Maternal Medical Conditions Flashcards
Type I Diabetes
Autoimmune disorder that destroys Beta cells in pancreas > progressive decline in insulin (complete lack of insulin results > body cells are unable to uptake glucose from blood >hyperglycaemia
Type II Diabetes
Insulin resistance possibly caused by:
- down regulation of insulin receptors due to large amounts of fat stores
- decreased cell sensitivity to insulin due to age, infection, insulin opposing drugs
Leads to decrease in glucose uptake > hyperglycaemia
Gestational Diabetes
(could be undiagnosed type I or II)
Decreased insulin production > decreased cell response to insulin or exaggerated insulin resistance > hyperglycaemia. Most GDM cases resolve after birth
Hyperglycaemia- two compnonets
Glucose deprivation and of body cells and excessive amount of glucose in the blood
Glucosuria
Glucose transporters for reabsorbing glucose back in to blood are saturated > glucose is lost in urine
Diabetes: thirst
Glucose in filtrate creates osmotic gradiant attracting water retaining > increased water volume > increased plasma osmolarity > thirst mechanism triggured
Glucolysation
deposition of glucose on blood vessels and nerves
- NERVES: impacts function leading to neuropathies: sensory/motor reception/response slow increasing risk of injury and lack of response to stimuli
- BLOOD VESSELS reduces gas exchange and filtration in capillaries resulting in ischemia and reduced inflammation response (healing time)
Cellular deprivation of glucose
- Cell signalling to hypothelamus is disrupted > feelings of hunger
- Increased lipolysis > ketoacidosis >fat deposition in blood vessels
Hyperglycaemia in pregnancy
foetal blood is also hyperglycaemic > foetal pancreas develops with overactive Beta cells and underactive alpha cells that produce glycogen > longer time for neonatal pancreas to adjust
Hyperthyroidism
increas in TH production > inc BMR > O2 consumption. Temp remission in pregnancy may occur due to the increase in thyroid binding globulins that bind excess TH
Hypothyroidism
Decrease TH > Decreases BMR > dec O2 consumption and use of metabolic fuel
ulcerative colitis
Mucosal inflammation of the bowel, comonlly the rectum characterised by active phases
Ulcerative colitis manifestations
bloody diarrhoea
fecal incontinence
abdominal pain
ulcerative colitis causes
auto immune disease stimulating inflammatory response of bowel mucosa > ulcers
ulcerative colitis in pregnancy
remission: no problems active phase: increased risk of: - preterm birth - IUGR - inc chance of CS
Chron’s
chronic inflammation and scarring of GI tract > dec nutrient absorption (anaemia common).
Chron’s in pregnancy
inactive = no inc risk in pregnancy active = will remain active during pregnancy and is associated with pregnancy loss, IUGR, preterm labour and birth
Cholelithiasis and cholecytitis definitions
Cholelithiasis: crystallisation of cholesterol due to super saturation of bile with cholesterol
Cholecytitiis: inflammation of gallbladder often caused by gall stones irritating mucosa layers
Pathophysiology of cholelithiasis
Gall stones inc risk of biliary inflammation, obstruction and pancreatitis
Obstruction > further bile concentration > reduced breakdown and absorption of fat > liver dysfunction as bile ‘backs up’ in to liver
Cholelithiasis and pregnancy (3 x aetiology 1 x outcome)
- increased cholesterol production in pregnancy
- oestrogens increase saturation of cholesterol in bile
- progesterone relaxes gall bladder and bile ducts
- cholelithiasis increases likelihood of preterm labour and birth
Demands on normal cardiac function in pregnancy
- Increase workload (inc CO, plasma volume, SR)
- labour and birth further increase workload
- hypercoagulable state of pregnancy increase chance of thromboembolism
Rheumatic heart disease pathophysiology
GAS causes infalmmation of endocardium > necrosis of tissue > scarring and lesion formation > permanent deformity of heart valves (mitral valve stenosis is most common)
