The document discusses various physiological changes that occur in pregnancy across multiple body systems. The uterus increases dramatically in size from 70g and 10mL non-pregnant to approximately 1100g and 5L by the end of pregnancy. Hormonal changes include increased estrogen, progesterone, hCG, hPL, prolactin, IGF, and decreased hGH levels. This leads to adaptations in various organ systems like increased blood volume by 45%, enlarged heart and increased cardiac output, mild anemia and thrombocytopenia, immunosuppression to tolerate the fetus, and metabolic changes in carbohydrate and fat metabolism. Respiration is also altered to support higher oxygen demands.
Puerperium is the period following childbirth during which the body tissues, specially the pelvic organs revert back approximately to the pre-pregnant state both anatomically and physiologically. puerperium begins as soon as the placenta is expelled and lasts for approximately 6 weeks when the uterus becomes regressed almost to the non-pregnant size.
Puerperium is the period following childbirth during which the body tissues, specially the pelvic organs revert back approximately to the pre-pregnant state both anatomically and physiologically. puerperium begins as soon as the placenta is expelled and lasts for approximately 6 weeks when the uterus becomes regressed almost to the non-pregnant size.
Threatened abortion by dr alka mukherjee dr apurva mukherjee nagpur m.s.alka mukherjee
Threatened abortion is associated with bleeding and/or uterine cramping while the cervix is closed. This stage of abortion may progress to spontaneous incomplete or complete abortion. While this event may be considered a part of the quality control process in human reproduction, it is important to know the possible etiologies and when therapy might prevent pregnancy loss. The World Health Organization estimated that 15% of all clinically recognizable pregnancies and in spontaneous abortion, 50-60% of which are due to chromosomal abnormalities. Apart from the fetal factors, several maternal and probably paternal factors contribute to the causes of spontaneous abortion. The maternal factors that may be responsible for abortion include both local and systemic conditions such as infections, maternal disease states, genital tract abnormalities, endocrine factors and other miscellaneous causes (antiphospholipid antibodies, maternal-fetal histocompatibility, excessive smoking and other environmental toxicants, etc.). This review focuses on the management of threatened abortion, but it should be emphasized that the management to maintain pregnancy is reasonable only in those cases, in which the fetus is not seriously affected. It would not be beneficial to provide treatment that would permit chromosomally and anatomically abnormal embryos to survive to term. Treatment is feasible first of all in cases with maternal factors. Surgical procedures may precede pregnancy (correction of septate uterus, removal of a submucous leiomyomata) or may be performed usually in the second trimester (cervical cerclage). Maternal general diseases (diabetes, hypothyroidism) and infections should be treated accordingly. The most common entity to be treated in this category is luteal phase deficiency. Progesterone is the most important hormone for the maintenance of an early human pregnancy. Besides progesterone administration, human chorionic gonadotropin (hCG) also is the logical endocrine treatment of choice. In the pregnant woman hCG stimulates and optimizes hormonal production in the corpus luteum and may also influence the fetoplacental unit. The contribution of environmental, physical and chemical agents to the incidence of spontaneous abortion is controversial. They may be abortifacient even if they are not teratogenic. Exposure to environmental toxicants should be avoided. Paternal leukocyte immunotherapy has been associated with successful outcome in patients with unexplained repeated spontaneous abortion. This therapeutic approach is considered experimental, as there may be some significant risks. Associating maternal antiphospholipid antibodies with reproductive failure is a rapidly developing field. Administration of corticosteroids with low doses of aspirin has resulted in fetal salvage in women in whom antiphospholipid antibodies are present.
Rh Incompatibility in Pregnancy. Rh incompatibility occurs when a pregnant woman whose blood type is Rh-negative is exposed to Rh-positive blood from her fetus, leading to the mother's development of Rh antibodies
obstetric and gyneacology; Changes in pregnancy, cardiovascular changes, respiratory changes, endocrine changes, gastrointestinal changes, related organ changes in pregnancy. hormonal changes during pregnancy.
Threatened abortion by dr alka mukherjee dr apurva mukherjee nagpur m.s.alka mukherjee
Threatened abortion is associated with bleeding and/or uterine cramping while the cervix is closed. This stage of abortion may progress to spontaneous incomplete or complete abortion. While this event may be considered a part of the quality control process in human reproduction, it is important to know the possible etiologies and when therapy might prevent pregnancy loss. The World Health Organization estimated that 15% of all clinically recognizable pregnancies and in spontaneous abortion, 50-60% of which are due to chromosomal abnormalities. Apart from the fetal factors, several maternal and probably paternal factors contribute to the causes of spontaneous abortion. The maternal factors that may be responsible for abortion include both local and systemic conditions such as infections, maternal disease states, genital tract abnormalities, endocrine factors and other miscellaneous causes (antiphospholipid antibodies, maternal-fetal histocompatibility, excessive smoking and other environmental toxicants, etc.). This review focuses on the management of threatened abortion, but it should be emphasized that the management to maintain pregnancy is reasonable only in those cases, in which the fetus is not seriously affected. It would not be beneficial to provide treatment that would permit chromosomally and anatomically abnormal embryos to survive to term. Treatment is feasible first of all in cases with maternal factors. Surgical procedures may precede pregnancy (correction of septate uterus, removal of a submucous leiomyomata) or may be performed usually in the second trimester (cervical cerclage). Maternal general diseases (diabetes, hypothyroidism) and infections should be treated accordingly. The most common entity to be treated in this category is luteal phase deficiency. Progesterone is the most important hormone for the maintenance of an early human pregnancy. Besides progesterone administration, human chorionic gonadotropin (hCG) also is the logical endocrine treatment of choice. In the pregnant woman hCG stimulates and optimizes hormonal production in the corpus luteum and may also influence the fetoplacental unit. The contribution of environmental, physical and chemical agents to the incidence of spontaneous abortion is controversial. They may be abortifacient even if they are not teratogenic. Exposure to environmental toxicants should be avoided. Paternal leukocyte immunotherapy has been associated with successful outcome in patients with unexplained repeated spontaneous abortion. This therapeutic approach is considered experimental, as there may be some significant risks. Associating maternal antiphospholipid antibodies with reproductive failure is a rapidly developing field. Administration of corticosteroids with low doses of aspirin has resulted in fetal salvage in women in whom antiphospholipid antibodies are present.
Rh Incompatibility in Pregnancy. Rh incompatibility occurs when a pregnant woman whose blood type is Rh-negative is exposed to Rh-positive blood from her fetus, leading to the mother's development of Rh antibodies
obstetric and gyneacology; Changes in pregnancy, cardiovascular changes, respiratory changes, endocrine changes, gastrointestinal changes, related organ changes in pregnancy. hormonal changes during pregnancy.
Detailed account of the various changes that occur in maternal anatomy, physiology, and metabolism of pregnant women. These physiological changes are often very precise, and deviations of physiological responses can be a prelude to possible disease/infectious states. In this second part of Labor, we will examine the various systems of the human body,its altered states during pregnancy, and how those changes affect the woman preparing for delivery. Special care is imperative in properly determining the needs of an expecting mother, so developing an intimate, trusting relationship between the mother and fully understanding her physiological output will lead to the best chances of a successful delivery.
physiological changes during pregnancy
effect of pregnancy on physiological functions during pregnancy
cardiovascular, respiratory and hormonal changes
Shifa Riaz
gynecology
obstetrics
females
Maternal physiological changes in pregnancy are the adaptations during pregnancy that a woman's body undergoes to accommodate the growing embryo or fetus. ... The pregnant woman and the placenta also produce many other hormones that have a broad range of effects during the pregnancy.
Biochemical changes in pregnancy, Physiological changes in pregnancy, maternal and fetal health assessment, assessment of complications in pregnancy, hormonal changes and physiological evaluations in pregnancy
Similar to Physiological changes in pregnancy (20)
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
3. Uterus
Non PregnantNon Pregnant
UterusUterus
Pregnant UterusPregnant Uterus
MuscularMuscular
StructureStructure
Almost SolidAlmost Solid Relatively thin –Relatively thin –
walled (≤ 1.5 cm)walled (≤ 1.5 cm)
weightweight ≈≈ 70 gm70 gm Approx. 1100 gm byApprox. 1100 gm by
the end ofthe end of
pregnancypregnancy
VolumeVolume ≤≤ 10 mL10 mL ≈≈ 5 L by the end of5 L by the end of
pregnancypregnancy
5. Uterine size, shape & position
• First few weeks, original peer shaped organ
• As pregnancy advances, corpus & fundus
assumes a more globular form.
• By 12 weeks, the uterus becomes almost
spherical .
• Subsequently, uterus increases rapidly in
length than in width & assumes an ovoid
shape.
• With ascent of uterus from pelvis, it usually
undergoes Dextrorotation (caused by the
rectosigmoid colon on the left side)
6. CERVIX
• Estradiol + progesterone swollen and softer during pregnancy
• Estradiol stimulates growth of columnar ep. of cervical canal
ectropion (visible on ectocervix) prone to contact bleeding
• ↑ vascularity look bluer
• Mucous glands distended + complexity↑ secretion↑
mucus thickened operculum @ os (protective plug)
• PG (remodelling of cervical collagen) + collagenase (from
leukocytes) softening
7. • Estrogen vaginal epithelium thicker ↑
desquamation rate vaginal discharge↑ > acidic
protect against ascending infection
• Vagina become more vascular
8. BREAST
• Deposition of fat around the glandular tissue
• Estrogen number of↑ glandular ducts
• Progesterone + hPL number↑ of gland alveoli
• hPL stimulate synthesis of alveolar casein + lactoglobulin +
lactalbumin
• ↑ [serum prolactin] in pregnancy antagonized by estrogen
no lactation
9. • 48 hours after birth rapid of [estrogen]↓ lactation
• End of pregnancy and early puerperium colostrum
produced (thick yellow secretion + immunoglobulin)↑
• Early + frequent suckling stimulates ant. and post.
Pituitary gland prolactin + oxytocin promotion of
lactation
• Stress + fear dopamine↑ synthesis and release of↓
prolactin
10. • 2-3 days of puerperium prolactin alveoli distended by
milk breast engorgement
• oxytocin myoepithelial cells surrounding alveoli and small
ducts contract squeezes milk into larger ducts and
subareolar reservoirs
• Oxytocin inhibit dopamine prolactin↑ successful
lactation
13. • Peptide and steroid hormones produced by
• Non-pregnant: endocrine glands
• Pregnant: intrauterine tissues
14. Hormones
Pregnancy specific
• Human chorionic gonadotrophin
(hCG)
• α and β (pregnancy specific; produced by
trophoblast detectable w/in days of
implantation)
• production influenced by leukemia
inhibitory factor (LIF) and isoform of GnRH
• Maintain corpus luteum’s fx
• peak values @10w progesterone by
placenta to plateau @>12w↓
• α hCG ≈ α of LH, FSH, TSH supress FSH
and LH secretion by ant. pituitary
• Human placental lactogen (hPL) • Produced by placenta
• partial homology with prolactin and hGH
15. Hormones
Steroids • produced by placenta and fetus
• Concentration earliest weeks of pregnancy↑ plateau
•Effects upon myometrium and (+prolactin) breast tissue
• effects on smooth muscle of vascular tree, GIT, GUT
• estrogen • max 30-40mg/day (80% estriol)↑
• encourages cellular hypertrophy (uterus, breast)
•Alter chemical constitution of con. tissue more pliable
• Water retention
• Reduce sodium excretion
• progesterone • reduce smooth muscle tone
• ↓ stomach motility nausea
• ↓ colon activity delayed emptying water reabsorb↑
constipation
• ↓ uterine tone prevent contraction
• ↓ vascular tone diastolic P ↓ venous dilatation
• ↑ temperature
• ↑ fat storage
• Induce over-breathing
• Induce development of breast
16. Hormones
Pituitary related
• Prolactin • produced by lactotrophs of ant
pituitary and cells of decidua
• Rc in trophoblast cells and w/in
amniotic fluid
• Stimulated by estrogen and sleep
•Inhibited by hPL and dopamine agonist
• essential of lactation
•Human growth hormone (hGH) • production by ant pituitary supressed
in pregnancy
• [hGH] ↓
• hPL supress hGH
•Adrenocorticotrophic hormone
(ACTH)
• placental clock theory
Pituitary gland increase 30% in weight in first pregnancy (50% in next
pregnancy) can produce headache
17. Hormones
Hypothalamus related
• Gonadotrophin-releasing
hormone (GnRH)
• Corticotrophin-releasing factor
(CRF)
CRF placental clock theory
Other peptides
• Insulin-like growth factor I and
II (IGF)
•1,25-Dihydroxycholecalciferol
•Parathyroid hormone-related
peptide
•Renin
•Angiotensin II
• IGF regulates fetal growth
• IGF I and II: produced by fetal cells
(in liver) and maternal cells (in
uterus)
• IGF II predominated in fetal
circulation
• 1,25-(OH)2D3: calcium absorption↑
18. Carbohydrate metabolism
• First half of pregnancy
• Fasting plasma glucose concentration ↓
• Little change in plasma insulin level
• OGGT enhance respond compared to non-pregnant, normal insulin release
but blood glucose value↓
• Second half of pregnancy
• Delay in reaching peak glucose value
• ↑ glucose value + [plasma insulin] =↑ relative insulin resistance ( sensitivity↓
by 80%)
• May involve hPL or other growth-related hormones
• Reduced peripheral insulin sensitivity
• Characteristic of insulin binding to Rc also altered (= obese and NIDDM)
19. • In pancreas:
• ↑ size of Langerhans cell
• ↑ number of β cell
• ↑ Rc for insulin
20.
21. Fat metabolism
• 4kg fat is stored by 30 weeks of gestation
• Mostly in form of depot in abdominal wall, back and thighs.
• Modest amount stored in breast
• Three points to be noted
• Total metabolism and energy demand ↑
• Glycogen stores are diminished energy from KH ↓
• Although blood fat in greatly increase only a moderate amount stored
22.
23. Thyroid function
• hCG ≈ TSH hCG maximal suppress maternal TSH
production @ trimester I
• hCG or TSH nausea and vomiting improve after trimester I
• Biochemical hyperthyroidism + free T4 + suppressed TSH↑
hyperemesis gravidarum
• Iodine active transport to feto-placental unit + urine excretion↑
plasma level ↓ uptake of iodine from blood by thyroid↑
gland
• Diet insufficiency of iodine hypertrophy of thyroid gland
trap iodine
• ↑ thyroid-binding globulin, bound T4 and T3
• Free T4 and T3 fall a little in trimester II and III
24. Calcium metabolism
• 40% bound to albumin
• Pregnancy: [plasma albumin]↓ [plasma calcium]↓
• Little changes to unbound calcium
• ↑ demand from fetus transplacental flux 6.5 mmol/day (~ 80%
absorbed in GIT by non-pregnant)
• Mother: absorption and excretion↑ ↓ little changes in bone
(failed = osteopenia)
25. • ↑ calcium absorption by 1,25-dihydroxycholecalciferol
(metabolite of vit D3) which is influenced by PTH
• PTH 1/3 in pregnancy↑
• No changes in calcitonin or other D3 metabolites
• [plasma calcium] fetus > maternal and independent
regulation of PTH and calcitonin
26. Placental corticotrophin-releasing factor
• Mid-pregnancy: trophoblast produces CRF stimulates fetal
pituitary ACTH↑ fetal adrenal fetal↑
dihydroepiandrosterone (DHEA) precursor of placental estrogen
secretion estrogen↑ @ end of pregnancy gap junc↑
synthesis @myometrial aid conduction regular uterine
contractions labour = placental clock theory
• CRF synthesis regulated by +ve feedback by estrogen
27. Corticosteroid and renin-angiotensin system
• Trophoblast cell CRF and ACTH regulate activity of fetal
adrenal glands, myometrium and possibly maternal adrenal glands.
• Cortisol progressively, mostly bound to cortisol-binding globulin↑
(CBG)
• ACTH may regulate maternal cortisol level because there’s lack of
diurnal fluctuation of cortisol and attenuated response to
dexamethasone supression
29. • Metabolic changes + fetal growth increase weight↑
~25% of non-pregnant (~12.5 kg)
• First half: weight increase is varied
• Second half: 0.5kg/week (2kg/month)↑
• At term the gain stopped
• After 40 weeks, may fall
• Weight increase due to:
• Growth of conceptus
• Enlargement of maternal organs
• Maternal storage of fat and protein
• ↑ maternal blood volume and interstitial fluid
32. concentrations of estrogen &
progesterone
Directly act on kidney
Causing release of renin
Activates aldosterone-renin-
angiotensin mechanism
Renal sodium retention & in
total body water
in plasma volume
(45%)
Blood volume
PREGNANCY
hb
ht
Physiological
anemia
Physiological
anemia
•To allow adequate perfusion of vital
organs including placenta and fetus
•To anticipate blood loss a/w
delivery
33. Hypercoagulable State
Increase in: Decrease in:
PROCOAGULANT
FACTORS
•Factor VII
•Factor VIII
•Factor IX
•Factor X
•Factor XII
•Fibrinogen
ANTICOAGULANT
•Protein S activity
•Antithrombin IIIa
•Activated
Protein C
resistance
ESR
34. Increased production of:
RBC mass (20%) WBCPlatelet
Due to increase in renal
erythropoietin production
Supports higher metabolic
requirement for O2 during
pregnancy
BUT platelet
consumption increase
more
Fall to low normal
value
Mild thrombocytopenia
Mainly due to increase
in no of PMN cells as
early as 3 wks AOG
Difficult to
differentiate with
infection
Neutrophilia
35. Immunosuppresive State
Approximately 30% of women
develop IgG abs against the
inherited paternal human leukocyte
ag of fetus
BUT, the role of these abs is
UNCLEAR & there is no evidence of
attack on fetus
Lack of maternal immunity towards
the fetus
Due to reduced no of cytotoxic T
cells (CD8+) during pregnancy
Potentially harmful T cell-mediated
immune responses downregulated &
components of innate immune system
activated instead
Allowed fetal
allograft to implant
& develop
51. Gastrointestinal
• As the gestational age in pregnancy increase so does the size of
uterus.
• This increase in size of the uterus causes the stomach and the
intestine to be displace upwards
• The position of the appendix is usually displace upwards towards
the right upper flank region.
• Because of the alteration of the intra-abdominal structure this
makes it very difficult to diagnose any disease associated with the
intra abdominal
52. • Increase in progesterone level causes
• Lower esophageal sphincter tone to be reduced (esophageal reflux)
• Increase placenta production of gastrin, which increases gastric acidity.
(heart burn)
• Reduced motility of the gut which result in delay of the gastric emptying
time. (constipation)
53. • During labour the motility of the gut decreases further and even
during the pueriperium period, emptying of the gut is still
delayed.
• This increases the risk of pregnant women to develop aspiration of
gastric content-especially if they are sedated after 16 weeks of
gestation.
54. Liver
• Liver may become more difficult to examine during pregnancy due
to the expanding uterus.
• Due to hyperoestrogeninc state in pregnancy, clinical findings such
as telangiectasia and palmar erythema that are associated with
liver disease in non pregnant state are found in 60% of the
pregnant woman
55. • Despite of the increase of the portal vein pressure in pregnancy,
the size of the liver and the hepatic blood flow remains unaltered.
• Liver function also remains mostly the same.
• Total alkaline phosphate serum increases up to double the normal
amount due to fetal and placenta production.
56. • Hepatic production of protein increases but because of the
expanding maternal placenta volume serum albumin level still
remain low.
• Most important changes in pregnancy to the liver is the increased
in production and plasma fibrinogen and the clotting factors
57. Gall bladder
• During pregnancy, contractility of the gallbladder is reduced.
• Progesterone may impairs gallbladder contraction by inhibiting
cholecystokinin-mediated smooth muscle stimulation (primary
regulator of gallbladder contraction).
• This impairment leads to stasis, and is associated with the
increased cholesterol saturation of pregnancy
58. • Intrahepatic cholestasis has been linked to high circulating levels
of estrogen, which inhibit intraductal transport of bile acids
62. Anatomic Changes
• Increase in length for about 1 - 2 cm.
• Calyces, renal pelvis & ureters dilate impression of obstruction.→
• Anatomical changes predispose pregnant women to ascending UTI.
• By 6 weeks postpartum, renal dimensions return to pre-pregnancy
values.
63.
64.
65. Functional Changes
• Renal vascular resistance decreases renal plasma flow increases→
50 – 85% above nonpregnant values during first half of pregnancy.
• Renal perfusion increases rise in GFR by approximately 50%.→
• GFR returns to normal within 12 weeks of delivery.
66. Functional Changes
• Renal clearance of creatinine increases as the GFR rises.
• Urinary protein loss normally does not exceed 300 mg over 24
hours, which is similar to nonpregnant state.
67. Functional Changes
• Increase in GFR plus saturated ‘renal threshold’ in the proximal
convoluted tubule explain the increase amount of glucose in urine
glycosuria.→
• More than 50% of women have glycosuria sometime during
pregnancy.
↑ estradiol + progesterone hyperplasia + hypertrophy of myometrial cells Uterus weight 50-60g 1000g (at term) Early: uterine growth independent of the growing fetus Later on hypertrophy > hyperplasia Muscle fibres ↑ in length x15 Uterine arteries undergo hypertrophy
The average blood loss associated with: - vaginal delivery 500 – 600 ml - cesarean delivery 1000 ml - twin delivery 1000 ml
The erythrocyte sedimentation rate (ESR), also called a sedimentation rate or Biernacki Reaction , is the rate at which red blood cells sediment in a period of 1 hour The ESR is governed by the balance between pro-sedimentation factors, mainly fibrinogen , and those factors resisting sedimentation, namely the negative charge of the erythrocytes ( zeta potential ). When an inflammatory process is present, the high proportion of fibrinogen in the blood causes red blood cells to stick to each other. The red cells form stacks called ' rouleaux ,' which settle faster. The flat surface of the discoid RBCs give them a large surface area to make contact and stick to each other; thus, forming a rouleau. They occur when the plasma protein concentration is high, and because of them the ESR ( erythrocyte sedimentation rate ) is also increased.
Erythrocyte lifespan slightly decrease during pregnancy A greater expansion of plasma volume relative to the increase in hemoglobin mass and erythrocyte volume is responsible for the modest fall in hemoglobin levels (i.e., physiological or dilutional anemia of pregnancy) observed in healthy pregnant women. The greatest disproportion between the rates at which plasma and erythrocytes are added to the maternal circulation occurs during the late second to early third trimester. (Lowest hematocrit is typically measured at 28–36 weeks [16].) Nearer to term, hemoglobin concentration increases due to cessation of plasma expansion and continuing increase in hemoglobin mass. Conversely, the absence of physiologic anemia appears to be a risk factor for Stillbirth The neutrophil count begins to increase in the second month of pregnancy and plateaus in the second or third trimester, at which time the total white blood cell counts ranges from 9000 to 15,000 cells/L The white blood cell count falls to the normal nonpregnant range by the sixth day postpartum