Professional Documents
Culture Documents
Causes:
MAIN CAUSES OF EARLY HEMORRHAGE:
• Overdistention of uterus (large baby, multiple
• Uterine atony – first 2 hours, which is critical
gestation)
• Lacerations
o Large baby and multiple gestation excessively
• Retained placental fragments
stretches the uterine wall making the uterus fail to
• Inversion of the uterus
contract after it empties
• Placenta accreta
• Uterine muscle exhaustion (prolonged labor)
o The uterus failed to contract since it got tired
because contraction and the labor process are
exhausting
• Uterine infection
o It is important to prevent UTI or any infection in uterus isn’t fully healed during that pregnancy =
general since the bacteria can ascend to the difficulty to contract which would lead to uterine
uterus causing infection. rupture since uterus is stretched again even if it
o Uterine infection = failure to contract isn’t fully healed.
• Uterine relaxants (general anesthetic) • Chorioamnionitis
o Local anesthesia is usually used for episiotomy o Inflammation of the bag of water
o The effect of general anesthesia (GA) is o Can cause uterine infection
vasodilation. If GA is used, usually during CS, the • Full bladder: Distended Uterus = Uterine Atony
blood and muscles are relaxed leading to uterine o After delivery, the uterus should be on top of the
atony bladder at the middle of the umbilicus at the
• Retained placental fragments fundus,
o Since a portion of the placenta is left in the uterus, o If the bladder is full, the uterus is distended to
the chorionic villi is still there which is the pathway either left or right, which will lead to uterine atony
of blood from mother to fetus. If the chorionic villi
is left, it will continue to receive blood and will Additional Notes:
continue to bleed. ✓ Hydramnios, large baby, uterine myoma, over
distended uterus, macrosomia, multiparity – can
FACTORS CAUSING UTERINE ATONY all make uterus distended
o Over distention of the uterine muscle wall will
• Multiple Gestation eventually allow failure of uterine contraction
• Precipitate Labor after delivery
o The stronger contraction and shorter intervals
during precipitate labor would allow the uterus to
get tired, which will cause uterine atony
• Hydramnios
o Polyhydramnios
• Large Baby
• Uterine Myoma
• Over distended uterus
• Macrosomia
• History of PPH
o Most likely to have the same condition on
succeeding pregnancies
• MgSo4 use
o Although it is used to prevent seizures for PIH, it
is also a tocolytic (uterus relaxant). When given
before delivery, it will make the uterus less likely
to contract after delivery since the effect is still in Fig. 2 Uterine Atony
the body SIGNS AND SYMPTOMS
• General anesthesia
• Oxytocic drugs 1. Boggy Uterus
o Oxytocin (Pitocin) and Methergin 2. Large uterus
o Stimulates contraction of the uterus, however, 3. Expulsion of large clots
when more doses are given, it will stimulate the 4. Bright red vaginal bleeding: Dehydration: leads to
uterine muscles to get tired = failure to contract Hypovolemic shock
o Bright red vaginal bleeding came from the arteries
• Multiparity
that has been cut, which is from either episiotomy
• Advanced maternal age
or laceration
• Prolonged tocolytic agents
5. Hypotension, tachycardia, tachypnea
o Ex. duvadilan, isoxsuprine HCL
o highlight from any fluid loss
o Ex. duvadilan is given to a mother to prevent
6. Pallor, poor capillary refill test (CRT), dry skin, dry
preterm labor. However, the bag of water ruptured
mucous membrane, dry lips
so the baby should be delivered to avoid infection.
o Dahil nawalan ng dugo, ang water from cellular
Duvadilan is a muscle relaxant that directly affects
level is pupunta sa blood stream to refill the
the smooth muscles. Since the mother has been
losses. Yung cells, particularly sa skin is
using duvadilan, there would be difficulty of
dehydrated.
contraction after delivery
7. Decrease urine output, concentrated urine
• Dystocia
o Low urine output is the kidney’s compensatory
o Prolonged labor = tired uterus = failure to contract
mechanism to conserve or keep water in the body
• Previous uterine surgery
▪ Brought about by the antidiuretic hormone
o Should allow the exact time of healing of the
which will be released in cases bleeding,
uterine wall and uterine muscles where the
water loss, plasma loss. Antidiuretic
incision took place
hormone will tell the kidney to conserve
o If there is a short interval (ex. less than a year)
water
between the surgery and next pregnancy, the
8. Dizziness, headache, delirium, confusion
o Blood loss - decreased oxygen to the brain since Additional Notes:
blood (hemoglobin) carries oxygen
✓ Oxytocin: promotes/stimulates uterine contraction,
Additional Notes: good for the 1st until 4th stage of labor
✓ Contraction: methergin (increases BP, can only be
✓ Boggy uterus = malambot na uterus given on the 4th stage of labor considering the
✓ Hypovelemic shock: patient’s BP is normal and the placenta is out), the
o 10% murag standard na percent for effect is more on the blood vessel
hypovolemic shock ▪ If BP is high and methergin is given, the BP
o >10%: irreversible will continue to increase, which could lead to
o <10%: buhay ka pa seizure, will worsen eclampsia, etc.
✓ E.g the patient is 50kls. ▪ If given before placental delivery, the uterus
will trap the placenta inside = CS
50kls x 60= 30 kls fluids/blood x 10 %=
3kls = 3000g = 1ml
MEDICAL MANAGEMENT OF UTERINE ATONY
Therefore, 3000ml blood loss. This is irreversible
and may likely result to death, and it denotes hypovolemic 1. Intravenous Fluid: D5LR 1L, PNSS with BT
shock. 2. Oxytocic medications:
A. Oxytocin: Pitocin
SIGNS AND SYMPTOMS OF SECONDARY B. Methylergonovine maleate: Methergin
POSTPARTUM HEMORRHAGE: ▪ Methergin: contracts vascular smooth
muscles. Only given IM if the BP of the client
General is within Normal level
▪ Contraindicated to elevated BP because the
• Tachycardia and low grade fever methergin further increase BP
C. Cytotec: prostaglandin
Abdominal Examination
D. Antibiotics: Amoxicillin
• Subinvolution of uterus 3. Blood transfusion: replace blood loss for vaginal bleeding
4. Catheterization: Full bladder causes uterine distention =
Vaginal Examination uterine atony
5. Oxygen administration
• Lochia heavier in amount; fresh in color and offensive
odor
• If infection occurs, retained placenta may present Additional Notes:
LACERATIONS
Vaginal
• Anterior
• Posterior
• Lateral wall
Perineal
• Lateral
Fig. 7 Degree of Lacerations
PERINEAL TEARS
First Degree SURGICAL MANAGEMENT OF LACERATIONS
HEMATOMA
Postpartum Hematoma
Fig. 16 Vaginal
Hematoma
Fig. 14 Surgical Repair
• Rectal pain, vague lower abdominal pain but hematoma
NURSING CARE: MEDICAL MANAGEMENT will not be obvious externally but can be diagnosed by
vaginal examination
• Vaginal Pack: compress the site of lacerations. Must be
• The mass often occludes the vaginal canal and extends
removed after 2 hours and/or before transfer to the
into the ischiorectal fossa
room/ward
o Roll ang OS then ipasok sa vagina
o Napkin gamit sa lying-in
FACTORS CAUSING HEMATOMA
o Remove to prevent infection
• Analgesics: Mefenamic Acid • Rapid spontaneous birth
• Varicosities
• Episiorrhaphy
• Lacerations
Incomplete
MEDICAL MANAGEMENT OF UTERINE RUPTURE
• Intact perimetrium
• Intravenous fluid
• Blood transfusion
• Antibiotics: Amoxcilline
• Oxytoxics: Oxytocin, Methergin
• Laparotomy
• Tubal ligation
• Hysterectomy
Fig. 17 Uterine Rupture Posterior and Anterior View NURSING DIAGNOSIS AND INTERVENTIONS
Nursing Diagnosis
Nursing Diagnosis
Fig. 18 Uterine Rupture
• Dysfunction Grieving
SIGNS AND SYMPTOMS OF UTERINE RUPTURE
• Anxiety
• Localized abdominal pain • Fear
• Abdominal tenderness Interventions
• Tearing feeling
• Hypovolemic shock ✓ Obtain consent for surgery
✓ Give factual information • Prevent infection
✓ Explain procedures • Prevent death
✓ Do not give reassurances
MEDICAL MANAGEMENT
✓ Emotional support
Initially
UTERINE INVERSION
• Tocolytic: Duvadilan – relaxes uterus to perform
Johnson’s Manuever
• General anesthesia
• Nitroglycerin patch: potent vasodilator
Later: When Uterus is Back in Place
SURGICAL MANAGEMENT
• Johnson’s Maneuver
• Surgical Replacement
• Hysterectomy
• Laparotomy
• General Anesthesia
Fig. 24 Johnson’s
Maneuver
NURSING DIAGNOSIS AND INTERVENTIONS
Nursing Diagnosis
RETAINED PLACENTA
Fig. 26 Abnormal
CAUSES OF RETAINED PLACENTA
Placental Attachments
• Placenta separated but not expelled: the placenta may
separate completely from the uterine muscle but may still Additional Notes:
be retained within the uterus. There are three causes for ✓ Placenta accreta – attachment of the chorionic villi
this retention: (placenta root) to the endometrial lining
o Failure of the woman to push out the placenta due ✓ Placenta increta – involving the myometrium
to exhaustion of prolonged labor ✓ Placenta percreta – involves the entire layer of the
o Closure of the cervix preventing the placenta from uterus + surrounding organs
being expelled
o A constriction ring in the uterus can hold up the
placenta
RETAINED PLACENTA
Causes
Normal Pregnancy
Fig. 28 Normal
Placental Attachment
Placenta accreta
Fig. 30 Placenta
Placenta percreta increta
Fig. 34 Adherent Placenta
• When the placenta goes completely
through the uterine wall, sometimes
invading nearby organs like the
bladder
Fig. 31 Placenta
percreta
• Shock
• Postpartum hemorrhage
• Puerperal sepsis
• Subinvolution
• Hysterectomy
• Inform anesthetist
• Insertion of large bore IV (18g) cannula
• Insert urinary catheter
• Commence/continue oxytocin infusion 20 units in 1L / rate
– 60drops per min Fig. 38 Subinvolution of Uterus
• Measure and accurately record blood loss
• Prepare and transfer patient to theatre for manual
removal of placenta (MROP)
MEDICAL MANAGEMENT
• Oxytocin
• Methylergonovine maleate Hemorrhagic syndrome
• IVF: hydration, BT
Called
Surgical Management
DIC
• Hysterectomy
Additional Notes:
NURSING CARE
✓ Thrombus formation at the site of injury +
• Massage the fundus microcirculation – clot formation sa cervix, uterus,
• Put ice pack over the fundus vaginal area, perineum pero mag clot din sa
o Prevent vasoconstriction therefore stimulating systemic circulation that’s why effect ng DIC is
vascular contraction whole body naga clot
• Teach client on nipple stimulation
• Encourage breastfeeding: stimulate release of oxytocin
FACTORS CAUSING DIC
• Monitor for lochial flow
• Measure for vaginal bleeding • PIH
• Regulate IVF with Oxytocin o Promotes microcoagulation causing thrombus
• Monitor I&O formation and thus DIC
• Abruption Placenta
NURSING DIAGNOSIS AND MANAGEMENT • Incomplete Placenta
• Septic Abortion
• Fluid Volume Deficit r/t
• Prolonged retention of dead fetus
• Decrease Cardiac Output r/t
• Amniotic fluid embolism
• Altered Tissue Perfusion r/t
• Hypertonic labor
• Hyperthermia r/t
• Sepsis
• Anxiety r/t
• Fear r/t OTHER CAUSES OF DIC
DISSEMINATED INTRAVASCULAR COAGULATION Hemolysis
(DIC)
• Hemolytic transfusion reaction
• Sometimes a complication of PIH or any bleeding • Massive transfusions
disorders • Malaria
• Systemic effect • Other severe hemolysis
• Pathological activation of clotting in response to
septicemia, cancers, obstetric (e.g. retained dead Malignant Disorders
fetus, amniotic fluid embolism)
• Metastatic malignancy
• Thrombotic phase: Numerous small thrombi and emboli
• Tumors producing cancer procoagulant
form throughout the microvasculature causing block of
• Tumor with tissue necrosis (usually breast cancer)
Vascular Abnormalities Additional Notes:
• Pancreatitis
• Acute liver necrosis
• Transplant rejection PATHOPHYSIOLOGY OF DIC
• Heat stroke
Precipitating event
Coagulation cascade
Conversion of
Excess thrombin
plasminogen to plasmin
Microvascular
clotting
Microvascular
clotting
Fig. 40 DIC Causes
Thrombocytopenia Consumption of Excess thrombin
clotting factors
Ischemia Shock
Impaired organ perfusion Hypotension
End-organ damage Increased vascular
permeability
Additional Notes:
1. Bleeding
o Bleeding on mucous membrane, GI & GU tracts,
and all other orifices (all other exit sites)
Fig. 41 DIC o Petechiae and ecchymosis
o Intravenous (IV) lines and catheters bleed
o Venipuncture sites, surgical sites, drains, and
tracheostomies and within serous cavities
2. Renal Failure
o Blood loss = decreased oxygen to organs, or in
this case the kidneys = renal failure
3. Pulmonary Involvement D. Hemorrhage
o Dyspnea, Hemoptysis, Diaphoresis o Blood escapes through ruptured vessel
4. Jaundice o Insufficient clotting agent available to control
bleeding
Other Signs and Symptoms
Central Nervous System Signs Include the Following: • Heparin: anticoagulant – prevents formation of blood
clots
1. Nonspecific altered consciousness or stupor • Blood transfusion for blood replacement
2. Transient focal or neurologic deficits o Hemoglobin of 8 or 9 = subject to BT
• Fresh frozen plasma transfusion for plasma
Cardiovascular Signs Include the Following:
replacement
1. Hypotension • Platelet transfusion for platelet replacement
2. Tachycardia
3. Circulatory collapse DIC MANAGEMENT
Respiratory Signs Include the Following: • Treatment of underlying cause
• Fluid replacement
1. Pleural friction rub
• Blood products
2. Signs of acute respiratory distress syndrome (ARDS)
o FFP
o Platelets
o PRBCs
• Management of clotting
o Plasmapheresis
o Heparin
• Management of bleeding
o Aminocaproic acid (promote coagulation)
o Antithrombin III (prevent bleeding)
POSTPARTUM INFECTION
TYPES OF INFECTION
Fig. 1 Endometritis
MANAGEMENT
BREAST ENGORGEMENT
Causes
MANAGEMENT
• Delayed or infrequent feeding
• Right dosage of antibiotics
• Improper latching and positioning
• NGT to relieve vomiting and rest the bowel
• Engorged breast: swollen, hard, warm and painful
• IVF
• Parenteral feeding (ex. Kaviben) Prevention
• Analgesics
• Antipyretics • Early and frequent feeds
• Correct attachment
MASTITIS Treatment
• Infection of the breast tissues • Warm water packs, breast massage, analgesics
• Occurs as early as 7 days postpartum or not until the baby • Milk expressed to soften breast
is weeks or months of age
• Breastfeeding and lactation are the most likely causes of SIGNS AND SYMPTOMS
mastitis
• Localized pain and swelling
• Breastfeeding places stress on the nipple and
• Fever
surrounding breast tissues, which often results in small
cracks. • Body malaise
• Rapid pulse
• Bacteria from the baby’s mouth or the mother’s skin may
enter these abrasion and infect breast tissue • Scanty breast milk
o Nag narrow and duct since inflamed ang breast so
• The nipples on an engorged breast are flat or inverted.
Sometimes it may lead to striae on nipples, mainly hindi makalabas ng maayos ang milk
preceding symptoms of septation mastitis
• Note for: cracked nipples, clogged ducts, bruises on the
breasts
Additional Notes: o Soup with malunggay
• Alternate breast for breastfeeding
✓ The main symptoms of mastitis are: breast pain, • Administer antibiotics as ordered
swelling, redness, fever, enlargement, changed • Administer anti-inflammatory meds
nipple sensation, discharge, itching, tenderness, • Administer analgesics
and/or breast lump
NURSING DIAGNOSIS AND INTERVENTIONS
NURSING CARE
Dilatation of veins
OTHER FACTORS
• Varicosities
o Patient has varicose before delivery
o Pwede mag lodge ang thrombus which can cause
swelling
Decrease fibrinolytic factors
• Obesity Thromboxane (plasminogen & antithrombin)
o Slow venous return
• History of thrombophlebitis
• Oral contraceptives Elevate coagulation
• Age > 35 years old factors
• Multiparity
• Diabetes mellitus
o Slow blood flow Thrombus Formation
• Smoking
Additional Notes:
CLASSIFICATIONS OF THROMBOPHLEBITIS
ACCORDING TO DEPTH
Additional Notes:
• Nurse-patient relationship
o Therapeutic relationship
FACTORS CAUSING POSTPARTUM BLUES o Stay with the patient, listen to their concerns, give
them feedback, etc.
• Sudden drop of hormones at about 72 hours postpartum
• Psychopharmacologic
o In relevance to HCG and HPL since the placenta
o Anti-depressive drugs
is already separated from the uterus
o Selective serotonin reuptake inhibitors (SSRI)–
serotonin problems with the neurotransmitters
• Disappointments of body changes
▪ Brand name: Citalopram
• Extreme disappointments of labor and birth
o Escitalopram Oxalate
• Inadequate emotional support from partner
▪ Brand name: Lexapro
• Extreme stress of mothering role o Zoloft – commonly heard
▪ Generic Name: Sertraline • Psychotherapy and Milieu Therapy (for depression and
• Milieu therapy psychosis)
o Forceful manipulation of the environment o Psychotherapy – emotional and mental support,
o Scheduled activity counselling
o Ex. breakfast sa morning, 30 mins walking, then ▪ Counselling, Psychologist, Psychiatrist,
rest for a while, read at least 2 pages, the lunch, Nurses
then sharing with lain mothers with postpartum o Milieu Therapy – change the environment and
depression, then walking naman, so on activities that is therapeutic in a way
• Observe for suicidal and infanticide thoughts
Additional Notes: o Observe self-inflicting harm and wounds with
different rates of healing, particularly on the wrist
✓ If postpartum depression is not immediately o Keep away from sharp objects or anything that
assessed and managed, this could progress to can be used to harm the patient and baby
postpartum psychosis
• Suicidal precautions (Away from sharp objects)
o Raise the side rails, away from sharp objects, etc.
POSTPARTUM PSYCHOSIS
NURSING DIAGNOSIS AND MANAGEMENT OF
• It is a disrupted mental state in which an individual POSTPARTUM EMOTIONAL DISTURBANCES
struggles to distinguish the external world from his
• Risk for/Actual Ineffective Coping r/t
internally generated perceptions ✓ Convey a caring attitude
• The disorder may become apparent 20 to 3 weeks after ✓ Acknowledge that the woman feels depressed
birth to as long as 6 to 12 months ✓ Assure that it is not her fault
• Much more worse than postpartum depression ✓ Encourage support from family members
✓ Adequate rest and nutrition
FACTORS CAUSING POSTPARTUM PSYCHOSIS
• Self-Isolation r/t
• Major life crisis • Anxiety r/t
• Previous mental illness • Sleep pattern disturbance r/t
• Family history of mental illness • Altered sensory perceptions (Visual) (Hearing) r/t
• Hormonal changes • Imbalance nutrition less than body requirements r/t
• Altered parenting r/t
SIGNS AND SYMPTOMS
NURSING CARE
• Use therapeutic technique of communication
• Stay with the client
• Listen attentively
• Allow client to verbalize feelings
• Re-orient client to reality
• Counselling
• Encourage support from partner and family
• Provide adequate nutrition
• Encourage rest
• Use non-judgmental response
INFERTILITY
Tubal
OUTLINE • Scarring
o Mahirapan na maglabas ang egg due to the
I. Infertility scarring
II. Factors Causing Infertility • PID
III. Etiology • Endometriosis Will lead to scarring
IV. Diagnostic Studies Ovarian
V. Management of Infertility
VI. Role of the Nurse in Contraception and • Anovulation
Infertility o when an egg doesn't release from your ovary
VII. Management during your menstrual cycle (hindi naga
VIII. Nursing Care menstruate)
IX. Nursing Diagnosis • Oligo-ovulation
o Infrequent menstruation (ex. mag menstruate
INFERTILITY once every 6 months)
• Secretory
• Normally, 50% of recently married couples conceive o Hormonal
within 6 months and 35% conceive within 12 months
MALE INFERTILITY
• Infertility is the inability to conceive after at least 1 year of
sexual intercourse at leats 4 times a week without Congenital
contraception
• Absence of vas deferens and testes
Primary Infertility
Ejaculatory
• No previous history of conception
• Retrograde ejaculation
Secondary Infertility
o Pabalik ang ejaculation instead na palabas
• Inability to conceive after previous successful pregnancy Sperm Abnormalities
FACTORS CAUSING INFERTILITY • Oligospermia
o Low sperm production
• Not ovulating
• Aspermia
• Male infertility
o No sperm at all
• Age (menopause)
• Inadequate maturation
• Blocked fallopian tubes - egg and sperm aren’t able to
o Hindi naga mature ang sperm na pwede mag
meet due to the obstruction
conceive
• Endometriosis
• Inadequate motility
• Underlying medical problems (ex. diabetes) o Short or slow tail so by the time mag meet sila ng
ETIOLOGY egg, dead na ang egg
• Inability to deposit sperm into the vagina
FEMALE INFERTILITY • Blockage of sperm (ex. vas deferens obstruction)
Vaginal Problems Testicular
Additional Notes:
OUTLINE
I. Pathophysiology of GDM
II. Pathophysiology of PIH
PATHOPHYSIOLOGY OF GDM
Cell no nutrients Increase G in blood concentration Increase Glucose in Fetal Circulation – Fetal
pancreas will be stimulated to release fetal
insulin – Glucose absorption
Cellular hunger Increase blood viscosity
MACROSOMIA
Water for ICS – Shift to IVS
Cell message the brain (Osmosis) in an attempt to
to tell = hunger; brain dilute the blood viscosity Water & Glucose = Kidneys
response for the body to
eat
More water escape = Cellular dehydration Filtration
Increase eating
Cell message - thirsty GLYCOSURIA Increase in Filtered water
Increase in Urine Output
POLYPHAGIA
Brain response –
POLYDIPSIA POLYURIA
Increase OFI
GDM DIAGRAM 2: EFFECTS ON VITAL ORGANS
HYPERGLYCEMIA
Amputation Increase in
peripheral resistance Increase Lactic Acid
• Once Estrogen, Progesteron, and HPL crosses maternal • There is decreased blood flow since the blood is already
circulation, this causes insuling resistance. Without viscous.
insulin, the glucose cannot enter the cell therefore, the • Decreased blood flow and oxygen to the retina would
glucose will stay in the bloodstream = hyperglycemia cause inadequate supply of oxygen and glucose to the
blood vessels which helps the eyesight = blurring of
POLYPHAGIA visions
• The client will eventually manifest blindless if not properly
• In the presence of hyperglycemia, the glucose stays in
managed. It is a must to regulate the sugar level at all
the blood stream and the cell does not receive any
times to prevent blurring of vision and blindness
nutrients therefore, they will be hungry (cellular hunger)
• The cell will then message the brain telling the brain that SKIN
the cell is hungry. In response, the brain will tell the
patient to eat (polyphagia). • Decreased blood flow and oxygen to the skin causes
decreased sensation (peripherial neuropathy) or
POLYDIPSIA numbness
• The client will then be at risk for injury on the skin. Since
• Since the patient has hyperglycemic blood, the blood is healing is delayed for patients with diabetes, this will lead
concentrated. When the blood is concentrated, it is to necrosis of affected extremity (usually feet), and will
viscous (malapot). eventually lead to amputation
• Increased blood viscosity will allow the fluid from the o More common on type 1 and 2 DM not GDM
intracellular space (ICS) to shift to the intravascular space • Wound healing requires a lot of nutrients, oxygen, etc.
(IVS) in the process of osmosis in an attempt to dilute the Since the blood is viscous, the circulation is slow and
high concentration of glucose in the intravascular space. most of the time the distal portion of the toes and fingers
o Osmosis - transfer of water from low concentration receive less amount of oxygen and nutrients. Therefore,
to higher concentration in a semi-permeable there is a tendency for the cell tissue of the affected site
membrane to die and become necrotic. Once necrosis spreads and
• More water escape will lead to cellular dehydration ascends, the affected part will be amputated.
• The cell will message the brain that the body is thirsty. In HEART
response, the brain will tell the patient to increase OFI
(polydipsia). • Chance of having cardiac arrest or CVA is low
• Most common complication would be a combination of
POLYURIA GDM and hypertension or combination of GDM and PIH
• Since the water shifted from the ICS to the IVS, the water LUNGS
is already mixed with the glucose and the cell is already
• Hyperventilation – rapid, shallow breathing so there is
somehow empty that’s why there’s cellular dehydration.
more CO2 rather than O2 which will result to respiratory
• The majority of the water/fluid from the cell is already in
acidosis
the bloodstream. The water and glucose will go to the
kidneys and there will be filtration. MUSCULOSKELETAL (MSS)
• Since there is a mixture of glucose and water going to the
kidney where filtration happens, there will be glycosuria • There is decreased blood flow and O2 to the muscles and
(presence of glucose in the urine) cells, and there is cellular hunger.
• Normally, big molecules like glucose cannot escape in the • To feed the cell while the client is not yet eating, the
urine or in the kidneys. However, since there is a problem, muscle will result to anaerobic metabolism wherein the
like GDM, some big particles of this molecules escaped stored glycogen from the muscles and fat are converted
along with the water into glucose
• Filtered glucose and water will result in increase filtered o Anaerobic metabolism – a metabolism that occurs
water and increase urine output (polyuria) without the usage of oxygen because the body
does not receive enough oxygen in compensation
MACROSOMIA to produce glucose to feed the cell while the client
is not yet eating.
• Since the mother’s blood contains a lot of glucose, this • Aside from producing glucose (good product), anaerobic
glucose will circulate to the maternal and fetal circulation metabolism also produces a waste product called lactic
so it will reach the baby = increase glucose circulation acid
• Increase glucose in the fetal circulation will stimulate the • Increase lactic acid will lead to metabolic acidosis
pancreas to release fetal insulin
• After the baby releases insulin, the glucose from the
mother will be absorbed by the fetus (glucose
absorption). So more glucose will be absorbed =
macrosomia
Additional Notes:
PATHOPHYSIOLOGY OF PIH
Vasospasm Uteroplacental
Insufficiency
Vasoconstriction
Decrease O2 to
Increase blood pressure the fetus
(hypertension)
Abortion
Preterm labor
Intrauterine Growth Restriction
SGA
FDIU (Fetal death in utero)
Abruptio
PIH DIAGRAM 2: VITAL ORGANS AFFECTED
HYPERTENSION / VASOCONSTRICTION
Seizure
AST/ALT Risk for
release bleeding
Increase
DIC
AST/ALT
Increase
Cardiac Output Less O2, More CO2 Decrease urine
output
Increase BP
PIH DIAGRAM 1 Additional Notes:
• There is no exact explanation on the cause of PIH but ✓ Keep the edema localized as much as possible so
there are theories: it will not ascend.
o relevant to infection; relevant to immunity; relevant
to genetics SEIZURE
o damage on the endothelial cells – most common
and nearest reason • If the patient has preeclampsia, there are two reasons
• Endothelial cells are found in the inner lining of the blood why the patient will have seizures = eclampsia
vessels (arteries and veins). If there are damage on the 1. Vasoconstriction – blood vessels in the brain are
endothelial cells, it will cause vasospasm also constricted
• They say that during placental development there is an ▪ If blood vessels are constricted, there is
invasion of abnormal cytotrophoblast on the uterine wall, decreased O2 in the CNS, causing
which decreases placental blood flow alteration in firing of electrical impulses
• Placental ischemia – decrease oxygen in a particular from synapses thereby, causing seizure
tissue that comprises of a lot of blood vessels 2. Cerebal edema – if the edema ascends in the
• Since the endothelial cells are located in the innermost brain, the accumulation in the brain causes
layer of the arteries and veins and if there is endothelial decrease intracranial pressure (ICP), promoting
dysnfuction then it would create vasospasm seizure
• In the presence of hypertension and vasoconstriction, this UTEROPLACENTAL INSUFFICIENCY
will greatly affect the systemic function at the same time
it will affect the organs • Effect of hypertension on the baby
• In the presence of vasoconstriction, it is expected that the • Since there is vasoconstriction, there is decreased O2
blood flow will decrease and the vital organs will receive supply from the mother towards the baby.
inadequate amount of oxygen = organ ischemia
o Kidney – renal ischemia; Liver – hepatic ischemia PIH DIAGRAM 2: EFFECTS ON VITAL ORGANS
etc.
CNS
PROTEINURIA
• Initial symptoms of seizure are dizzines, headache,
• Decrease O2 in the kidney has two effects: lethargy, and confusion
o Decrease renal function, which would lead to
decrease GFR, resulting in decrease urine output MSS
o Nephrotic damage will allow big molecules like
CHON to escape, resulting in proteinuria • Myalgia – muscle pain
• GFR – glomerular filtration rate • Arthralgia – bone pain
• Proteinuria – presence of protein in the urine = protein LIVER
loss
EDEMA • Since there is decrease O2, the liver will work double to
the point that it will swell (hepatomegaly)
• Since there is loss of protein in the blood stream, this will • Since the liver is also responsible for the maturity of the
result to hypoalbuminemia platelet, there will be decrease platelet if the liver is
• There is decreased oncotic pressure since protein exerts damaged.
oncotic pressure • If the platelet goes down from the normal value (below
o Oncotic pressure – pulling force to hold water in 150,000) the client will most likely be at risk for bleeding.
place (inside the cell and blood vessels) If not treated, this will progress to DIC.
• Since there is decreased oncotic pressure, wala nay mag
KIDNEYS
hold sa water. This will allow fluid to escape from ICS/IVS
to ISS • The kidney should receive 20% of oxygenated blood.
o ICS – intracellular space; IVS - intravascular However, due to vasoconstriction, there is decrease O2 to
space; ISS - interstitial space (space outside or in the kidney.
between the cells)
• If the kidney receive less oxygenated blood, the nephrons
• Bipedal edema – edema on the lower extremities; usually (kidney’s functional unit) will start to die. If there are
starts on the foot and goes up if there is more water accumulated dead nephrons, the function of the kidney
retention will reduce.
• Ascites – abdominal edema • If there is nephrotic damage, there would be decrease
• Pulmonary edema – if naabot na sa lungs ang water GFR then decrease urine output. If this worsens and the
retention renal ischemia is left untreated/unmanaged, this will
• If edema the edema is ascending, the water will pass result to acute renal failure. Unmanaged or untreated
through the vein, causing cerebral edema acute renal failure will eventuallty progress to chronic
• ANASARCA – generalized edema/edema all over the renal failure.
body
Additional Notes: