Shock is a clinical condition caused by inadequate tissue perfusion leading to cellular ischemia. The main causes of death in surgical patients are from shock. Shock can be classified as cardiogenic, hypovolemic, distributive, or obstructive. The key features of shock are hypotension, tachycardia, altered mental status, and signs of poor peripheral perfusion. Treatment involves rapid fluid resuscitation to restore perfusion, with blood products as needed. Ongoing fluid needs and use of vasopressors depends on the type and severity of shock. Monitoring includes vital signs, urine output, lactate, and base deficit to guide resuscitation efforts until tissues are fully resuscitated.
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
It will help to understand heart diseases in newborn, infants and children.
Acute coronary syndrome is a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart.
One such condition is a heart attack (myocardial infarction) — when cell death results in damaged or destroyed heart tissue. Even when acute coronary syndrome causes no cell death, the reduced blood flow changes how your heart works and is a sign of a high risk of heart attack.
Acute coronary syndrome often causes severe chest pain or discomfort. It is a medical emergency that requires prompt diagnosis and care. The goals of treatment include improving blood flow, treating complications and preventing future problems.
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
It will help to understand heart diseases in newborn, infants and children.
Acute coronary syndrome is a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart.
One such condition is a heart attack (myocardial infarction) — when cell death results in damaged or destroyed heart tissue. Even when acute coronary syndrome causes no cell death, the reduced blood flow changes how your heart works and is a sign of a high risk of heart attack.
Acute coronary syndrome often causes severe chest pain or discomfort. It is a medical emergency that requires prompt diagnosis and care. The goals of treatment include improving blood flow, treating complications and preventing future problems.
TAPVC defines the anomaly in which the pulmonary veins have no connection with the left atrium. Rather, the pulmonary veins connect directly to one of the systemic veins (TAPVC) or drain in to right atrium.
A PFO or ASD is present essentially in those who survive after birth
When pulmonary veins drain anomalously into the right atrium either because of complete absence of the interatrial septum or malattachment of the septum primum , then it is known as total anomalous pulmonary venous drainage.
When some or all of the pulmonary veins drain anomalously in to RA or its tributaries without being abnormally connected, the terms partially anomalous pulmonary venous drainage (PAPVD) or totally anomalous pulmonary venous drainage (TAPVD) with normal pulmonary venous connections are used.
TAPVC defines the anomaly in which the pulmonary veins have no connection with the left atrium. Rather, the pulmonary veins connect directly to one of the systemic veins (TAPVC) or drain in to right atrium.
A PFO or ASD is present essentially in those who survive after birth
When pulmonary veins drain anomalously into the right atrium either because of complete absence of the interatrial septum or malattachment of the septum primum , then it is known as total anomalous pulmonary venous drainage.
When some or all of the pulmonary veins drain anomalously in to RA or its tributaries without being abnormally connected, the terms partially anomalous pulmonary venous drainage (PAPVD) or totally anomalous pulmonary venous drainage (TAPVD) with normal pulmonary venous connections are used.
History
3 year old boy.
Taken to Pediatrician with fever and cough.
Started on Paracetamol and oral antibiotics.
One week later still low grade fever, tachypnea.
Referred to hospital.
Basics of Shock and its management. Compentency and SLO based learning for undergraduate medical training (MBBS)
Check out the lecture by clicking on the link below
https://www.youtube.com/watch?v=J5m4kh4FO7k
د/باسم السيد
Management of shocked patient
المحاضرة التي قدمت يوم الثلاثاء 8 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
SHOCK SYNDROMESHOCK SYNDROME
• Shock is a condition in which the cardiovascular system
fails to perfuse tissues adequately
• An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to tissues
• Inadequate tissue perfusion can result in:
– generalized cellular hypoxia (starvation)
– widespread impairment of cellular metabolism
– tissue damage organ failure
– death
ATHOPHYSIOLOGYPATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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 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
- 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
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
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
1. Vi k a s h B h a t t a r a i ( I n t e r n )
F o r S u r g e r y D e p a r t m e n t
C M S - T H B h a r a t p u r
SHOCK
2. Introduction
Shock is a clinical syndrome that results from inadequate tissue
perfusion leading to imbalance between delivery and requirement
for oxygen and substrates which causes cellular ischemia and
dysfunction.
The cellular ischemia which occurs induces the production and
release of inflammatory mediators that further compromises the
perfusion.
It is the most common so, important cause of deaths among
surgical patients. So every surgeons must know…..
3. Pathophysiology of shock
Cellular level:
Micro-vascular level:
Systemic:
Cardiovascular
Respiratory
Renal
Endocine
Ischemia-perfusion syndrome:
perfusion to the tissues is reduced
cells are deprived of oxygen
switch from aerobic to anaerobic metabolism.
Accumulation of lactic acid in the blood
systemic metabolic acidosis.
glucose within cells is exhausted, anaerobic respiration
ceases
failure of sodium/potassium pumps
Intracellular lysosomes release autodigestive enzymes
cell lysis
Intracellular contents, including potassium are released
into the blood stream.
tissue ischaemia progresses
activation of the immune and coagulation systems
Hypoxia and acidosis activate complement and prime
neutrophils
generation of oxygen free radicals and cytokine
injury of the capillary endothelial cells
further activate the immune and coagulation systems
Damaged endothelium becomes ‘leaky’
tissue edema, exacerbating cellular hypoxia
As preload and afterload decrease
Compensatory baroreceptor response
increased sympathetic activity
release of catecholamines into the circulation
tachycardia and systemic vasoconstriction
(except in sepsis)
metabolic acidosis and
increased sympathetic response
increased respiratory rate
increased minute ventilation
excretion of carbon dioxide
compensatory respiratory alkalosis
Decreased perfusion to kidney
Reduced filtration at the glomerulus
renin–angiotensin–aldosterone axis
is stimulated
further vasoconstriction
increased sodium and water
reabsorption
decreased urine output
decreased preload
activation of the adrenal and
renin–angiotensin systems
vasopressin (antidiuretic
hormone)- hypothalamus
Cortisol – adrenal cortex
vasoconstriction and
resorption of water
decreased urine output
During systemic hypoperfusion
cellular and organ damage due to tissue hypoxia and
local activation of inflammation.
Further injury occurs once normal circulation is restored
The acid and potassium load
direct myocardial depression, vascular dilatation and further hypotension
cellular and humoral elements activated by the hypoxia (complement,
neutrophils, microvascular thrombi)
flushed back into circulation
further endothelial injury to organs such as the lungs and the kidneys
acute lung injury
acute renal injury
multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing
the extent and duration of tissue hypoperfusion.
7. Pitfalls
• The classic cardiovascular responses are not elicited in every patient.
• The patient in shock may not be recognized.
• Tachycardia:
Patients on beta-blockers, pacemakers, penetrating injury with
less tissue injury
• Blood pressure: one should recognise it as one of the last signs of shock
Children and young fit patients, elderly who are normally
hypertensive
• Capillary refill:
Distributive shock, patients are not cold, clammy but have brisk
capillary refill
8. Possible consequences
Unresuscitable Shock:
profound shock for prolonged period
delayed, inadequate or inappropriate resuscitation
death is inevitable
Multiple organ failure:
defined as 2 or more failed organ systems
prolonged ongoing systemic ischemia (Occult hypoperfusion)
Ischemia reperfusion syndrome……..Mgt?
9. Resuscitation
Immediate – Ensure airway and adequate oxygenation and
ventilation
Then attention is directed to Cardiovascular resuscitation
NEVER DELAY resuscitation for definitive Dx
Rapid and careful clinical examination – clues to make appropriate
initial determination
People actively bleeding high volume therapy is
counterproductive immediate operation for control of bleeding
with parallel resuscitation should be done
10. While securing ABC, also don’t forget to draw blood for investigations
like:
CBC, haematocrit (remember in Hypovolemia……..)
Blood grouping and cross matching
Blood culture and Culture sensitivity ( if septic shock suspected…)
PT, INR, PTT, D - dimer
ABG, Base deficit
Electrolytes
Lactate level
LFT, RFT
Other Inv’s:
Urinalysis
Gram stain and culture of sputum, urine, and other suspected sites
Obtain ECG (myocardial ischemia or acute arrhythmia)
Chest x-ray(heart failure, tension pneumothorax, pneumonia)
Echocardiogram (cardiac tamponade, left/right ventricular
dysfunction, aortic dissection)
11. In all cases of shock, FIRST LINE THERAPY SHOULD ALWAYS
BE iv FLUIDS to correct hypovolemia and inadequate pre-load
Otherwise, EMPTY heart will rapidly and permanently deplete
myocardium of oxygen store becomes unresponsive to
resuscitation
For initial resuscitation wide short bore catheters better than
long narrow line Central venous catheter, which is more
appropriate for monitoring than Fluid replacement
12. Types of fluids
There is no ideal Res. Fluid and is matter of debate
Studies show no overt differences b/n crystalloids and colloids
Rather colloids are more expensive and have worse side-effect
profiles
MOST IMPtly Both have ZERO oxygen carrying capacity, and if
blood is lost ideal replacement is blood but they help buying
time while awaiting blood products
Don’t use hypotonic solutions like Dextrose Poor plasma
volume expanders (exception, if free water loss as in DI, and
sodium overload in cirrhosis.)
13. Dynamic Fluid response
One of the methods to determine Shock status of patient
250-500 mL fluid given over 5-10 mins and Cardiovascular
response observed (HR, BP, CVP)
Responders: not actively losing fluid but require filling
Transient responders: moderate ongoing fluid loss
Non-responders: severely volume depleted
14. After fluid challenge, There should be raise in CVP of 2-5 cmH2O
which gradually drifts back over 10-20 mins
Those not showing change further fluid resuscitation
Vasopressors/Inotropic therapy may be required
Once HR, BP, CVP, UO restored patient is kept on maintenance fluid
therapy.
4-2-1 mL/kg/hr for 1st 10 kg, 2nd 10kg and rest respectively
or,
100-50-20 mL/kg/day for 1st 10 kg, 2nd 10kg and rest respectively
16. Monitoring
CO, SVR and preload monitoring (real time monitoring of cardiovascular response)
Invasive: Pulmonary Artery Catheter
Non-invasive: Doppler Ultrasound, Pulse waveform analysis and Indicator dilution method
Mixed Venous Oxygen saturation (N- 50-70%, Sepsis > 70%, Others - <50%)
Level of consciousness adequate marker of cerebral perfusion
New methods: monitoring regional tissue perfusion
Muscular tissue oxygen probes
Near infrared spectroscopy
Sub lingual capnometry
ICU setup is
appropriate
17. Base excess: Normal range +2 to -2 mEq/L
Base deficit - when base excess is negative.
Patients with a base deficit over 6 mmol/L have a much higher morbidity and mortality than those with no
metabolic acidosis
• Lactate Level: Normal – 0.5 to 1.6 mmol/L in arterial blood
0.5 to 2.2 mmol/L in venous blood
mild to moderate hyperlactatemia 2-4 mmol/L
Lactic acidosis = >4-5 mmol/L with pH = <7.35
18. Endpoints of resuscitation
Easy to know WHEN TO START, hard to know WHEN TO STOP
Traditionally patients resuscitated until vitals and U.O. normalized
Which is WRONG, as some tissues may still be in OH, Later MOF
New concept, resuscitation not stopped until sensitive parameters
like Base deficit, Lactate level and mixed venous oxygen saturation
are normalised.
19. Antimicrobial Regimens (IV Therapy)
• Immunocompetent adult
(1) piperacillin-tazobactam (3.375 g q4–6h)
(2) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h); or (3)
cefepime (2 g q12h).
If the pt is allergic to β- lactam agents, use ciprofloxacin(400 mg q12h)
orlevofloxacin (500–750 mg q12h)plus clindamycin (600 mg q8h).
Vancomycin(15 mg/kg q12h) should be added to each of the above
regimens.
• Neutropenia (<500 neutrophils/μL)
(1) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h) or cefepime
(2 g q8h)
(2) piperacillin-tazobactam (3.375 g q4h)plus tobramycin (5–7 mg/kg
q24h).
Vancomycin(15 mg/kg q12h) should be added if the pt has an indwelling
vascular catheter, has received quinolone prophylaxis, or has received
intensive chemotherapy that produces mucosal damage
20. • Splenectomy
Cefotaxime (2 g q6–8h) or ceftriaxone (2 g q12h)should be
used. If the local prevalence of cephalosporin-resistant
pneumococci is high, add vancomycin.
If the pt is allergic to β- lactam drugs, vancomycin (15 mg/kg
q12h) plus either moxifloxacin (400 mg q24h) or levofloxacin
(750 mg q24h) or aztreonam (2 g q8h) should be used.
• IV drug user
Vancomycin (15 mg/kg q12h)
• AIDS
Cefepime (2 g q8h) or piperacillin-tazobactam (3.375 g q4h)
plus tobramycin (5–7 mg/kg q24h) should be used.
If the pt is allergic to β- lactam drugs, ciprofloxacin (400 mg
q12h) or levofloxacin 750 mg q12h) plus vancomycin (15
mg/kg q12h) plus tobramycin should be used.
21. Management of Hemorrhagic shock
Every effort directed towards rapidly identifying and
stopping Haemorrhage
Identify haemorrhage
Immediate resuscitative manoeuvres
Identify the site of haemorrhage
Haemorrhage control
The bleeding, shocked patient must
be moved rapidly to a place
of haemorrhage control.