hypertension and pre-e

Question 1

what are the three different types of hypertensive disorders in pg

Answer 1

chronic or pre-existing hypertension, gestational hypertension, and pre-e

Question 2

what are women with chronic/pre-existing hypertension at greater risk of

Answer 2

[20-30 percent] developing superimposed pre-e compared to a woman with normal bp

Question 3

what are some complications or variation os pre-e

Answer 3

eclampsia, HELLP syndrome and acute fatty liver disease of pg

Question 4

hypertension

Answer 4

bp of 140/90 mmHg or higher

Question 5

chronic hypertension

Answer 5

identified at the initial booking visit, or before 20 weeks.

Question 6

gestational hypertension

Answer 6

new hypertension presenting after 20 wga w/o significant proteinuria or any other features of pre-e

Question 7

pre-e

Answer 7

hypertension developing after 20 wga and the coexistence of one or more the following new onset conditions- proteinuria, other maternal organ dysfunction [renal, liver, neurological, hematological complications] or uteroplacental dysfunction [fetal growth restriction]

Question 8

severe pre-e

Answer 8

BP of 160/110 mmHg or higher associated with significant proteinuria, features of PET [severe headaches, visual scotomata, n or v, epigastric pain, oliguria, reduced fetal growth] and/or laboratory evidence of renal, hepatic or coagulation dysfunction

Question 9

Eclampsia

Answer 9

new onset grand mal convulsions associated with pre-e

Question 10

HELLP syndrome

Answer 10

an acronym for a complication of pre-e with the following features- hemolysis, elevated liver enzymes and low platelet count

Question 11

what is bp

Answer 11

the force exerted on the wall of the blood vessel by the blood.

Question 12

what is systolic and diasotlic pressure

Answer 12

maximum pressure as the left ventricle expels blood into the aorta [systolic] and falls when the aortic valve closes and the heart is filling [diastolic]

Question 13

what does bp depend on

Answer 13

cardiac output [stroke volume x heart rate]

systemic vascular resistance

Question 14

what are key components of bp

Answer 14

the amount of circulating fluid [plasma volume], the heart rate, and the diameter [lumen] of the blood vessel are key components of bp

Question 15

bp is controlled by

Answer 15

• cardiovascular center in the base of the brain via the autonomic nervous system
• the diameter of vessels- altered by relaxation or constriction of smooth muscle in walls of the vessel
• baroreceptors that detect changes from sitting to standing and adjust the heart rate
• chemicals carried in the blood [like adrenalin, noradrenaline, and histamine]
• chemoreceptors that are sensitive to changes in oxygen and co2
• endothelin-derived relaxing factor [EDRF][nitric oxide] that plays a role in vasodilation of pg
• kidney [anti-diuretic hormone, renin-angiotensin balance] control of fluid balance to maintain BP

Question 16

why does bp drop even with increase in blood volume and cardiac output during pg

Answer 16

vasodilation of blood vessels and a corresponding reduction in peripheral vascular resistance which dominates the changes to the cardiovascular system in pg

Question 17

With pre-existing hypertension what is primary or essential hypertension

Answer 17

there is no identifiable direct disorder that causes the hypertension but it arises from a combination of genetic and environmental factors.

Question 18

what makes up for majority of [90 percent] pre-existing hypertension

Answer 18

primary or essential hypertension

Question 19

what factors increase the risk of pre-existing hypertension

Answer 19

more common in black women, incidence increases with age, raised BMI, increased salt intake and physical inactivity.

Question 20

what is secondary hypertension when it comes to pre-existing hypertension

Answer 20

arises as a consequence of disorders like renal disease, diabetes, thyroid disorders, cardiac disease, SLE or adrenal gland abnormalities

Question 21

what are some risks or complications of chronic hypertension

Answer 21

increased risk [20-30 percent] of superimposed pre-eclampsia, PET include risk of stroke, placental abruption HELLP syndrome, low birth weight babies, preterm birth, still birth, and increased c-section

Question 22

pathophysiology of pre-e

Answer 22

complex interplay of abnormal genetic, immunological and placental factors. early changes in the way the placenta embeds in the uterus is a strong predisposing factor in the development of pre-e, but it is the generalized response in the maternal endothelial system which leads to the widespread inflammation, platelet aggregation and vasoconstriction that underlines multi-organ dysfunction

Question 23

What normally happens with placenta in an healthy uncomplicated pregnancy by pre-e

Answer 23

trophoblastic cells of the placenta invade the maternal uterine arteries at both the decidual and myometrial level. The aim is to establish an effective blood supply for the placenta and the fetus. The trophoblast cells bring about an erosion of the muscle later of the blood vessel walls, which allows the vessel lumen to enlarge. The spiral arteries are transformed from high-resistance, low flow vessels into large dilated vessels with an increased blood flow.

Question 24

what happens with pregnancy complicated by pre-e [placenta]

Answer 24

invasion of trophoblast cells is confined to the decidual level of the blood vessels causing a problem with normal uterine placental blood flow. this results in a relatively under-perfused [ischemic] placenta. this placental hypo perfusion is accompanied by an imbalance of key angiogenic factors that are important in the development of blood vessels. the persistently under-perfused placenta causes oxidative stress which results in the release of inflammatory cytokines and an imbalance of angiogenic factors that result in widespread damage to the maternal endothelial cells.

Question 25

why does damage to the endothelial cells underline the varied multi-organ dysfunction seen in pre-e

Answer 25

the endothelial cells that line the maternal blood vessels mediate immune and inflammatory responses, maintain the integrity of the vascular compartment, prevent intravascular coagulation and modify the contractile response of the underlying smooth muscle. endothelial dysfunction in pre-e causes increased cell permeability, increased platelet aggregation, increased thrombosis, decreased production of nitric oxide [a powerful vasodilator] and an imbalance of the ratio of thromboxane A2 and prostacyclin. the result is profound vasoconstriction leading to hypo perfusion of organs ‘leaky’ vessels and raised bp

Question 26

how does the kidneys get involved with pre-e

Answer 26

in the kidneys, glomerular capillary endothelial swelling occurs accompanied by deposits of fibrinogen within and under the endothelial cells. this results in the general renal function being impaired, causing rising serum creatine, uric acid and urea levels. in addition, increased glomerular permeability allows protein to escape into the urine.

Question 27

how does edema occur with pre-e

Answer 27

hypoalbuminemia of pre-e causes a lower colloid osmotic pressure, affecting fluid transport across the capillaries, resulting in too much fluid in the interstitial spaces [edema] and too little in the vascular compartment [hypovolemia] .

Question 28

what are other serious complications of pre-e

Answer 28

reduced organ perfusion in the liver and the brain can contribute to serious potentially fatal outcomes.

Question 29

summary of pre-e

Answer 29

• failure of the invading trophoblast cells to maximize uterine spiral artery modification
• decreased uterine blood flow, decreased plasma expansion
• relative placental ischemia
• generalized intravascular inflammatory reaction
• endothelial dysfunction
• vasoconstriction of arterioles of major body organs

Question 30

potential fetal complications of relative placental ischemia

Answer 30

growth restriction, reduced amniotic fluid, reduced umbilical artery blood flow

Question 31

how does vasoconstriction of arterioles affect the cardiovascular system

Answer 31

• bp increase to compensate for low perfusion
• plasma volume expansion decreases
• low colloid osmotic pressure edema

Question 32

how does vasoconstriction of arterioles affect the hematological system

Answer 32

• high hematocrit and high Hb
• high platelet consumption
• activation of clotting systems
• formation of microthrombi

Question 33

how does vasoconstriction of arterioles affect the renal system

Answer 33

• decrease renal blood flow
• damage to glomerular membrane
• loss of protein
• impaired uric acid and creatinine excretion
• increase sensitivity to angiotensin

Question 34

how does vasoconstriction of arterioles affect the liver

Answer 34

• hemorrhage, ischemic damage, and thrombosis
• epigastric pain and vomiting
• HELLP syndrome

Question 35

how does vasoconstriction of arterioles affect the neurological system

Answer 35

• headache
• hyperreflexia
• eclamptic fits
• visual disturbance
• cerebral hemorrhage

Question 36

how to monitor clients with suspected chronic hypertension

Answer 36

self-monitor in addition to attending antenatal care. benefits include identification of hypertension, sense of empowerment and responsibility for care, and reduced anxiety

Question 37

what are some potential complications from HELLP

Answer 37

eclampsia, hemorrhage, stroke, renal failure, deterioration of fetal condition

Question 38

what is a specific consequence of HELLP

Answer 38

liver damage or even rupture is possible.