PSYCHOPATHOPHYSIOLOGY Host       Agent Filipino (a woman of color) Has been pregnant with twins of History of multiple gestations Low

socioeconomic background as a factor to poor nutrition Unable to follow low-fat high-calorie diet prescribed at 6 months AOG Preference to fatty and salty food Drinks a glass of coffee and hot chocolate drink (sikwate) both twice a week Environment  Stress

Fatty acids serve as substrates for lipid peroxidation

Cytotrophoblast invasion of the uterine spiral arteries is limited to the proximal decidua Myometrial segments of arteries escaping trophoblast remodeling remain anatomically intact andundilated and adrenergic nerve supply to the spiral arteries is not affected

Increased blood volume during pregnancy

Increased cardiac output Prevents an adequate response to increased fetal demands for blood flow that occur as gestation progresses Generation of free radicals, lipid peroxides and reactive oxygen species Reduced uteroplacental perfusion Placental ischemia Placental release of cytokines (Tissue Necrosis Factor- ) Directly induces oxidative damage on endothelial cells Increased pressure along the walls of the arteries Direct endothelial cell injury in the arteries Prostaglandin action, i.e. increased thromboxane and decreased prostacyclin SEQUEL I

Widespread activation/dysfunction of the maternal vascular endothelium

Enhanced formation of endothelin and thromboxane (vasoconstrictors)

Induces structural and functional alterations in endothelial cells

Reduces acetylcholine-induced vasodilatation

Increased vascular sensitivity to angiotensin II and norepinephrine (pressor substances

Decreased formation of vasodilators such as nitric oxide and prostacyclin

SEQUEL II

SEQUEL II Vasospasm in the arteries Arterial vasoconstriction

The heart is forced to pump against rising peripheral resistance Further injury to arterial endothelium

Decreases perfusion and blood supply to body organs

Increase in blood pressure

Causes the bulk of the blood volume in the maternal circulation to be pooled in the venous circulation Deceptively low arterial intravascular volume

SEQUEL I

Platelets cluster at the sites of endothelial damage Thrombocytopenia Retina Retinal hemorrhage Blindness

Pancreas

Liver

Kidney Increased blood flow resistance in the kidneys Degenerative changes develop in kidney glomeruli due to back pressure

Brain SEQUEL VI

Placenta SEQUEL VII Vision changes

Ischemia

SEQUEL III

Epigastric pain, nausea, general malaise

Increased permeability of the glomerular membrane Allows serum proteins albumin and globulin to escape into the urine Proteinuria SEQUEL IV

Decreased glomerular filtration rate

Elevated amylasecreatinine ratio

Increased kidney tubular reabsorption of sodium SEQUEL V

Decreased urine output

Decreased clearance of creatinine and other substances

Increased serum BUN, uric acid and creatinine

SEQUEL IV Loss of proteins from the blood plasma Osmotic pressure of the circulating blood falls Plasma fluid diffuses from the circulatory system into denser interstitial spaces to equalize pressure Higher concentration of formed elements in the blood versus plasma Increased hematocrit Edema

SEQUEL V Reabsorbed sodium retains water in the body Increased plasma volume Hydrostatic pressure of the blood against blood vessels rises Plasma leaks out the capillaries and goes into interstitial spaces

Peripheral Pitting or nonpitting; noticeable as puffiness in a womans face and extremities, most readily palpated over bony surfaces

Cerebral Excessive water causes the volume of the brain as well as the blood inside the skull to be compressed As the brain, blood or cerebrospinal fluid continue to increase in volume, accommodative mechanisms fail

Pulmonary Fluid transfer isincreased into the lung interstitium; because lymphatic flow also increases, no net increase in interstitial volume occurs The capacity of the lymphatics to drain excess fluid is exceeded and liquid begins to accumulate in the interstitial spaces that surround the bronchioles and lung vasculature Increased pressure causes fluid to track into the interstitial space around the alveoli and finally disrupt the tight junctions of the alveolar membranes SEQUEL X

Damaged cells swell

Injured blood vessels leak

Blocked absorption pathways force fluid to enter brain tissues Injury cascade SEQUEL VIII

SEQUEL VIII Glutamate release into the extracellular space Calcium and sodium entry channels on cell membranes are opened by glutamate stimulation Membrane ATPase pumps extrude one calcium ion exchange for 3 sodium ions Sodium builds up within the cells Creates an osmotic gradient and increasing cell volume by entry of water Increase in water causes dysfunction but not necessarily permanent damage

SEQUEL X Gas exchange becomes impaired Dyspnea, tachypnea, orthopnea, tachycardia, hypertension, thoracic oppression, cold extremities with or without cyanosis, cough with a frothy or pink sputum, extensive use of accessory muscles or respiration, moist rales with or without wheezing

Hypoxia depletes the cells energy stores disabling the sodium-potassium ATPase and reducing calcium exchange Failure of the energy-dependent sodium pump in the cellular membrane causes sodium to accumulate intracellularly and water moves from the extracellular to the intracellular space to maintain osmotic equilibrium Calcium accumulates inside the cell activating intracellular cytotoxic processes

Inflammatory response is initiated by the formation of immediate early genes (c-foc and cjun), cytokines and other intermediary substances

Microglial cells are activated and release free radicals and proteases Free radicals attack cell membranes and capillaries Further increase in brain edema (secondary) Exponential increase in intracranial pressure SEQUEL IX Membranes are disrupted causing irreversible damage to cells

SEQUEL IX

Reduction of cerebral blood flow throughout the brain Widespread brain ischemia Alteration in neuronal environment Seizures Widespread brain infarction

Brain herniation Irreversible brain damage

Alterations in neurological function (e.g. visual disturbances [blurred vision, seeing spots before the eyes], severe headache, marked hyperreflexia, ankle clonus, seizures)

Brain death SEQUEL VII

Placenta begins to separate from the uterus Reduces fetal nutrient and oxygen supply Fetal organ infarction Fetal death Hemorrhage into the decidua basalis

Vaginal bleeding or concealed hemorrhage in the pregnant woman Platelets and fibrin from the general circulation increasingly rush to the site of bleeding Not enough are left in the rest of the body for further clotting SEQUEL XI

SEQUEL XI High thrombin level continues to encourage anticoagulation Paradoxical effect: at one point, the person has increased coagulation but throughout the rest of the system, a bleeding defect exists SEQUEL XII Causes extreme blood loss from lack of fibrinogen Maternal circulatory collapse/shock Maternal and fetal distress Maternal and fetal death

SEQUEL III Liver inflammation RUQ tenderness Liver injury

Impaired production of clotting factors X, IX, VII, II and platelets Hypoglycemia Poor clotting ability Maternal hemorrhage (especially at birth) SEQUEL XII Subcapsular liver hematoma

Hemolysis of RBC

Elevated liver enzymes (ALT, AST)

Renal failure

Hyponatremia

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