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GU / GYN & Renal > Clinical Obstetrics: HTN > Flashcards

Clinical Obstetrics: HTN Flashcards

1
Q

Plasma volume / Blood volume

Normal CV Changes in Pregnancy

A

Increase w/ weeks gestation

Blood volume increases ~60%

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2
Q

Red cell mass

Normal CV Changes in Pregnancy

A

Increases w/ weeks gestation

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3
Q

Hematocrit

Normal CV Changes in Pregnancy

A

Decreases w/ weeks gestation
* Physiological anemia

Greater increase in plasma volume than red cell mass

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4
Q

Heart rate

Normal Physiological Changes in Pregnancy

A

Increases w/ weeks gestation

HR increases 10-15 bpm

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5
Q

Stroke volume

Normal Physiological Changes in Pregnancy

A

Increases w/ weeks gestation

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6
Q

Cardiac output
* Undetected heart problems may present during pregnancy due to increased demand on heart

Normal Physiological Changes in Pregnancy

A

Increases w/ weeks gestation

Normal CO = 5 L/min; at 20 weeks gestation = 7 L/min

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7
Q

Blood pressure

Normal Physiological Changes in Pregnancy

A

Decreases w/ weeks gestation

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8
Q

Systemic vascular resistance (SVR)

Normal Physiological Changes in Pregnancy

A

Decreases w/ week gestation
* Vasopressor (Ang II) resistance during pregnancy
* Increased endothelium-dependent factors: NO
* Upregulated by estradiol & vasodilatory prostaglandins (PGI2)

Peripheral vasodilation leads to 25-30% decrease in SVR

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9
Q

Hypertensive disorders of pregnancy

A
  • Gestational HTN
  • Preeclampsia
  • Eclampsia
  • Chronic HTN
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10
Q

SBP >140 or DBP >90 mm Hg
* >20 weeks gestation
* Absence of proteinuria, systemic signs/symptoms

A

Gestational HTN

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11
Q
  • SBP >140 or DBP >90 mm Hg
  • > 20 weeks gestation
  • Proteinuria with or without signs/symptos
  • Preeclampsia signs/Sx/labs w/o proteinuria
A

Preeclampsia

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12
Q
  • SBP > 140 or DBP > 90
  • Pregestational or <20 wks gestation
A

Chronic HTN

Physiological changes of pregnancy should resolve by 6 weeks postpartum

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13
Q

Blood Pressure
* SBP >140 mm Hg OR DBP >90 mm Hg on 2 occasions at least 4 hrs apart after 20 wks gestation in woman w/ previously normal BP
OR
* SBP >160 mm Hg OR DBP >110 mm Hg confirmed within short interval (15 min)

Proteinuria
* >300 mg per 24-hour urine collection
OR
* Protein/creatinine ratio >0.3
OR
* Dipstick reading of 2+ (used only if other quantitative methods not available)

A

Preeclampsia

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14
Q
  • Nulliparity
  • Multifetal gestations (i.e., twins)
  • Chronic HTN
  • Pregestational / gestational diabetes
  • SLE
  • Pregestational BMI >30
  • Antiphospholipid antibody syndrome
  • Maternal age >35 years
  • Kidney disease
  • Thrombophilia
  • Assisted reproductive technology
  • Obstructive sleep apnea

Risk Factors

A

Preeclampsia

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15
Q

Two-stage theory of pre-eclampsia

Etiology

A
  • Lack of remodeling of spiral arteriole intima by cytotrophoblasts leading to less capacitance, decreased blood flow, and hypoxia
    * Remodeling normally dilates spiral arterioles, results in lower resistance, greater capacitance, increased blood flow
  • Placental hypoxia damages syncytium
    * Increased maternal oxidative stress and endothelial & immunological dysfunction leading to maternal end-organ damage
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16
Q

Mediators of preeclampsia

A
  • Hypoxia results in upregulation of sFlt1
  • Increased sFlt1 reduces free VEGF & PIGF
  • Decreased free VEGF & PIGF results in endothelial dysfunction of maternal blood vessel

sFlt1: soluble EGF transporter

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17
Q

Maternal end-organ damage in preeclampsia

A
  • HTN
  • Glomerular dysfunction
  • Proteinuria
  • Brain & liver edema
  • Coagulation abnormalities
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18
Q

Preeclampsia

Etiology

A

Vasospasm
* Uterine vessels (two-stage theory)
* Inadequate maternal vascular response to trophoblast-mediated vascular changes
* Endothelial damage
* Hemostasis
* Prostanoid balance
* PGI2:TXA2 balance shifted to favor TXA2
* TXA2 promotes: vasoconstriction; platelet aggregation
* Endothelium-derived factors
* Decreased NO in pts w/ preeclampsia resulting in vasoconstriction
* Lipid peroxide, free radicals & antioxidants
* Increase in preeclampsia resulting in vascular injury

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19
Q

Preeclampsia

Pathophysiology

A

Mediated by systemic vasospasm
* Cardiovascular effects
* Hematologic effects
* Neurologic effects
* Pulmonary effects
* Renal effects
* Fetal effects

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20
Q

Cardiovascular effects of vasospasm

Pathophysiology

A
  • Hypertension
  • Increased CO
  • Increased SVR
21
Q

Hematologic effects of vasospasm

Pathophysiology

A
  • Volume contraction / hypovolemia
  • Elevated hematocrit
  • Thrombocytopenia
  • Microangiopathic hemolytic anemia
  • Third spacing of fluid
  • Low oncotic pressure
22
Q

Neurologic effects of vasospasm

Pathophysiology

A
  • Hyperreflexia
  • Headache
  • Cerebral edema
  • Seizures (eclampsia)
  • PRES radiological findings
23
Q

Pulmonary effects of vasospasm

Pathophysiology

A
  • Capillary leak
  • Reduced colloid osmotic pressure
  • Pulmonary edema
24
Q

Renal effects of vasospasm

Pathophysiology

A
  • Decreased GFR
  • Glomerular endotheliosis
  • Proteinuria
  • Oliguria
  • Acute tubular necrosis
25
Q

Fetal effects of vasospasm

Pathophysiology

A
  • Placental abruption
  • Fetal growth restriction
  • Oligohydramnios
  • Fetal distress
  • Increased perinetal morbidity & mortality
26
Q
  • Headache
  • Visual changes
  • Epigastric / RUQ pain

Symptoms

A

Severe preeclampsia

27
Q
  • SBP >160 or DBP >110
  • Papilledema
  • Pulmonary edema

Signs

A

Severe preeclampsia

28
Q
  • Platelets: < 100,000 x 10^9 /L
  • AST, ALT: elevated (>2x normal)
  • Serum creatinine: >1.1 mg/dL
  • Hemolysis
  • Abnormal coagulation: increased PT, PTT

Labs

A

Severe preeclampsia

29
Q

Defined as severe preeclampsia with new onset tonic-clonic, focal or multifocal seizures in absence of other causative conditions

A

Eclampsia

Other cause: epilepsy, cerebral ischemia, intracranial hemorrhage, drugs

30
Q

Eclampsia

Epidemiology

A

Incidence (US): 1/1,000 deliveries
Mortality: 1% developed world; 15% developing world

31
Q
  • LDH: >600 IU/L
  • AST & ALT: >2x ULN
  • Platelets: < 100,000
A

HELLP syndrome

HELLP: Hemolysis, Elevated Liver Enzynes, Low Platelets

32
Q

HELLP syndrome

Epidemiology

A

20% of women with severe preeclampsia
* Occurs in young women, early in pregnancy

33
Q

HELLP syndrome

Potential Complications

A
  • Placental abruption
  • Renal failure
  • Subcapsular hepatic hematoma
  • Preterm delivery
  • Fetal / maternal death
  • Recurrent preeclampsia
34
Q

Non-severe preeclampsia

Approach to Therapy

A

Conservative management
* Modified bedrest (rest at home; no activity)
* BP monitoring 2-3x/day
* Call MD if any Sx of headache, visual changes, or decreased fetal movement
* Biweekly MD visit
* Weekly labs
* Biweekly fetal well-being tests (sonogram, NST)

35
Q

Severe preeclampsia

Approach to Therapy

A

Delivery
* Pitocin: induce labor
* Magnesium sulfate: prevent seizures
* Antihypertensives (some cases)

36
Q

MoA: Pitocin

Severe Preeclampsia Treatment

A
  • Oxytocin stimulates Ca2+-mediated activation of myometrial receptors
    • Also causes release of Ca2+ from sarcoplasmic reticulum
  • Activation of Ca2+ receptors induces contraction

Pitocin = oxytocin analog

37
Q

MoA: Magnesium Sulfate

Severe Preeclampsia Treatment

A
  • CNS depression
    • Mg2+ competes with Ca2+ for calcium channels blocking intracellular flow of Ca2+ needed to initiate neuronal firing
      • Raises threshold for neuronal triggering of seizure activity
    • Antagonistic effects of Mg2+ can also affect cerebral endothelium that forms BBB
      • Decreased cell calcium inhibits endothelial contraction & opening of tight junctions
  • Increased blood flow to CNS
    • Small vessel vasodilation
38
Q
  • Loss of deep tendon reflexes (DTRs)
  • Respiratory depression
  • Cardiac arrest

Symptoms

A

Magnesium sulfate toxicity
* Loss of DTRs: >10 mEq/L
* RD: >15 mEq/L
* CA: >20 mEq/L

Recommended Mg levels: 4-7 mEq/L; monitor DTRs

39
Q

Indication for antihypertensives in preeclampsia

Approach to Therapy

A

Severe HTN: SBP >160 or DBP >110

40
Q

Optimal intervention to prevent deaths due to stroke in women with preeclampsia

A

Blood pressure control

41
Q

First-line antihypertensive agents for preeclampsia

Approach to Therapy

A
  1. Labetalol IV
  2. Hydralazine IV
  3. Nifedipine PO: if no IV route available
42
Q

MoA: Labetolol

Severe Preeclampsia BP Control

A
  • Non-specific antiadrenergic agent
  • Alpha1-blocker: vasodilation
    • Decreases SVR
  • Beta-blocker: prevents reflex tachycardia
    • Decreases BP
43
Q
  • Flushing
  • Light headedness
  • Palpitations
  • Scalp tingling

Symptoms

A

Labetolol side effects

Severe Preeclampsia BP Control

44
Q

MoA: Hydralazine

Severe Preeclampsia BP Control

A
  • Activates arteriolar endothelium receptors & induces release of NO
  • Promotes vasodialtion
  • Decreases SVR
45
Q
  • Reflex tachycardia
  • Flushing
  • Nausea
  • Salt & water retention
  • Drug-induced SLE

Symptoms

A

Hydralazine side effects

Severe Preeclampsia BP Control

46
Q
  • Reflex tachycardia
  • Flushing
  • Nausea
  • Salt & water retention
  • Drug-induced SLE

Symptoms

A

Hydralazine side effects

Severe Preeclampsia BP Control

47
Q

MoA: Nifedipine

Severe Preeclampsia BP Control

A
  • Blocks Ca2+ channels & reduces intracellular Ca2+ in vascular smooth muscle
  • Prevents contraction of vascular smooth muscle
  • Promotes vasodilation
  • Decreases SVR
48
Q

Chronic HTN & superimposed preeclampsia

Approach to Diagnosis

A
  • Chronic HTN
    • HTN diagnosed pregestation or <20 wks gestation
      OR
    • HTN first diagnosed during pregnancy & does not resolve in postpartum period
  • Superimposed preeclampsia
    • Preeclampsia w/ Hx of HTN before pregnancy or <20 wks gestation
49
Q

Chronic HTN & superimposed preeclampsia

Approach to Diagnosis

A
  • Chronic HTN
    • HTN diagnosed pregestation or <20 wks gestation
      OR
    • HTN first diagnosed during pregnancy & does not resolve in postpartum period
  • Superimposed preeclampsia
    • Preeclampsia w/ Hx of HTN before pregnancy or <20 wks gestation

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GU / GYN & Renal (23 decks)

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