ICL 15.7: Maternal Hypertension and Diabetes Flashcards
what time in gestation differentiates chronic HTN from gestational HTN?
chronic HTN is HTN before 20 weeks gestation
gestational HTN and preeclampsia are after 20 weeks
how does blood pressure change in pregnancy?
it drops for the first 20 weeks then comes back to baseline
progesterone causes vasodilation and is the reason that BP drops
how do you diagnose chronic HTN?
HTN before pregnancy OR was elevated before 20 weeks gestation
after 20 weeks, elevated BP is defined as gestational HTN
over 140/90
what organ is involved with preeclampsia?
preeclampsia is a placental disorder!!
what vessel gives rise to the spiral arteries of the uterus?
uterine artery
what are the risk factors for preeclampsia?
- immune maladaptation
- genetic factors
- metabolic factors (obesity)
what is the pathophysiology of preeclampsia?
immune maladaptations, genetic factors and metabolic factors all lead to abnormal placental implantation, endothelial dysfunction and ultimately preeclampsia
in order for implantation to occur, trophoblasts need to invade the spiral arteries so that they can remodel the spiral arteries to remove the smooth muscle layer of the spiral arteries so that it becomes more dilated! we want this remodeling to occur and we want the spiral arteries to lose their muscular layer because resistance in the spiral arteries will go down!
maternal blood volume increases during pregnancy but in order for the placenta to handle this increased volume, we need blood vessels that can deliver this increased blood volume to the placenta
in preeclampsia, the trophoblasts don’t remodel the spiral arteries and so there’s more muscular layer left so they’re more receptive to the low oxygen levels in the amniotic sac and they are more prone to vasospasm and vasoconstrictive agents – you end up with endothelial dysfunction and damage which leads to HTN, proteinuria, liver dysfunction, and cerebral edema
what is the clinical presentation of preeclampsia
- HTN
- proteinuria
- liver dysfunction
- cerebral edema
- HELLP
what is the main pathophysiologic problem that results in preeclampsia?
trophoblastic dysfunction
link the pathophysiology of preeclampsia with the clinical presentation of seizures?
seizures occur because of the impact of the vasactive mediators on the BBB
link the pathophysiology of preeclampsia with the clinical presentation of liver dysfunction?
there is a robust capillary circulation between liver capsule and parenchyma
during preeclampsia you get hepatic swelling as a result of hepatic vein vasocongestion –> the capsule gets stretched and can rupture and patient will present with RUQ pain since the sensory fibers of the liver are in the capsule, not the parenchyma
link the pathophysiology of preeclampsia with the clinical presentation of pulmonary edema?
pulmonary edema results from venous congestion due to the leaky endothelial cells in the pulmonary circulation that are being damaged by the vasoconstrictive agents released by the damaged spiral arteries
link the pathophysiology of preeclampsia with the clinical presentation of thrombocytopenia?
the damaged endothelial cells are going to bind platelets and use them up
link the pathophysiology of preeclampsia with the clinical presentation of heart failure?
CHF is going to work harder due to venous congestion and vasospasm
link the pathophysiology of preeclampsia with the clinical presentation of kidney damage?
the endothelial cells in the glomerulus get damaged too which allows protein to be filtered through and you get proteinuria
34 yr G1 at 8 weeks presents for her first prenatal visit. she has no history of HTN. BP is 140/92. 4 hrs later the repeated BP is 144/90.
diagnosis?
chronic HTN
even though she has no history of HTN, she has 2 repeat measures with HTN before 20 weeks gestation
27 year old who is 30 weeks and at routine follow up with bP of 150/105. she was previously normotensive. platelet count and liver function tests are normal. 24 hr urine protein collection is 1.1 grams.
diagnosis?
preeclampsia w/o severe features
it’s not just gestational HTN because she is showing signs of kidney damage
when diagnosin
how do you diagnose preeclampsia?
- elevated BP with more than 200 mg protein in urine during 24 hr urine
- HTN and any lab changes that can occur during:
- elevated AST/ALT
- platelets under 100,000
- elevated creatinine over 1
proteinuria is not necessary to make the diagnosis of preeclampsia
27 year old who is 30 weeks and at routine follow up with bP of 165/105. she was previously normotensive. platelet count and liver function tests are normal. 24 hr urine protein collection is 1.1 grams.
diagnosis?
if over 160/110 it becomes preeclampsia with severe features
this means there’s more vasospasm causing arterial HTN
there is associated risk with eclampsia once you have severe features…
which physiologic adaptation during pregnancy exacerbates the risk of pulmonary edema in women with preeclampsia?
decreased serum albumin
what are the criteria for preeclampsia with severe features?
- thrombocytopenia
- BP greater than 160/110
- elevation of ALT/AST
- doubling of creatinine
- pulmonary edema
- oliguria
if someone has a seizure it becomes eclampsia
do preeclampsia symptoms recover fully after pregnancy?
preeclampsia with severe features risk factor for CVD!!
what is gestational diabetes?
impaired glucose tolerance that begins or is first recognized during pregnancy?
why does DM develop during pregnancy?
pregnancy is characterized by a state of insulin resistance and hyperinsulinemia due to placental secretion of hormones like cortisol, hPL, and progesterone
what are the normal glucose changes involved in a normal pregnancy without GDM?
- fasting hypoglycemia
- postprandial hyperglycemia
- hyperinsulinemia
- peripheral insulin resistance (leads to increased glucose for fetus)
how does glucose get to placental circulation from maternal circulation?
facilitated diffusion via glucose transporters
how hPL effect glucose levels?
- anti-insulin effects
- promotes lipolysis resulting in increased free fatty acids, decreased maternal which leads to decreased gluconeogenesis
produced by syncytiotrophoblasts of placenta
which 3 homrones are responsible for increased insulin resistance in pregnancy?
- hPL
- estrogen
- cortisol
what happens to the insulin receptors during pregnancy?
there is a modifications to the GLUT4 transporter leading to a 25% reduction the amount of glucose transport into cells!
there is also a down regulation and decreased concentration of insulin receptors
of the insulin receptors that are left, they have a decreased ability to undergo tyrosine phosphorylation which is necessary for the insulin receptor to work! when insulin binds to its receptor, it causes a change in the GLUT4 receptor which allows glucose to enter the cell so without insulin receptor phosphorylation, glucose can’t enter!
this all results in increased glucose in the peripheral circulation which can then be transported to the fetus
how do glucose and insulin levels change during pregnancy?
they both increase a lot!!
even though there’s higher insulin levels there’s still high glucose levels due to insulin resistance that occurs in pregnancy
what are ht risk factors for GDM?
- obesity
- prior pregnancy with GDM
- h/o macrocosmic neonate (big baby)
- over 25 years old
- AA, NA or hispanic
- h/p unexplained stillbirth
- family history of diabetes
- multiple gestation because more placenta present producing more hPL
- medical condition associated with development of DM like HTN
who is screened for GDM?
everybody!!!
for people with risk factors you do it at the very first prenatal visit and for people w/o risks you do it at 24-28 weeks
how do you treat GDM?
- nutritional therapy
- life style modifications
- oral hypoglycemia agents
- insulin
really important because increased risk of type II DM after birth so do glucose challenge test at 6 weeks post-partum
what are the neonatal effects on GDM?
- macrosomia
- growth restriction
- hypoglycemia
- hyperbilirubinemia
- polycythemia
- respiratory distress
- stillbirth
- Erbs palsy because the babies are usually bigger and the shoulders can get stuck under the pubic symphysis which can damage nerves and cause Erbs palsy
what are the long term impacts of GDM after delivery?
maternal hyperglycemia have fetal hyperinsulinemia which increases fetal fat cells
this is a risk factor for childhood obesity and insulin resistance leading to impaired glucose tolerance and DM in adulthood
