Vaginal bleeding in late pregnancy can be caused by placenta previa, placental abruption, or other local causes. Placental abruption occurs in about 1-2% of pregnancies and is a significant cause of perinatal mortality. Risk factors include hypertension, smoking, trauma, and sudden uterine decompression. Clinical features range from mild pain and bleeding to severe abdominal pain, heavy bleeding, and maternal shock. Management depends on fetal maturity, severity of bleeding, and presence of complications, and may include expectant monitoring, induction of labor, or caesarean section.
Please find the power point on Puerperal sepsis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Puerperal sepsis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
Under the topic of (APH) I talked about the most common causes of (APH) which are placental causes, including Placental Abruption, Placenta Previa and Vasa previa and I depended on the most famous obstetric and gynecological books, Like:
1-An evidence-based text for MRCOG, THIRD EDITION. 2016
2-Bedside Obstetrics and Gynecology (2010)
3-Differential_Diagnosis_in_Obstetrics and gynecology
And other books
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
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.
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
8. ABRUPTIO PLACENTA
Definition:
Early separation of the normally
implanted placenta after 28/40 and
before the end of second stage of
labour
Recurrence:
The risk of recurrent abruption in a
subsequent pregnancy is high.
9. Epidemiology of Abruption
Occurs in 1-2% of pregnancies
20% of all third-trimester bleeders
Recurrence risk
10% in first pregnancy
25% in second pregnancy
10. Epidemiology of Abruption
It is a significant cause of perinatal
mortality – 15-20%
Maternal mortality- 2-5%
11. Risk factors
Prevalence is high in
Smoking or substance abuse (e.g.
cocaine)
History of previous abruption
High birth order
Advancing maternal age
Poor-socioeconomic condition
Malnutrition
Placental insufficiency
13. Etiology
Hypertension in pregnancy
• Spasm of utero-placental blood vessels
• Anoxic endothelial damage
• Rupture of vessels or
• Extravasations' of blood in decidual basalis
17. Pathogenesis
Decidual hematoma leads to degeneration and necrosis
of decidua basalis and adjacent placental parts
Hemorrhage into decidua basilais initiate placental
separation
Etiological factors
21. Features of retroplacental
clots
Depression found in maternal surface
of placenta
Area of infraction with varying
degree of organization
22. Abruptio placenta:
Classifications
Are based on
1. Extent of separation: Partial vs complete
2. Location of separation: Marginal Vs
central
3. Clinical presentation: Revealed, concealed
and mixed
4. Clinical Severity: Mild, Moderate and
Severe
23. Grade 1 Mildest form:
approx 40 of all
cases.
• No vaginal bleeding to
mild vaginal bleeding
• Slightly tender uterus
• Normal maternal BP
and heart rate
• No coagulopathy
(clotting problems)
• No fetal distress
Clinical Severity
Grade 2: moderate -
approx
45% of all cases.
• No vaginal bleeding to moderate
vaginal bleeding
• Moderate-to-severe uterine
tenderness with possible tetanic
contractions
• Maternal tachycardia with
orthostatic changes in BP and
heart rate
• Fetal distress or even death
• Low fibrinogen levels present
(causing clotting problems)
Grade 0: no clinical features
•Diagnosis made after placental exmaninatio
24. Grade 3: Severe form: Approx 15% of all cases.
• No vaginal bleeding to heavy vaginal bleeding
• Very painful tetanic uterus
• Maternal shock
• Coagulopathy
• Fetal death
Clinical Severity
25. Abruptio Placenta: Features
Pain and tenderness
Initially localized then becomes
generalized due to endometrial injury –
extravasations of blood
Vaginal bleeding
Maternal distress
Often I.U.F.D
26. Clinical manifestation of
hemorrhage
Concealed type: blood accumulates
behind placenta
Revealed type: blood dissect
downwards between membranes and
uterine wall and ultimately escape
out through the cervix or may be kep
concealed by the pressure of fetal
head on the lower uterine segment
27.
28. Clinical manifestation of
hemorrhage
Blood may gain access to the amniotic
cavity after rupturing the membrane
Couvelaire uterus : blood may
percolate through the layer of
myometrium
29.
30. Couvelaire uterus
Naked eye features
Dark port wine color:patchy and
diffused
Sub peritoneal petechial
hemorrhage
Free blood may be present in
peritoneal cavity
31. Couvelaire uterus
Microscopic appearance:
Necrosed uterine muscles in the
affected part
Blood infiltration between the
muscle bundle
Blood vessels may show acute
degenerative changes
Muscular dissociation occurs in
middle and outer muscle layer
32. Clinical features
Revealed Mixed(Concealed
features predominate)
Symptoms Abdominal bleeding and
discomfort followed by
bleeding
Acute, intense
abdominal pain followed
by slight bleeding
Character of bleeding Continuous dark color Continuous dark color or
blood stained serous
discharge
General condition Proportionate to the
visible blood loss, shock
is usually absent
Shock may be
pronounced which is
proportionate to the
visible blood loss
Pallor Related with visible
blood loss
Pallor is usually severe
and out of proportion to
the visible blood loss
Features of pre- May be absent Frequent association
33. Revealed Mixed(Concealed
features predominate)
Uterine height Proportionate to the
POG
May be
disproportionately
enlarged and globular
Uterine feel Normal feel with
localized tenderness,
contractions frequent
and local amplitude
Uterus is tense ,tender
and rigid
Fetal parts Can be identified easily Difficult to make out
FHS Usually present Usually absent
34. Laboratory test
Revealed Mixed(Concealed features
predominate)
Hemoglobin Low value proportionate to
the blood loss
Markedly lower than vi
Coagulation profile Usually unchanged Variable changes
•Clotting time increased(>6min)
•Fibrinogen level
low(<150mg/dl)
•Low platelet count
•^ Partial thromboplastin time
•^ FDP and D-dimer
Urine for protein
Confusion in diagnosis
May be absent Usually present
Confusion in diagnosis Placenta previa Acute obstretrical-
gynaecological –surgical
complication
35. Ultrasound - Abruption
Abruption is a clinical diagnosis!
Placental location and appearance
Retroplacental echolucency
Abnormal thickening of placenta
“Torn” edge of placenta
Fetal lie
Estimated fetal weight
39. Laboratory - Abruption
Complete blood count
Type and Rh
Coagulation tests + “Clot test”
Kleihauer-Betke not diagnostic, but
useful to determine Rhogam dose
Preeclampsia labs, if indicated
Consider urine drug screen
40. Sher’s Classification -
Abruption
Grade I
Grade II
Grade III with fetal demise
III A - without
coagulopathy (2/3)
III B - with coagulopathy
(1/3)
mild, often retroplacental
clot identified at delivery
tense, tender abdomen and
live fetus
41. Placental Abruption: Complications
Shock
Acute renal failure
Cause: ?seriously impaired renal
perfusion 2° to ↓CO and intrarenal
vasospasm as in preeclampsia
DIC
Consumptive coagulopathy 2° to
hypofibrinogenemia along with elevated
levels of fibrinogen–fibrin degradation
products
42. Placental Abruption: Complications
Fetal distress/demise
PPH
Couvelaire Uterus:
Widespread extravasation of blood
into the uterine musculature and
beneath the uterine serosa.
Sheehan syndrome
Puerperal sepsis
43. Placental Abruption:
Management
Prevention : Aim
Elimination of the known factors
Correction of anemia
Prompt detection and institution of
the therapy to minimize
complication
44. Prevention of known
factors
Early detection and effective therapy
Needle puncture: USG guided
Avoidance of trauma
Avoid sudden decompression of the
uterus
To avoid supine hypotension
Routine administration of folic acid
46. Assessment of case
Blood loss
Maturity of fetus
Whether patient is in labor or not
Presence of complication
Types and grade of abruption
47. Emergency measures
Sent blood for Hb and hematocrit,
coagulation profile, ABO and Rh
grouping
Urine for detection of protein
IV RL drip with wide bore cannula and
arrangement for BT
Close monitoring of maternal and
fetal well being
48. Treatment modalities
Expectant management of
pregnancy
Definitive management
Induction/augmentation of labor
Caesarean section
49. If patient in labor
Low Rupture of membrane
Augmentation
Bed site clotting time
Done regularly
50. Vaginal delivery
Limited placental abruption
Reassuring FHS
Facilities of continous FHS
monitoring
Prospect of vaginal delivery is soon
Placental abruption with dead fetus
51. The patient not in labor
Bleeding continues
> grade 1 abruption
Delivery either by
• Induction of labor
• C/S
52. Placental Abruption: General Management
1. Delivery
Resuscitation
FFP, whole blood, IV fluids
Monitor BP
Catherization - monitor urine output
53. Placental Abruption: General Management
2. Caesarean Section
Indications for Caesarean Section
salvageable baby,
Severe vaginal bleeding,
Poor progress,
Transverse lie, inadequate pelvis
Post delivery -watch out for PPH
Myometrial myofibrin loose contractility
Failure to clot
54. Expectant management
If bleeding stopped
Grade 1
Fetus reactive and remote from term
Goal :
prolong pregnancy
Meanwhile administer betamethasone
for fetal lung maturity