then descends in preparation for delivery
Uterus blood flow increases from 50mL/min at 10 weeks to 500mL/min at term
Cervix Changes Druing Pregnancy
mucous glands secrete operculum (mucous plug) which seals the uterus and protects from infection
Vaginal Changes During Pregnancy
blood supply increases due to uterus and embryo demands
blood causes colour changes in the vulva leading to a bluish discoloration
feeling of fullness and heaviness
increased discharge
Musculoskeletal Postural Changes During Pregnancy
equilibrium of the spine and pelvis
centre of gravity no longer falls over the feet
need to lean backwards to gain equilibrium resulting in disorganisation of spinal curves
Musculoskeletal Muscle Changes During Pregnancy
alterations in collagen metabolism due to altered levels of relaxin, oestrogen and progesterone
connective tissue more pliable and laxative
reduced joint stability especially in symphysis pubis and sacroiliac joints
elongation of abdominal muscles can cause pelvic girdle pain and linea alba (abdominal separation)
Haematological Changes During Pregnancy
major alteration to blood composition to protect against:
normal blood loss during delivery (round 500ml)
maintain cardiac output despite widespread vasodilation
promote rapid haemostasis during placental separation
bacterial infection
Haemodilution
blood volume increase by 30-40% (approx. 1500mL) between 7 and 34 weeks
plasma increases at a faster rate than other cellular components
plasma increase begins around 7 weeks, rapidly during second trimester, reaching 40-50% by 32 weeks
RBC volume increases slower, reaching 2-30% increase
RBC increase is less than the total plasma increase = physiological aneamia
blood viscosity reduced by 20% which decreases heart’s workload
haemoglobin concentration falls due to haemodilution - can be concern due to increased iron requirements
WBC (neutrophil) increases to protect against bacterial infections
hypercoagulability due to increase in clotting factors incl fibrinogen
Cardiovascular Changes During Pregnancy
progesterone decreases BP causing decreased systemic vascular resistance
cardiac output increases by 30 – 50% peaking in 3rd trimester due to increased blood volume
HR increases 15% and stroke volume 30%
IVC compression at later stages (25-30% drop in CO lying supine)
can all lead to dizziness, light headedness, palpitations, decreased exercise tolerance.
Respiratory Changes During Pregnancy
changes in ventilation due to:
BMR increase causes increased oxygen consumption (20%)
progesterone increases sensitivity of chemoreceptors to CO2 and leads to 40% ventilation increase
40% increase in tidal volume by end of first trimester (from 500ml – 700ml)
35-45% decrease in chest wall compliance, decreasing functional residual capacity (FRC) and residual volume (RV)
Progesterone production enhances response to hypercapnia and water retention
Gastrointestinal Changes During Pregnancy
progesterone relaxes muscles decreasing GI motility and lower oesophageal sphincter tone causing:
reflux
nausea and vomiting
constipation
Renal Changes During Pregnancy
Systemic vasodilation early in pregnancy increases renal plasma volume and GFR
dilation of the kidney’s collecting system causes retention of electrolytes necessary for foetal growth limiting proteins, glucose and amino acids in urine
increase in total body sodium increases plasma volume
progesterone dilates kidneys and potentially kinks the ureters from 10 weeks and can cause urinary stasis and increased risk of infection
Integumentary Changes During Pregnancy
Melanocyte stimulating hormone increases and causes deeper pigmentation of the skin leading to:
patchy mask on the face (chloasma)
pigmented line on the abdomen from the pubis to the umbilicus (linea niagra)
Areola darken and toughen up
Stretch marks in the collagen layer of the skin causing red stripes (stria gravidarum)
Hyperemesis Gravidarum (HG)
Onset 6 – 8 weeks and in some settles around 21 weeks, others until full term
causes chronic dehydration and malnutrition and can lead to excessive weight loss
if Pts don’t receive aggressive and consistent management they are at extreme risk of:
loss of > 5-10% of pre-pregnancy body weight
dehydration and production of ketones
nutritional deficiencies
metabolic imbalances
severe fatigue and debility
depression/anxiety and trauma
premature labour/delivery
Morning Sickness (NVP)
usually begin at 6 – 8 weeks, peaking at 9 weeks and settles at 14 weeks
lose little if any, weight
don’t impact ability to eat/drink normally
vomit infrequently and the nausea is episodic but not severe or constant
diet or lifestyle changes are enough most of the time
typically improve after first trimester, but may have brief period of it later in pregnancy
still able to work most days and fulfill normal life duties
Role of oxytocin during labour
love hormone
causes feelings of euphoria
helps uterine contractions
helps bonding with baby
responsible for milk ejection
Role of prolactin during labour
the ‘mothering’ hormone
major hormone of breastfeeding
may play a role in helping baby
adjust to life outside the womb
peaks at the start of labour
Role of endorphins during labour
causes feelings of euphoria
natural pain relief
increased with feelings of love
works on same area of our brain as morphine and heroin
Role of adrenaline during labour
fight or flight response
initially slows labour, natural reaction to birth
gives sudden rush of energy before delivery
Role of melatonin during labour
improves and initates oxytoxin function to work more effectively
makesg contractions longer and labour quicker
higher levels at night - why more labour at night
Respiratory Distress Syndrome (RDS) Pathophysiology
surfactant deficiency, especially in immature lungs which increases the surface tension in small airways and alveoli, reducing the lungs compliance
What effect does Asthma have?
Decreased flow rates and reduced gas exchange
Air gets into lungs due to decreased intrapulmonary pressure on inspiration, but struggles to get out on expiration due to the increased pressures and further narrowing
Lung stretch receptors sense hyperinflation and trigger hyperventilation
More air is trapped and CO2 builds up
Decrease in alveoli perfusion
Intrathoracic pressure impedes venous return
Asthma Mortality
rare
3 major contributing factors of severity, management and psychological factors
Stages of Cognitive Development
Stage 1 - Sensorimotor Period
Stage 2 - Preoperational Period
Stage 3 - Concrete Operational Period
Stage 4 - Formal Operational Period
Paget’s Stage 1 Sensorimotor Period
Birth to 2 years
coordination of sensory input and motor responses
development of object permanence
Paget’s Stage 2 Preoperational Period
2 to 7 years
development of symbolic thought marked by irreversibility, centration, and egocentrism
Paget’s Stage 3 Concrete Operational Period
7 - 11 years
Mental operations applied to concrete events
mastery of conservation, hierarchical classification
Paget’s Stage 4 Formal Operational Period
11 through to adulthood
Mental operations applied to abstract ideas; logical, systematic thinking
Neurological Differences in Paediatric Patients
Undeveloped temperature regulation
Large head in relation to body size
(More susceptible to head injuries)
Incomplete motor development
(Increased risk of falls)
Thinner cranial bones
(increased risk of head trauma)
Presence of fontanelles at birth
(Anterior fontanelle closes 12-18months, Posterior closes 2-3 months)
(Neonates and infants increased risk of hypothermia)
Anatomical Respiratory Differences in Paediatric Patients
Narrower airways
Large tongue with smaller mouth|
(Greater risk of obstructions)
Soft cricoid cartiledge
(External pressures can obstruct airway)
Larynx is higher and more anterior
(More difficult airway management)
Trachea is soft and compressible and smaller in diameter
(Hyperextension or hyperflexion of neck can fully compress airway and difficult airway management)
(Greater risk of obstructions -Swelling (inhalation burns, croup etc), -Foreign bodies, -Nasal mucous (RSV))
Physiologicaly Respiratory Differences in Paediatric Patients
Higher basal metabolic rate
Smaller and fewer alveoli
(Smaller area for gas exchange and increased dead space - must breathe faster to achieve adequate minute ventilation)
Infants are obligatory nasal breathers
(partially blocked results in increased resistance, laboured breathing and difficult feeding)
Infants use abdominal muscles for breathing
(Any distention of injury can quickly lead to respiratory distress)
(Naturally higher respiratory rates and oxygen consumption resulting in greater loss of water from lungs)
Cardiovascular Differences in Paediatric Patients
Large body surface area
Decreased contractile efficiency of heart
(Difficulting manipulating their cardiac stroke volume - increased HR to increase stroke volume.)
Smaller volumes of circulating blood
(Small amounts of blood loss constitute a large percentage of their volume.)
Cardiac output, oxygen consumption and delivery are higher
(Anything that causes an increase in oxygen consumption and a decrease in delivery can cause decompensation)
Smaller veins and more subcutaneous tissue
(Difficult cannulation)
Higher metabolic rate
(Increased cardiac workload and HR)
(Greater fluid losses through evaporation. Require greater fluid requirements to maintain adequate circulating volume.)
Gastrointestinal Differences in Paediatric Patients
Increased glucose requirements with poor glycogen stores
Reliance on others for fluid and nutrition
(Hard for caregivers to meet the childs needs, especially when sick)
Higher metabolic rate
(ncreased waste production and increased nutrition and fluid requirements)
Cylindrical abdomen (Poor protection of vital organs)
Proportionally longer intestinal length
(Greater fluid losses)
Immature lower oesophageal sphincter tone (up to 12 months)
(Regurgitation)
(Can rapidly develop hypoglycemia and muscular fatigue)
Musculoskeletal Differences in Paediatric Patients
Lack of tone, muscle and power
Bones are soft until puberty
(Bones will break and bend more easily)
Bones are more flexible
(Serious internal injuries can result without fractures present)
Growth plates are still active
(Fractures to these long bones can have significant impacts on growth)
Babies born with more bones than adults
(Many of these will fuse together as they grow)
(Rely on others to keep stable and safe, Large head held by weak neck so more prone to head and spinal injuries, cannot initiate shivering with poor muscle tone)
Renal Differences in Paediatric Patients
Immature tubular function
Decreased ability to concentrate urine
(loss of water)
Age related changes in pharmokinetics and pharmodynamics
(slower excretion of some drugs)
(sodium wasting)
Other Differences in Paediatric Patients
body to surface area ratio is 4 times that of adults and heat production is only 1 and a half times as high
nerve endings in the retinas are not fully developed
(Blurred images and shapes seen in the first few weeks - will start to smile at you when clearly sees you smiling)
(More prone to accidental hypothermia)
