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NUR 113 Unit 3 Questions And Answers With Verified Study Solutions
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NUR 113 Unit 3 Questions And Answers With Verified Study Solutions
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NUR 113 Unit 3 Questions And Answers With VerifiedStudy Solutions
Chronic Hypertension ANS ✅ History > BP 140/90 prior to pregnancy, during, & after pregnancy
Meds:
labetalol - BETA blocker (slows HR and force)
nifedipine - antianginal calcium channel blocker slows down calcium ions that slow the heart down
methyldopa - alpha-2 agonist releases/relaxes blood vessels to make blood pass easier
a client will not be on meds unless it reaches that dangerous threshold
Gestational Hypertension ANS ✅ > BP in pregnancy (140/90 mm Hg) or systolic elevation of > 30
+diastolic elevation of > 15
No proteinuria
BP resolves after birth within 12 weeks
Preeclampsia/
Eclampsia ANS ✅ Most common
Hypertension occurs at or >20 wks
Previous normotensive Proteinuria
Progressive
Chronic Hypertension with superimposed preeclampsia or eclampsia ANS ✅ Worsening >20wk
> Serum uric acid
*normally uric acid is 6.8 (anything higher than that is the only thing that stands out for
superimposed preeclampsia)*
*urine protein > 300*
,preeclampsia ANS ✅ is increased blood pressure in pregnancy after 20 weeks gestation
accompanied by proteinuria in a previously normotensive woman.
*urine protein > 300*
eclampsia definition ANS ✅ the occurrence of a seizure in a woman with preeclampsia who has no
other cause for a seizure.
risk factors (PIH) ANS ✅ First pregnancy
Age younger than 18 years or older than 40 years
Prior history of preeclampsia
African American race
Medical risk factors:
Twins or multiples
Family history
Current theories (PIH) ANS ✅ 1. Abnormal trophoblast invasion
2. Dietary deficiencies
3. Genetic abnormalities
4. Immunologic response to partially foreign genetic placental & fetal tissue.
,5. Stimulation of the inflammatory system by the cardiovascular changes of pregnancy
Pathophysiology OF PIH ANS ✅ The normal response during pregnancy is to lower the peripheral
vascular resistance and to increase maternal resistance to the pressor effects of Angiotensin II results
in lowering the blood pressure.
Gradual loss of resistance to angiotensin II occurs for preeclampsia women.
Loss of normal pregnancy vasodilation of uterine arterioles and concurrent maternal vasospasm
results in decreased placenta perfusion.
Angiotensin II and blood vessels Effect ANS ✅ drop in BP/drop in fluid volume
Renin release from the kidney
angiotensinogen -> renin acts on angiotensinogen to form angiotensin I.
ACE (angiotensin-converting enzyme) releases from the lungs
ACE acts on angiotensin I to form angiotensin II. *(angiotensin II also acts directly on the blood
vessels stimulating vasoconstriction - narrowing)*
Angiotensin II acts on the adrenal gland to stimulate the release of aldosterone.
Aldosterone acts on the kidneys to stimulate reabsorption of salt (NaCl) and water (H2O)
Pathophysiology Of PIH ANS ✅ Normal renal perfusion is decreased with reduced GFR
Stretching of capillary walls of the endothelial cell walls of the glomerulus allows large protein to
escape in urine.
Cycle of PIH ANS ✅ vasospasm
, increased peripheral resistance
decreased tissue perfusion
hypertension
in pregnancy, it is normal to have 0 - trace amounts of protein in the urine
when you are not pregnant you should have zero protein in your urine
protein in the urine during pregnancy vs not pregnant ANS ✅ in pregnancy, it is normal to have 0 -
trace amounts of protein in the urine
when you are not pregnant you should have zero protein in your urine
Clinical manifestations of PIH ANS ✅ Kidney:
<perfusion,
< GFR
manifestation: < UOP and edema
Brain:
< perfusion
< O2
>cerebral edema
manifestation: visual disturbances and seizures
Liver/
Pancreas:
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