1/25
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
name some cardiovascular changes in pregnancy
(increases and decreases)
increase in:
cardiac output
heart rate
oxygen consumption
blood flow to uterus, kidneys and brain
blood volume
sympathetic tone
decrease in:
systolic + diastolic BP
mean arterial pressure
colloid osmotic pressure
vagal tone
blood volume expansion
what pregnancy hormone is responsible for the synthesis of the other hormone responsible for this
the receptor for this is upregulated where in the body
what pregnancy hormone counterbalances vasoconstriction
what happens to RBCs
Blood volume expansion
Driven by oestrogen-stimulated hepatic synthesis of angiotensinogen
Activates RAAS system
Aldosterone increases sodium and water retention
Plasma volume increases before red cell mass expands
Oestrogen increases angiotensin II receptor density on vascular smooth muscle
PG counterbalances vasoconstriction
Reduces Ca influx into smooth muscle cells -> net vasodilation
RBC mass increases by erythropoietin upregulation, slowly
Expands preload -> ^SV
cardiac output increase
what happens to stroke volume in early pregnancy
what physiological effect does relaxin have on BVs
how does the placenta reduce afterload
why does it do this
Cardiac output increases
Early pregnancy: ^^ SV
Mid-late pregnancy: ^^ HR (10 bpm)
Sympathetic activation and reduced baroreceptor sensitivity
Relaxin
Enhances NO signalling to increase arterial compliance
OE + relaxin
NO synthase expression ^ in endothelial cells -> systemic vasodilation
Placenta acts as a low resistance vascular bed, reducing afterload
Ensures enough uteroplacental perfusion
drop in vascular resistance
what does PG do
what does relaxin do
what happens to blood pressure in early pregnancy
PG
Smooth muscle relaxation
Reduces MLCK activity
Relaxin
Increase VEGF and matrix metalloproteinases
Softens connective tissue in vessel walls
BP falls in early pregnancy
respiratory changes
what happens to the physical position of the diaphragm, ribs, subcostal angle and ligaments
what happens to tidal volume, inspiratory capacity, expiratory reserve, residual volume and functional residual capacity
what happens to total lung capacity and inspiratory reserve volume
Mechanical changes
Elevation of diaphragm
Robs flare
Subcostal angle increases
Ligaments relax
Changes in lung function
^^ tidal volume
^^ inspiratory capacity
-- expiratory reserve volume
-- residual volume and functional residual capacity
Total lung capacity, vital capacity, inspiratory reserve volume doesnt change much
increased ventilation
what hormone increased tidal volume
what is its effect on CO2
why is this needed (gradient established)
PG acts as a respiratory stimulant at medullary centre
TV ^^
Resp rate stays similar
PG ^^ central chemoreceptor sensitivity to CO2
Leads to chronic respiratory alkalosis (PaCO2- 30mmHg)
Enhances foetal CO2 clearance (F-> M gradient)
diaphragm elevation
due to this what happens to functional residual capacity and residual volume
what hormone soften the costochondral ligaments
what is the pregnancy symptom for this
Uterine enlargement elevates diaphragm by 4-5 cm
Reduces FRC (functional residual capacity) and RV (residual volume)
Ribcage widens (OE-mediated ligament laxity)
Relaxin: costochondral ligaments soften
Inspiratory capacity preserved despite reduced residual volume
Breathlessness is common
renal changes
how does PG, relaxin and NO increase renal plasma flow
what happens to renal vascular resistance and cardiac output
increased GFR
what happens to creatinine clearance, urea
Renal plasma flow ^^ 50-80%
Systemic vasodilation (PG, relaxin, NO)
Reduced renal vascular resistance
Increased cardiac output
Increased GFR 50% (glomerular filtration rate)
Creatinine clearance increases
Serum creatinine and urea falls
Glomerular barrier remain intact
tubular reabsorption
what hormone increases Na+ reabsorption
what is the effect on plasma volume because of this
what happens to glucose and amino acid reabsorption
why is bicarbonate secreted more (blood)
Sodium
Increased aldosterone -> increased Na+ reabsorption
Sodium retention -> supports plasma volume expansion
Glucose and amino acids
Increased filtered load exceeds reabsorption capacity
Glycosuria, aminoaciduria
Bicarbonate
Kidneys secrete more HCO3- to compensate for respiratory alkalosis
Leads to lower serum bicarbonate
fluid retention
what system is activated
increases sensitivity to what hormone
ureteric dilation
what hormone relaxes smooth muscle in the bladder
how does urinary stasis happen
Fluid retention
RAAS activation (renin-angiotensin-aldosterone system)
Increased antidiuretic hormone ADH sensitivity
Ureteric dilation
PG helps relax smooth muscle
Mechanical compression by uterus
Reduced peristalsis -> urinary stasis
> increased UTI risk
renal changes summary: affect on
ureters
bladder tone
renal plasma flow
GFR
sodium reabsorption
serum urea and creatinine levels
dilation
decreased tone
increase plasma flow
increase GFR and glucose excretion
increase
decrease in serum levels
GIT changes
mouth
oesophagus
stomach
intestines
caecum/appendix
gallbladder
liver
Mouth
More susceptible to gingivitis, caries
Oesophagus
Relaxation of oesophageal sphincters
Stomach
Decreased gastric tone and motility
Intestines
Decreased gut motility – constipation
Displaced caecum and appendix
Attention to site of pain in appendicitis – McBurneys point
Gallbladder
Decreased tone and motility
Liver
Alters production of liver enzymes, proteins, altered position
endocrine changes
OE/PG levels
what hormone is secreted once embryo implants
what increases milk production
PTHrP levels
^^ OE PG
HCG
Increased prolactin (pituitary enlarges by 50%)
Parathyroid hormone increased
insulin sensitivity
what happens to this
why
INSULIN RESISTANCE
Ensures glucose is diverted to foetus
Encourages mother to use fatty acids for her own energy
HPL
what does it stand for
increases the lysis of which energy store
effect on maternal glucose uptake
human placental lactogen
lipolysis - free fatty acids inhibit insulin signalling
reduces maternal glucose uptake
progesterone
effect on maternal fat deposition in early pregnancy
effect on insulin sensitivity
effect on metabolic activity
promotes maternal fat deposition
increases insulin resistance
supports shift towards fat use
placental TNF-a
effect on insulin signalling
effect on GLUT-4 translocation
metabolism
impairs insulin receptor signalling
reduced glucose translocation
increases lipolysis
cortisol
gluconeogenesis
peripheral glucose uptake
insulin resistance
increase
decrease
increase
prolactin
effect on B-cell mass
effect on insulin secretion
expands B-cell mass
increases insulin secretion
oestrogen
effect on lipogenesis
effect on hepatic glucose output
enhances lipogenesis
increases hepatic glucose output
thyroid
increase or decrease in T3,T4 (metabolism regulators)
change in iodine requirements
it is important for the development of what in the foetus
increase in T3/4
increase in iodine requirement
important for foetal neurodevelopment
adrenal gland
what hormone stimulates ACTH hormone
what happens to cortisol levels
aldosterone increase
sodium levels
what happens to BP
Placental and maternal corticotropin releasing hormone CRH stimulates maternal ACTH
Cortisol ^^ 2/3x
Aldosterone increases
Sodium retention
Despite high aldosterone, BP falls due to systemic vasodilation
Explains cushingoid appearance and fluid retention in pregnancy
MSK, sensory, neural system changes
increased strain on body bc of what spine shape change
weight change
blood flow to ENT, airways
Change in posture/gait
Increased strain bc of lordosis
Altered sleep pattern
ENT - ^ vascularity, oedema
Airway - ^ mucosal oedema
Eyes – corneal oedema, -- ocular pressure
11kg weight gain
haematological changes
plasma volume
red cell mass
WCC
iron binding capacity and rquirement
coagulation state
platelet and HB count
colloid osmotic pressure
Plasma volume increases by 50%
Red cell mass increases
WCC increases
Reticulocyte count increases
Increase in iron binding capacity, and increase in iron requirement
Hypercoagulable state – fibrinogen and FVII, VIII, X, vWF and ristocetin co-factor activity increased
Decrease platelet count
Decrease in haemoglobin (physiologic anaemia)
Total protein decrease (reduce colloid osmotic pressure-oedema, drug absorption)
Decrease in osmolality (ADH reset)
hyoercoagulability
what hormone synthesises clotting factors
protein S count
fibrinolysis
platelet count
OE increases hepatic synthesis of clotting factors
Clotting cascade becomes primed – clots form faster and more robustly
Protein S decreases
System cant stop clot formation once it starts
Fibrinolysis is suppressed
Clots persist longer and are harder to dissolve
Platelet count decreased
Dilutional effect from plasma volume expansion
immune system changes
why is there a shift from Th1→Th2 immune response
which 4 pregnancy hormones suppress immune system
what happens to WCC
chemotaxis are reduced - why
what happens to IgG,A,M
Cell mediated immunity is reduced and complement system c1, c1a, B, D are reduced
Shift from Th1-> Th2
Protects foetus from rejection
OE, PG, hCG, HPL – suppress immune system
WCC ^^
Chemotaxis are reduced – prevents excess inflammation
Ig G, A, M decrease