The document discusses fluid, electrolyte, and acid-base balance in the human body. It covers topics like intracellular and extracellular fluid composition and balance, electrolytes like sodium, potassium, and their regulation. It also discusses acid-base balance, the bicarbonate buffer system, and four major acid-base imbalances - respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Key organs involved in regulation are the lungs and kidneys.
This PPT gives an idea to MBBS students about the Type of fluids, Calculating the daily requirements as well as the drop rate to be used in day today clinical practice.
fluid and electrolyte imbalance
normal physiology of fluid regulation
FLUID IMBALANCES- fluid volume excess, fluid volume deficit, third spacing,
ELECTROLYTE IMBALANCES- hypo and hypernatremia, hypo and hyperkalemia, hypo and hypercalcemia
Nsg care with Fluid & Electrolyte imbalance.pptxAbhishek Joshi
Helpful for first year GNM and B.Sc. Nurses students.
Keep Reading and i will keep uploading...i want to enhance the nursing profession and provide an ideal nursing care to one and every students of India. Thanks
This PPT gives an idea to MBBS students about the Type of fluids, Calculating the daily requirements as well as the drop rate to be used in day today clinical practice.
fluid and electrolyte imbalance
normal physiology of fluid regulation
FLUID IMBALANCES- fluid volume excess, fluid volume deficit, third spacing,
ELECTROLYTE IMBALANCES- hypo and hypernatremia, hypo and hyperkalemia, hypo and hypercalcemia
Nsg care with Fluid & Electrolyte imbalance.pptxAbhishek Joshi
Helpful for first year GNM and B.Sc. Nurses students.
Keep Reading and i will keep uploading...i want to enhance the nursing profession and provide an ideal nursing care to one and every students of India. Thanks
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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!
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
2.
Fluid and Electrolytes
At the end of this lecture, we will be able to:
Discuss the importance of homeostasis.
Enumerate and discuss the importance of
laboratory assessment of fluid and
electrolyte balance.
Interpret laboratory results of fluids and
electrolytes.
correlate clinically
3.
Acid-Base Balance
Discuss the control of pH in the blood with
emphasis on the role of lungs/kidneys
Enumerate and discuss the four major
possible abnormalities of acid-base balance
Metabolic vs Respiratory
Acidosis vs Alkalosis
Compensated vs Uncompensated
Correlate clinically
4.
A delicate balance of fluids, electrolytes,
acids and bases is required to maintain good
health.
This balance is called Homeostasis.
5.
Intracellular fluid (ICF)
found within the cells of the body
constitutes 2/3 of total body fluid in adults
major cation is potassium
Extracellular fluid (ECF)
found outside the cells
accounts of 1/3 of total body fluid
major cation is sodium
6.
Osmosis
Solutes
movement of water across cell
membranes from less concentrated to
more concentrated
substances dissolved in a liquid
Osmolality
the concentration within a fluid
7.
Diffusion
Filtration
movement of molecules in liquids from an area
of higher concentration to lower concentration
fluid and solutes move together across a
membrane from area of higher pressure to one of
lower pressure
Active Transport
substance moves across cell membranes from
less concentrated solution to more concentrated requires a carrier and energy.
12.
Hyperkalemia
Conditions causing absolute
increase in body K and
extracellular shift of K
Hypokalemia
Conditions causing loss of K,
decreased K intake, and
intracellular shift of K
13.
Hyperosmolality (osmolal gap)
Normal: dehydration, high Na,
azotemia, DI
Moderately elevated: Ketoacidosis,
Renal and lactic acidosis
Markedly elevated: alcohol ingestion
and poisoning of selected substances
14.
Water Distribution
60% of BW
60% ICF and 33% ECF
8% in plasma
freely permeable
Na, K, glucose, urea and protein
balance between intake and body
loss
15.
Sodium Distribution
major EC cation
135 to 145 mmol/L
relatively impermeable
leakage is actively pump out by
Na-K ATPase
balance intake and loss
excessive intake contributes to
hypertension
massive internal turnover
16.
Potassium Distribution
major IC cation
constant tendency to diffuse
down its concentration gradient
opposed by Na-K ATPase
EC concentration is accessible
for measurement
17. Changes in H2O content independent of the
amount of solute will alter osmolality
Water Loss
movement from ICF to ECF
stimulation of ADH secretion
stimulates thirst center
ECF volume is directly dependent upon the total
sodium content
Sodium Balance: regulated by its renal excretion
(GFR, aldosterone); atrial natriuretic hormone
and natriuretic factor (cardiac glycosides) which
acts against Na-K ATPase
18.
Abnormalities:
Combined Water and Sodium Depletion
Pure Water Depletion
Pure Sodium Depletion (Hyponatremia)
Combined Water and Sodium Excess
Pure Water Excess
Pure Sodium Excess (Hypernatremia)
19. Hypotonic fluid loss
thirst, dryness of mouth, difficulty of
swallowing, weakness, confusion
weight loss, dry mucous membrane,
decreased saliva secretion, loss of skin
turgor, decreased urine volume
Causes:
Increased Loss: renal, GIT, lungs, skin
Decreased Intake
20. Isotonic or hypotonic fluid loss
hypertonic loss (excessive sweating)
corresponding decrease in ECF
response: aldosterone, inc. reabsorption, low GFR
increased Hct and plasma protein
reduced ECF volume
peripheral circulatory failure
plasma Na concentration
isotonic loss = decreased
hypotonic loss = increased
Causes: Excessive Loss or Inadequate Intake
22. Impairment of water excretion
hyponatremia
load is shared by ICF and
ECF
cerebral over-hydration
causes: increased intake and
decreased excretion
23. Peripheral edema, dyspnea,
pulmonary edema, venous
congestion, HPN, effusions,
weight gain
Causes: Increased Intake,
Decreased Excretion
mostly has paradoxical
hyponatremia due to defect in
free water excretion
24.
Plasma Na is dependent upon relative
amounts of Na and water in the plasma
Indications for serum Na determination:
dehydration or excessive fluid loss - as a
guide to appropriate replacement
on parenteral fluid replacement who are
unable to indicate or respond to thirst
with unexplained confusion, abnormal
behavior or signs of CNS irritability
Correlated with clinical observations
25.
Balance is controlled by kidneys and GIT
related to Hydrogen Ions
Kidney: complete reabsorption and active
secretion
amount of Na for reabsorption
relative availability of K and H
ability to secrete H
aldosterone concentration
rate of flow of tubular fluid
26.
GIT: secreted in gastric juice,
reabsorb in the SI, secreted in LI in
exchange of Na
movement between ECF and ICF
influence of insulin
integrity of cell membranes
Na-K ATPase
H ion concentration
27.
Output exceeds intake
inadequate intake is rarely the sole
cause
increased loss
drug therapy
redistribution in the ECF and ICF
asymptomatic, neuromuscular
disturbance, cardiac, renal (impaired
concentration), metabolic alkalosis
28.
Excessive intake if excretion is
decreased
iatrogenic and parenteral
decreased excretion
redistribution of ECF and ICF
spurious (hemolysis, delayed
separation, contamination)
29.
Hypokalemia
low ST wave
T depression/inversion
prolonged PR interval
prominent U wave
Hyperkalemia
peaking of T waves
loss of P waves
abnormal QRS complexes
ventricular fibrillation
31.
The acidity or alkalinity of a solution is
measured as pH.
The more acidic a solution, the lower
the pH.
The more alkaline a solution , the
higher the pH.
Water has a pH of 7 and is neutral.
The pH of arterial blood is normally
between 7.35 and 7.45
32.
The more Hydrogen ions, the more acidic the
solution and the LOWER the pH
The lower Hydrogen concentration, the more
alkaline the solution and the HIGHER the pH
34.
Regulate pH by binding or releasing
Hydrogen
Most important buffer system:
Bicarbonate-Carbonic Acid Buffer System
(Blood Buffer systems act
instantaneously and thus constitute the
body’s first line of defense against acidbase imbalance)
35.
36.
Lungs
help regulate acid-base balance by eliminating
or retaining carbon dioxide
pH may be regulated by altering the rate and
depth of respirations
changes in pH are rapid,
occurring within minutes
normal
CO2 level
35 to 45 mm Hg
37.
Kidneys
the long-term regulator of acid-base balance
slower to respond
may take hours or days to correct pH
kidneys maintain balance by excreting or
conserving bicarbonate and hydrogen ions
normal
bicarbonate level
22 to 26 mEq/L.
38.
Age
especially infants and the elderly
Gender and Body Size
amount of fat
Environmental Temperature
Lifestyle
stress
40.
Mechanism
Hypoventilation or Excess CO2 Production
Etiology
COPD
Neuromuscular Disease
Respiratory Center Depression
Late ARDS
Inadequate mechanical ventilation
Sepsis or Burns
Excess carbohydrate intake
41.
Symptoms
Dyspnea, Disorientation or coma
Dysrhythmias
pH < 7.35, PaCO2 > 45mm Hg
Hyperkalemia or Hypoxemia
Treatment
Treat underlying cause
Support ventilation
Correct electrolyte imbalance
IV Sodium Bicarb
42.
Risk Factors and etiology
Hyperventilation due to
extreme anxiety, stress, or pain
elevated body temperature
overventilation with ventilator
hypoxia
salicylate overdose
hypoxemia (emphysema or pneumonia)
CNS trauma or tumor
43.
Symptoms
Tachypnea or Hyperpnea
Complaints of SOB, chest pain
Light-headedness, syncope, coma, seizures
Numbness and tingling of extremities
Difficult concentrating, tremors, blurred vision
Weakness, paresthesias, tetany
Lab findings
pH above 7.45
CO2 less than 35
44.
Treatment
Monitor VS and ABGs
Treat underlying disease
Assist client to breathe more slowly
Help client breathe in a paper bag
or apply rebreather mask
Sedation
45.
Risk Factors/Etiology
Conditions that increase acids in the blood
Renal Failure
DKA
Starvation
Lactic acidosis
Prolonged
Toxins
diarrhea
(antifreeze or aspirin)
Carbonic anhydrase inhibitors - Diamox
46.
Symptoms
Kussmaul’s respiration
Lethargy, confusion, headache, weakness
Nausea and Vomiting
Lab:
pH below 7.35
Bicarb less than 22
Treatment
treat underlying cause
monitor ABG, I&O, VS, LOC, NaHCO3
47.
Risk Factors/Etiology
Acid loss due to
vomiting
gastric suction
Loss of potassium due to
steroids
diuresis
Antacids (overuse of)
48.
Symptoms
Hypoventilation (compensatory)
Dysrhythmias, dizziness
Paresthesia, numbness, tingling of extremities
Hypertonic muscles, tetany
Lab: pH above 7.45, Bicarb above 26
CO2 normal or increased w/comp
Hypokalmia, Hypocalcemia
Treatment
I&O, VS, LOC
give potassium
treat underlying cause
49.
50.
1. Look at the pH
is the primary problem acidosis (low) or alkalosis (high)
2. Check the CO2 (respiratory indicator)
is it less than 35 (alkalosis) or more than 45 (acidosis)
3. Check the HCO3 (metabolic indicator)
is it less than 22 (acidosis) or more than 26 (alkalosis)
4. Which is primary disorder (Respiratory
or Metabolic)?
If the pH is low (acidosis), then look to see if CO2 or HCO3 is
acidosis (which ever is acidosis will be primary).
If the pH is high (alkalosis), then look to see if CO2 or HCO3 is
alkalosis (which ever is alkalosis is the primary).
The one that matches the pH (acidosis or alkalosis), is the primary
disorder.
51.
The Respiratory system and Renal systems
compensate for each other
attempt
ABG’s show that compensation is present when
the
to return the pH to normal
pH returns to normal or near normal
If the nonprimary system is in the normal range
(CO2 35 to 45) (HCO3 22-26), then that system is
not compensating for the primary.
For example:
In respiratory acidosis (pH<7.35, CO2>45), if the HCO3
is >26, then the kidneys are compensating by retaining
bicarbonate.
If HCO3 is normal, then not compensating.