Hypertensive Disorders Flashcards
1
Q
What are the different hypertension disorder?
A
- Chronic hypertension
- White coat and masked hypertension
- Gestational PIH
- Pre-eclampsia
- HELLP syndrome
2
Q
What is chronic hypertension?
A
Chronic hypertension is associated with adverse maternal and fetal outcomes and is best managed by tightly controlling maternal blood pressure (BP, 110–140/85 mmHg), monitoring fetal growth, and repeatedly assessing for the development of preeclampsia and maternal complications. This can be done in an outpatient setting.
3
Q
What is White coat and masked Hypertension?
A
- White-coat hypertension refers to elevated office/clinic (≥140/90 mmHg) BP, but normal BP measured at home or work (<135/90mmHg). It is not an entirely benign condition and conveys an increased risk for preeclampsia
- Masked hypertension is another form of hypertension, more difficult to diagnose, characterized by BP that is normal at a clinic or office visit but elevated at other times, most typically diagnosed by 24-hour ambulatory BP monitoring (ABPM) or automated home BP monitoring.
- Repeat after 1-2 hours.
4
Q
What is Gestational Hypertension (PIH)?
A
Gestational hypertension is hypertension arising de novo after 20 weeks’ gestation in the absence of proteinuria and without biochemical or haematological abnormalities.
- It is usually not accompanied by fetal growth restriction.
- Outcomes in pregnancies complicated by gestational hypertension are normally good, but about a quarter of women with gestational hypertension (particularly those who present at <34/40 will progress to pre-eclampsia and have poorer outcomes
5
Q
What is pre-eclampsia?
A
- Pre-eclampsia is a complex medical disorder; Preeclampsia can deteriorate rapidly and without warning; we do not recommend classifying it as mild or severe.
- Proteinuria is not mandatory for a diagnosis of preeclampsia.
- BP 140/90
- PROTEIN- any protein in the urine is NOT NORMAL (ask woman to do another urine) if it comes back again as + then send an MSU.
- The first sign is abnormal fetal growth -> due to the placenta
- Rather, this is diagnosed by the presence of de novo hypertension after 20 weeks’ gestation accompanied by proteinuria and/or evidence of maternal acute kidney injury (AKI), liver dysfunction, neurological features, haemolysis or thrombocytopenia, or fetal growth restriction. Preeclampsia may develop or be recognized for the first time intrapartum or early postpartum in some cases.
6
Q
What is HELLP syndrome?
A
- The haemolysis, elevated liver enzymes, low platelets (HELLP) syndrome is a (serious) manifestation of preeclampsia and not a separate disorder.
- There is no linear symptoms of pre eclampsia.
7
Q
What is the aetiology of pre-eclampsia?
A
- Genetic predisposition
o Maternal family history of pre-eclampsia: 1st degree mum or sister.
o Previous personal history of pre-eclampsia - Immunological
o excessive maternal response occurs when there has been minimal exposure to paternal antigen.
o Results showed that a sexual relationship of under 4 months is associated with a 7-fold increase in high diastolic pressure (HDP)
o This may provide a partial explanation for the higher incidence of HDP with - Nulliparity
- Primipaternity
- Teenage pregnancy
- Artificial issemination by donor (AID),
- Previous history of pre-eclampsia with male partner
- Placental development and implantation
o Placental trigger is state of absolute or relative ischaemia due to: - Poor placentation which occurs when there is a failure of trophoblastic invasion of the uterine spinal arteries.
- in normal pregnancy, the muscle walls of these arteries are stripped as far as the inner third of the myometrium to result in greater perfusion of the intervillous spaces.
- placental insufficiency is also associated with deposition of fibrin and thrombosis in the spiral arterioles.
Transformation of the maternal intramyometrial portion of the spiral arterioles- Thins the endothelial layer. - Cardiovascular link
More recently a cardiovascular link has been suggested: women who suffer hypertensive pregnancies or have premature and/or low-weight babies are at an increased risk of presenting later in life with hypertension and cardiovascular events, such as coronary artery disease, stroke, obstruction of the carotid and lower limb arteries, cardiac failure, and thromboembolism. - Other factors include:
o Donor eggs
o Increased maternal age- more chance of higher BP which is a risk factor for PE in itself
o Sickle cell disorder
o Multiple pregnancies- there is a larger placental mass so increased maternal immune response to trophoblast debris so higher chance of endothelial damage
o Renal disease – Kidneys and endothelial cells already damaged.
8
Q
What occurs to a placenta that is complicated by pre-eclampsia?
A
- Second wave of trophoblast cell invasion of the spiral arterioles very early in 2nd trimester is abnormal, resulting in impaired perfusion of placental tissue (placental hypoxia theory)
- Spiral arteries retain intact endothelial and smooth muscle linings, and undergo much less than expected dilatation
- This is thought to result in the release of ‘factors’ into maternal circulation that may be responsible for the development of placental dysfunction, vasoconstriction and hypertension
- Outcome: decrease uteroplacental circulation & chronic fetal hypoxia
9
Q
What is the endothelial dysfunction that is caused by preeclampsia?
A
Endothelial dysfunction
- Circulating factors are released from the ischaemic placenta in response to hypoxia as a result of under perfusion-the factors are released in the maternal bloodstream which activates the endothelium (imbalance of vasoconstrictors and vasodilators) -> increase in vasoconstrictions -> higher BP (systolic of 150 or above) -> intracranial haemorrhage.
- Endothelial cells form the endothelium which lines the cardiovascular system, these cells play an important role in regulating capillary transport and modulating vascular smooth muscle reactivity in response to various stimuli
- Endothelial cells form the inner lining of blood vessels
- These cells play an important role in regulating capillary transport and modulating vascular smooth muscle reactivity in response to various stimuli
- Poor placental perfusion results in disruption to the integrity of endothelial cells
- Damage to endothelial cells will:
Reduce production of prostacyclin (PGI2) and nitric oxide (NO), potent local vasodilators and inhibitors of platelet aggregation
Increase vascular sensitivity to angiotensin II (controls BP and the excretion of salt/water)
Activate the coagulation cascade and stimulate the production of thromboxane A2 (potent vasoconstrictor)
Increase production of lipid peroxidase enzymes and decrease antioxidants (oxidative stress)
Effects of placental ischaemia + endothelial disruption
- Generalised vasoconstriction
- Increased systemic vascular resistance
- Increased vascular hydrostatic pressure
- Reduced tissue perfusion
- Multiple organ dysfunction/damage
- Increased vascular permeability
10
Q
What are the general signs and symptoms of preeclampsia?
A
- Severe Headaches – oedema and cerebral haemorrhage causing frontal headaches which can’t be resolved by pain killer.
- N+V – vasoconstriction in stomach so liquids become static
- Flashing lights – fluid from oedema and high BP presses an optic nerve
- Proteinuria – endothelial damage in glomerulus in kidneys so protein is not reabsorbed so leaks into urine
- Facial oedema – endothelial damage so fluid moves out of the blood vessels and leaks into the tissues
- RUQ pain – endothelial damage causes swelling in the liver, it cannot stretch with the fluid shift
- Blurred vision – vasoconstriction in the retina
- Increased Hb – movement of fluid into interstitial tissues, circulating blood becomes more concentrated
- Signs of clonus
- Liver tenderness – endothelial damage
11
Q
What causes hypertension in preeclampsia?
A
- Disturbed endothelial control of vascular tone -> associated with altered rennin-angiotensin function -> results in vasospasm, increased peripheral resistance and hence raised BP.
- Defined as systolic more or equal to 140 and/or diastolic more or equal to 90mmHg.
- BP should be repeated to confirm true hypertension
- If BP is severe (systolic more or equal to 160/ diastolic more or equal to 110 mmHg), then BP should be confirmed within 10 mins
- For less severe can be repeated after a couple of hours
- Use liquid crystal sphygmomanometer
- Make sure appropriate sized cuff is used
- Diastolic BP is more affected by peripheral resistance, therefore more useful for diagnosing pre-eclampsia
12
Q
What causes failure of renal function and proteinuria in preeclampsia?
A
- Occurs due to glomeruloendotheliosis which resolves after delivery.
- increased blood supply causes damage to the endothelial cells. Protein leaks out causing proteinuria
- vasospasm of arterioles decreased blood flow to the kidneys, preventing adequate excretion of waste products, so raised serum urate and urea.
- Reduced creatinine clearance and increased serum creatinine indicates the ability of the kidneys is compromised (through endothelial damage), as glomerular filtration rate falls so urea and creatinine accumulate in the blood and the serum concentration of both rises
- Proteinuria should be assessed initially by an automated dipstick urinalysis.
- If positive more than or equal to +1/30mg then spot protein/creatinine (PCr) should be performed.
- Avoid using the morning urine void
- A PCr ratio of more than or equal to 30mg is abnormal
- Massive proteinuria is associated with more severe neonatal outcomes
13
Q
What causes oedema in preeclampsia?
A
- results from increased endothelial permeability compounded by the loss of protein from the serum which alters the direction of osmotic pressure. As a consequence, reduced circulating volume and cardiac output further reduces organ perfusion and increased haemoglobin associated with poor perinatal outcome.
- Pathological oedema gives rise to several features of severe pre-eclampsia such as epigastric pain
14
Q
What causes cardiovascular problems in preeclampsia?
A
- Fluid shift into tissues causing hypovolaemia increasing Hb
- cardiac compromise due to hypertension and the extra effort to pump blood through the constricted circulatory system as there is hypovolemia (decrease blood volume in veins)
- An initial rise in platelets due to the stimulation of the immune system but a subsequent drop- thrombocytopenia – lowered Plt count less than 90- as fluid leaks out to other tissues
- C-reactive protein (CRP)- levels will rise due to inflammatory response due to endothelial damage. However, does not rule out infection so often omitted
- Disseminated intravascular coagulation
- Haemolysis: fibrin mesh formed breaks down RBC
15
Q
What causes problems with the liver in preeclampsia?
A
- Elevated liver enzymes
o Alanine transaminase (ALT)
o Aspartate transaminase (AST)
o Alkaline phosphate (ALP)- raised anyway due to placental production of phosphate) - Vasoconstriction causes hypoxia in the liver, resulting in liver cells becoming necrosed. This is indicated by the presence of liver enzymes (ALT, AST) in the blood.
- Damage to endothelial cells leads to a large amount of proteins and liquid leaking out of the liver, including serum albumin which causes the levels to decrease.
- Elevated liver function – due to the endothelial damage therefore the liver works harder
- Results from under perfusion due to vasoconstriction and local oedema. Raised levels of ALT, AST may also indicate damage to the heart, muscles, kidneys, pancreas and RBC as it is involved in tissue metabolism and is found in high levels in these areas
- Haemorrhage within the liver capsule may lead to capsular rupture -> which causes the right epigastric pain
