ICL 15.7: Maternal Hypertension and Diabetes

Question 1

what time in gestation differentiates chronic HTN from gestational HTN?

Answer 1

chronic HTN is HTN before 20 weeks gestation

gestational HTN and preeclampsia are after 20 weeks

Question 2

how does blood pressure change in pregnancy?

Answer 2

it drops for the first 20 weeks then comes back to baseline

progesterone causes vasodilation and is the reason that BP drops

Question 3

how do you diagnose chronic HTN?

Answer 3

HTN before pregnancy OR was elevated before 20 weeks gestation

after 20 weeks, elevated BP is defined as gestational HTN

over 140/90

Question 4

what organ is involved with preeclampsia?

Answer 4

preeclampsia is a placental disorder!!

Question 5

what vessel gives rise to the spiral arteries of the uterus?

Answer 5

uterine artery

Question 6

what are the risk factors for preeclampsia?

Answer 6

1. immune maladaptation
2. genetic factors
3. metabolic factors (obesity)

Question 7

what is the pathophysiology of preeclampsia?

Answer 7

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

Question 8

what is the clinical presentation of preeclampsia

Answer 8

1. HTN
2. proteinuria
3. liver dysfunction
4. cerebral edema
5. HELLP

Question 9

what is the main pathophysiologic problem that results in preeclampsia?

Answer 9

trophoblastic dysfunction

Question 10

link the pathophysiology of preeclampsia with the clinical presentation of seizures?

Answer 10

seizures occur because of the impact of the vasactive mediators on the BBB

Question 11

link the pathophysiology of preeclampsia with the clinical presentation of liver dysfunction?

Answer 11

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

Question 12

link the pathophysiology of preeclampsia with the clinical presentation of pulmonary edema?

Answer 12

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

Question 13

link the pathophysiology of preeclampsia with the clinical presentation of thrombocytopenia?

Answer 13

the damaged endothelial cells are going to bind platelets and use them up

Question 14

link the pathophysiology of preeclampsia with the clinical presentation of heart failure?

Answer 14

CHF is going to work harder due to venous congestion and vasospasm

Question 15

link the pathophysiology of preeclampsia with the clinical presentation of kidney damage?

Answer 15

the endothelial cells in the glomerulus get damaged too which allows protein to be filtered through and you get proteinuria

Question 16

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?

Answer 16

chronic HTN

even though she has no history of HTN, she has 2 repeat measures with HTN before 20 weeks gestation

Question 17

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?

Answer 17

preeclampsia w/o severe features

it’s not just gestational HTN because she is showing signs of kidney damage

when diagnosin

Question 18

how do you diagnose preeclampsia?

Answer 18

1. elevated BP with more than 200 mg protein in urine during 24 hr urine
2. 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

Question 19

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?

Answer 19

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…

Question 20

which physiologic adaptation during pregnancy exacerbates the risk of pulmonary edema in women with preeclampsia?

Answer 20

decreased serum albumin

Question 21

what are the criteria for preeclampsia with severe features?

Answer 21

1. thrombocytopenia
2. BP greater than 160/110
3. elevation of ALT/AST
4. doubling of creatinine
5. pulmonary edema
6. oliguria

if someone has a seizure it becomes eclampsia

Question 22

do preeclampsia symptoms recover fully after pregnancy?

Answer 22

preeclampsia with severe features risk factor for CVD!!

Question 23

what is gestational diabetes?

Answer 23

impaired glucose tolerance that begins or is first recognized during pregnancy?

Question 24

why does DM develop during pregnancy?

Answer 24

pregnancy is characterized by a state of insulin resistance and hyperinsulinemia due to placental secretion of hormones like cortisol, hPL, and progesterone

Question 25

what are the normal glucose changes involved in a normal pregnancy without GDM?

Answer 25

1. fasting hypoglycemia
2. postprandial hyperglycemia
3. hyperinsulinemia
4. peripheral insulin resistance (leads to increased glucose for fetus)

Question 26

how does glucose get to placental circulation from maternal circulation?

Answer 26

facilitated diffusion via glucose transporters

Question 27

how hPL effect glucose levels?

Answer 27

1. anti-insulin effects
2. promotes lipolysis resulting in increased free fatty acids, decreased maternal which leads to decreased gluconeogenesis

produced by syncytiotrophoblasts of placenta

Question 28

which 3 homrones are responsible for increased insulin resistance in pregnancy?

Answer 28

1. hPL
2. estrogen
3. cortisol

Question 29

what happens to the insulin receptors during pregnancy?

Answer 29

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

Question 30

how do glucose and insulin levels change during pregnancy?

Answer 30

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

Question 31

what are ht risk factors for GDM?

Answer 31

1. obesity
2. prior pregnancy with GDM
3. h/o macrocosmic neonate (big baby)
4. over 25 years old
5. AA, NA or hispanic
6. h/p unexplained stillbirth
7. family history of diabetes
8. multiple gestation because more placenta present producing more hPL
9. medical condition associated with development of DM like HTN

Question 32

who is screened for GDM?

Answer 32

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

Question 33

how do you treat GDM?

Answer 33

1. nutritional therapy
2. life style modifications
3. oral hypoglycemia agents
4. insulin

really important because increased risk of type II DM after birth so do glucose challenge test at 6 weeks post-partum

Question 34

what are the neonatal effects on GDM?

Answer 34

1. macrosomia
2. growth restriction
3. hypoglycemia
4. hyperbilirubinemia
5. polycythemia
6. respiratory distress
7. stillbirth
8. 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

Question 35

what are the long term impacts of GDM after delivery?

Answer 35

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