1. Metabolic acidosis and alkalosis occur due to issues with acid-base homeostasis and pH regulation in the body. Metabolic acidosis occurs when the body produces excessive acid or the kidneys cannot remove enough acid, while metabolic alkalosis is caused by decreased hydrogen ion concentration and increased bicarbonate.
2. The document discusses the causes, signs and symptoms, and compensation mechanisms for respiratory and metabolic acidosis and alkalosis. For metabolic conditions, compensation involves buffering, intracellular mechanisms, respiration, and the kidneys. Respiratory compensation aims to alter blood pH by varying breathing rate to expel or retain carbon dioxide.
3. The types and mechanisms of acute vs chronic respiratory
ABG test measures the blood gas tension values of the arterial partial pressure of oxygen, and the arterial partial pressure of carbon dioxide, and the blood's pH
An arterial-blood gas test measures the amounts of arterial gases, such as oxygen and carbon dioxide. An ABG test requires that a small volume of blood be drawn from the radial artery with a syringe and a thin needle, but sometimes the femoral artery in the groin or another site is used.
The common indications for ABGs are:
Respiratory compromise, which leads to hypoxia or diminished ventilation.
Peri- or postcardiopulmonary arrest or collapse.
Medical conditions that cause significant metabolic derangement, such as sepsis, diabetic ketoacidosis, renal failure, heart failure, toxic substance ingestion, drug overdose, trauma, or burns.
Evaluating the effectiveness of therapies, monitoring the patient's clinical status, and determining treatment needs. For instance, clinicians often titrate oxygenation therapy, adjust the level of ventilator support, and make decisions about fluid and electrolyte therapy based on ABG results.
During the perioperative phase of major surgeries, which includes the preoperative, intraoperative, and postoperative care of the patient.
The components of an ABG analysis are PaO2, SaO2, hydrogen ion concentration (pH), PaCO2, HCO3-, base excess, and serum levels of hemoglobin, lactate, glucose, and electrolytes (sodium, potassium, calcium, and chloride).
ABG test measures the blood gas tension values of the arterial partial pressure of oxygen, and the arterial partial pressure of carbon dioxide, and the blood's pH
An arterial-blood gas test measures the amounts of arterial gases, such as oxygen and carbon dioxide. An ABG test requires that a small volume of blood be drawn from the radial artery with a syringe and a thin needle, but sometimes the femoral artery in the groin or another site is used.
The common indications for ABGs are:
Respiratory compromise, which leads to hypoxia or diminished ventilation.
Peri- or postcardiopulmonary arrest or collapse.
Medical conditions that cause significant metabolic derangement, such as sepsis, diabetic ketoacidosis, renal failure, heart failure, toxic substance ingestion, drug overdose, trauma, or burns.
Evaluating the effectiveness of therapies, monitoring the patient's clinical status, and determining treatment needs. For instance, clinicians often titrate oxygenation therapy, adjust the level of ventilator support, and make decisions about fluid and electrolyte therapy based on ABG results.
During the perioperative phase of major surgeries, which includes the preoperative, intraoperative, and postoperative care of the patient.
The components of an ABG analysis are PaO2, SaO2, hydrogen ion concentration (pH), PaCO2, HCO3-, base excess, and serum levels of hemoglobin, lactate, glucose, and electrolytes (sodium, potassium, calcium, and chloride).
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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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
1. RESPIRATORY AND
METABOLIC ACIDOSIS
& ALKALOSIS
By Monisha Jayabalan
Ist MSc Medical Biochemistry
Dr.A.L.mudaliar post graduate institute of basic
medical sciences, University of Madras, Taramani.
14-03-2015 1
2. • Acids are hydrogen ion whereas A base is an
ion or a molecule that can accept an H+.
• H+ regulation is essential because the
activities of almost all enzyme systems in the
body are influenced by H+ concentration
• Acid-Base homeostasis is concerned about the
proper balancing of acid and bases, also called
the pH
14-03-2015 2
3. ACIDOSIS is the reduction in the pH due to
the presence of excess H+ ions
ALKALOSIS is the decrease in the pH
14-03-2015 3
4. Defences Against Changes in Hydrogen Ion
Concentration
1.Chemical acid- base buffer system
2.Respiratory centers
3.kidneys
14-03-2015 4
5. CHEMICAL ACID –BASE BUFFER SYSTEM
• This is the first line of defense.
• Chemical buffers include bicarbonate buffer,
phosphate buffer and protein buffer
• The bicarbonate buffering system is especially key,
as carbon dioxide (CO2) can be shifted through
carbonic acid (H2CO3) to hydrogen ions and
bicarbonate (HCO3-)
14-03-2015 5
6. Respiratory Regulation of Acid-Base Balance
• This is the second line of defense in acid-base
disturbances
• An increase in ventilation eliminates CO2 from
extracellular fluid, which, by mass action, reduces the
H+ concentration.
• Conversely, decreased ventilation increases CO2, thus
also increasing H+ concentration in the extracellular
fluid.
14-03-2015 6
7. • The buffering power of respiratory centers are one
to two times as great as the buffering power of all
the chemical buffers in the EC fluid combined
14-03-2015 7
8. RESPIRATORY ACIDOSIS
• Respiratory acidosis is a medical emergency in which
decreased ventilation causes increased blood carbon
dioxide concentration and ultimately leads to
decrease in the pH level
• During Alveolar hypoventilation there is an increase in
CO2 thus leads to an increased PaCO2.
Acidosis refers to disorders that lower
cell/tissue pH to < 7.35
Acidemia refers to an arterial pH < 7.3
14-03-2015 8
10. ACUTE RESPIRATORY ACIDOSIS
• PaCO2 is elevated above the upper limit of the
reference range (over 6.3 kPa or 45 mm Hg) with an
accompanying acidemia (pH <7.36).
• occurs when an abrupt failure of ventilation occurs
• failure in ventilation may be caused by depression of
the central respiratory center, inability to ventilate
adequately due to neuromuscular disease, or airway
obstruction related to asthma or chronic obstructive
pulmonary disease (COPD) exacerbation.
14-03-2015 10
11. CHRONIC RESPIRATORY ACIDOSIS
• Chronic respiratory acidosis may be secondary to
many disorders,including COPD
• Chronic respiratory acidosis also may be secondary to
Pickwickian syndrome, neuromuscular disorders, and
severe restrictive ventilatory defects as observed in
interstitial fibrosis and thoracic deformities.
14-03-2015 11
12. MECHANISM
• acute respiratory acidosis, compensation occurs in 2
steps.
• The initial response is cellular buffering that occurs
over minutes to hours. Cellular buffering elevates
plasma bicarbonate (HCO3
−) only slightly,
approximately 1 mEq/L for each 10-mm Hg increase in
PaCO2.
• The second step is renal compensation that occurs
over 3–5 days. With renal compensation, renal
excretion of carbonic acid is increased and
bicarbonate reabsorption is increased. For instance,
PEPCK is upregulated in renal proximal tubule brush
border cells, in order to secrete more NH3 and thus
to produce more HCO3
−
14-03-2015 12
13. RESPIRATORY ALKALOSIS
• Respiratory alkalosis is a medical condition in which
increased respiration elevates the blood pH beyond
the normal range (7.35-7.45) with a concurrent
reduction in arterial levels of CO2.
Alkalosis refers to disorders that elevate
cellular pH to > 7.45.
Alkalemia refers to an arterial pH > 7.45.
14-03-2015 13
15. ACUTE RESPIRATORY ALKALOSIS
• Acute respiratory alkalosis occurs rapidly. For every
10 mmHg drop in PCO2 in arterial blood, there is a
corresponding 2 mEq/L drop in bicarbonate ion due to
acute compensation. During acute respiratory
alkalosis, the person may lose consciousness where
the rate of ventilation will resume to normal.
14-03-2015 15
16. CHRONIC RESPIRATORY ALKALOSIS
• Chronic respiratory alkalosis is a more long-standing
condition. For every 10 mmHg drop in PCO2 in arterial
blood, there is a corresponding 5 mEq/L drop in
bicarbonate ion. The drop of 5 mEq/L of bicarbonate
ion is a compensation effect which reduces the
alkalosis effect of the drop in PCO2 in blood. This is
termed metabolic compensation.
14-03-2015 16
17. CAUSES
• psychiatric causes
• CNS causes
• drug use: doxapram, aspirin, caffeine and coffee
abuse
• moving into high altitude areas, where the low
atmospheric pressure of oxygen stimulates increased
ventilation
• lung disease such as pneumonia
• fever
• pregnancy
• high levels of NH4+ leading to brain swelling and
decreased blood flow to the brain
14-03-2015 17
18. MECHANISM
• Respiratory alkalosis generally occurs when some
stimulus makes a person hyperventilate. The
increased breathing produces increased alveolar
respiration, expelling CO2 from the circulation. This
alters the dynamic chemical equilibrium of carbon
dioxide in the circulatory system, and the system
reacts according to Le Chatelier's principle.
Circulating hydrogen ions and bicarbonate are shifted
through the carbonic acid (H2CO3) intermediate to
make more CO2 via the enzyme carbonic anhydrase.
14-03-2015 18
19. RENAL COMPENSATION
• Renal compensation is a mechanism by which the
kidneys can regulate the plasma pH. It is slower than
respiratory compensation, but has a greater ability to
restore normal values.
• In respiratory acidosis, the kidney produces and
excretes ammonium (NH4
+) and monophosphate,
generating bicarbonate in the process while clearing
acid.[1]
• In respiratory alkalosis, less HCO3
− is reabsorbed,
thus lowering the pH.[2]
14-03-2015 19
20. METABOLIC ACIDOSIS
• Metabolic acidosis is a condition that occurs when the
body produces excessive quantities of acid or when
the kidneys are not removing enough acid from the
body
• If untreated it leads to ACIDEMIA
• The consequences are so serious leading to coma and
death
14-03-2015 20
21. Signs and symptoms
• Symptoms are not specific
• Symptoms may include chest pain
• , palpitations,
• headache,
• altered mental status such as severe anxiety due to
hypoxia,
• decreased visual acuity,
• nausea,
• vomiting,
14-03-2015 21
22. • abdominal pain
• altered appetite and weight gain
• muscle weakness
• bone pain and joint pain.
• Extreme acidemia leads to neurological and cardiac
complications:
• Neurological: lethargy, stupor, coma, seizures.
• Cardiac: arrhythmias (ventricular tachycardia),
decreased response to epinephrine; both lead to
hypotension (low blood pressure).
14-03-2015 22
23. CAUSES
• Metabolic acidosis occurs when the body produces too
much acid, or when the kidneys are not removing
enough acid from the body. There are several types
of metabolic acidosis. The main causes are best
grouped by their influence on the anion gap.
The anion gap is the difference in the
measured cations and the measured anions
in serum, plasma, or urine.
14-03-2015 23
24. INCREASED ANION GAP
• lactic acidosis
• ketoacidosis
• chronic renal failure (accumulation of sulphates,
phosphates, urea)
• intoxication:
o organic acids (salicylates, ethanol, methanol, formaldehyde,
ethylene glycol, paraldehyde)
o Sulphates, metformin(Glucophage)
• massive rhabdomyolysis
14-03-2015 24
25. NORMAL ANION GAP
• longstanding diarrhoea (bicarbonate loss)
• bicarbonate loss due to taking topiramate
• pancreatic fistula
• uretero-sigmoidostomy
• intoxication:
o ammonium chloride
o acetazolamide (Diamox)
o isopropyl alcohol
• renal failure (occasionally)
• inhalant abuse
• toluene
14-03-2015 25
26. COMPENSATION MECHANISM
• Metabolic acidosis is either due to increased
generation of acid or an inability to generate
sufficient bicarbonate. The body regulates the
acidity of the blood by four buffering mechanisms.
• bicarbonate buffering system
• Intracellular buffering by absorption of hydrogen
atoms by various molecules, including proteins,
phosphates and carbonate in bone.
• Respiratory compensation
• Renal compensation
14-03-2015 26
27. METABOLIC ALKALOSIS
• Metabolic alkalosis is a metabolic condition in which
the pH of tissue is elevated beyond the normal range
(7.35-7.45).
• This is the result of decreased hydrogen ion
concentration, leading to increased bicarbonate.
14-03-2015 27
29. CHLORIDE RESPONSIVE
• Loss of hydrogen ions - Most often occurs via two
mechanisms, either vomiting or via the kidney.
o Vomiting results in the loss of hydrochloric acid
o Severe vomiting also causes loss of potassium (hypokalaemia)
and sodium (hyponatremia). The kidneys compensate for
these losses by retaining sodium in the collecting ducts at
the expense of hydrogen ions (sparing sodium/potassium
pumps to prevent further loss of potassium), leading to
metabolic alkalosis.
• Congenital chloride diarrhea - rare for being a
diarrhea that causes alkalosis instead of acidosis.
14-03-2015 29
30. • Contraction alkalosis
• Diuretic therapy - loop diuretics and thiazides
• Post hypercapnia - Hypoventilation (decreased
respiratory rate) causes hypercapnia (increased levels
of CO2), which results in respiratory acidosis. Renal
compensation with excess bicarbonate occurs to
lessen the effect of the acidosis. Once carbon
dioxide levels return to base line, the higher
bicarbonate levels reveal themselves putting the
patient into metabolic alkalosis.
• Cystic Fibrosis
14-03-2015 30
31. CHLORIDE RESISTANT
• Retention of bicarbonate
• Shift of hydrogen ions into intracellular space -
Seen in hypokalemia.
• Alkalotic agents - Alkalotic agents, such as
bicarbonate (administrated in cases of peptic ulcer or
hyperacidity) or antacids, administered in excess can
lead to an alkalosis.
• Hyperaldosteronism
14-03-2015 31
32. • Excess Glycyrrhizin consumption
• Bartter syndrome and Gitelman syndrome -
• Liddle syndrome
• 11β-hydroxylase deficiency and 17α-hydroxylase
deficiency - both characterized by hypertension
• Aminoglycoside toxicity can induce a hypokalemic
metabolic alkalosis via activating the calcium sensing
receptor in the thick ascending limb of the nephron,
inactivating the NKCC2 cotransporter, creating a
Bartter's syndrome like effect.
14-03-2015 32
33. RESPIRATORY COMPENSATION
• Respiratory compensation is a mechanism by which
plasma pH can be altered by varying the respiratory
rate. It is faster than renal compensation, but has
less ability to restore normal values.
• In metabolic acidosis, chemoreceptors sense a
deranged acid-base system, and there is increased
breathing.
• In metabolic alkalosis, the breathing rate is
decreased.
14-03-2015 33