Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious acute complications of diabetes characterized by high blood sugar levels. DKA involves ketones in the blood while HHS does not. Treatment for DKA involves rehydration with saline, potassium replacement, low-dose insulin therapy, monitoring blood sugars and electrolytes closely. The goals are to lower blood sugars and acid levels while replenishing fluids and salts. Complications can include low blood sugar, low potassium, or brain swelling.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
to download this presentation from this link
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Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
this power point descripe diabetic ketoacidosis in pediatric age group .. we talk about the risk of it .. management specially (fluid management) as case study .. complications and the treatment of brain oedema .. i hope to be auseful one .. enjoy
Announcement about my previous presentations - Thank youAreej Abu Hanieh
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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
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Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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2. Introduction
• Diabetic ketoacidosis (DKA) and hyperosmolar
hyperglycemic state (HHS) are two of the most
serious acute complications of diabetes.
• DKA is characterized by ketoacidosis and
hyperglycemia, while HHS usually has more severe
hyperglycemia but no ketoacidosis.
4. PRECIPITATING FACTORS
• Infection (often pneumonia or UTI).
• Discontinuation of or inadequate insulin therapy.
• Acute major illnesses.
• New onset type 1 diabetes.
• Drugs
5. CLINICAL PRESENTATION
• Diabetic ketoacidosis (DKA) usually evolves rapidly,
over a 24-hour period.
• The earliest symptoms of marked hyperglycemia are
polyuria, polydipsia, and weight loss.
• Patients with DKA may present with nausea,
vomiting, and abdominal pain.
6. Initial evaluation
• The initial evaluation of patients with hyperglycemic crises
should include assessment of cardiorespiratory status, volume
status, and mental status.
• The initial history and rapid but careful physical examination
should focus on:
• Airway, breathing, and circulation (ABC) status
• Mental status
• Possible precipitating events (eg, source of infection,
myocardial infarction)
• Volume status
7. Laboratory evaluation
• Serum glucose
• Serum electrolytes (with calculation of the anion gap), blood
urea nitrogen (BUN), and plasma creatinine
• Complete blood count (CBC) with differential
• Urinalysis and urine ketones by dipstick
• Plasma osmolality
• Serum ketones (if urine ketones are present)
• Arterial blood gas if the serum bicarbonate is substantially
reduced or hypoxia is suspected
• Electrocardiogram
8. Laboratory findings
• Serum glucose: Euglycemic DKA has been
described, particularly in patients with poor oral
intake, treatment with insulin prior to arrival in the
emergency department, or in pregnant women .
• Serum ketones: Three ketone bodies are produced
and accumulate in DKA: acetoacetic acid, beta-
hydroxybutyric acid and acetone.
9. • Serum potassium: Patients presenting with DKA or HHS have a
potassium deficit that averages 300 to 600 mEq .
• Insulin therapy shifts potassium into cells and lowers the
potassium concentration. Careful monitoring and timely
administration of potassium supplementation are essential.
• Serum creatinine: Most patients with uncontrolled
hyperglycemia have acute elevations in the BUN and serum
creatinine concentration.
10. • Serum amylase and lipase: These enzymes are often
elevated in patients with DKA who do not have any
other clinical or radiological evidence of
pancreatitis.
• Leukocytosis: The majority of patients with
hyperglycemic emergencies present with
leukocytosis.
• Lipids: Patients with DKA or HHS may present with
marked hyperlipidemia.
12. Treatment
• The first step in the treatment of DKA is infusion of
isotonic saline to expand extracellular volume and
stabilize cardiovascular status.
• The next step is correction of the potassium deficit.
• Low-dose intravenous (IV) insulin should be
administered to all patients with moderate to severe
DKA who have a serum potassium ≥3.3 mEq/L
13. Fluid replacement
• Fluid repletion is usually initiated with isotonic
saline (0.9 percent sodium chloride [NaCl]).
• The optimal rate of isotonic saline infusion is
dependent upon the clinical state of the patient.
• Adequate rehydration with correction of the
hyperosmolar state may enhance the response to
low-dose insulin therapy.
14.
15. Potassium replacement
• If the initial serum potassium is below 3.3 mEq/L, IV potassium
chloride (KCl 20 to 40 mEq/hour, which usually requires 20 to
40 mEq/L added to saline) should be given.
• If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV
KCl (20 to 30 mEq) is added to each liter of IV replacement
fluid.
• If the initial serum potassium concentration is greater than
5.3 mEq/L, then potassium replacement should be delayed
until its concentration has fallen below this level.
16.
17. Insulin
• Initiate treatment with low-dose IV insulin in all
patients with moderate to severe DKA who have a
serum potassium ≥3.3 mEq/L.
• IV regular insulin and rapid-acting insulin analogs
are equally effective in treating DKA . The choice of
IV insulin is based upon institutional preferences,
clinician experience, and cost concerns
18.
19. Bicarbonate and metabolic acidosis
• The venous pH and bicarbonate concentration
should be monitored every two hours, and
bicarbonate doses can be repeated until the pH
rises above 7.00 .
• When the bicarbonate concentration increases, the
serum potassium may fall, and more aggressive KCl
replacement may be required.
20. Phosphate depletion
• The routine use of phosphate replacement in the
treatment of DKA is not recommend.
• However, phosphate replacement should be
strongly considered if severe hypophosphatemia
occurs.
21. MONITORING
• The serum glucose should initially be measured
every hour until stable.
• While serum electrolytes, blood urea nitrogen
(BUN), creatinine, and venous pH should be
measured every (2-4) hours, depending upon
disease severity and the clinical response.
22. Converting to subcutaneous insulin
• The American Diabetes Association (ADA) guidelines for DKA
recommend that IV insulin infusion be tapered and a multiple-
dose, subcutaneous insulin schedule be started when the
blood glucose is <200 mg/dL (11.1 mmol/L) and at least two of
the following goals are met :
• Serum anion gap <12 mEq/L (or at the upper limit of normal
for the local laboratory)
• Serum bicarbonate ≥15 mEq/L
• Venous pH >7.30
23. COMPLICATIONS
• Hypoglycemia and hypokalemia are the most
common complications of the treatment of DKA.
• Cerebral edema
• Noncardiogenic pulmonary edema
Editor's Notes
Acute major illnesses such as myocardial infarction, cerebrovascular accident, sepsis, or pancreatitis.
Drugs that affect carbohydrate metabolism, including glucocorticoids, higher-dose thiazide diuretics, sympathomimetic agents (eg, dobutamineand terbutaline) , and second-generation “atypical” antipsychotic agents .
symptoms of hyperosmolar hyperglycemic state (HHS) develop more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission.
As the degree or duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation, can develop.
Neurologic symptoms are most common in HHS, while hyperventilation and abdominal pain are primarily limited to patients with DKA.
Possible causes of abdominal pain include delayed gastric emptying and ileus induced by the metabolic acidosis and associated electrolyte abnormalities .
Additional testing, such as cultures of urine, sputum, and blood, serum lipase and amylase, and chest radiograph should be performed on a case-by-case basis.
Measurement of glycated hemoglobin (A1C) may be useful in determining whether the acute episode is the culmination of an evolutionary process in previously undiagnosed or poorly controlled diabetes or a truly acute episode in an otherwise well-controlled patient.
acetoacetic acid, which is the only one that is a true ketoacid; beta-hydroxybutyric acid (a hydroxyacid formed by the reduction of acetoacetic acid); and acetone, which is derived from the decarboxylation of acetoacetic acid. Acetone is a true ketone, not an acid.
Urine ketone bodies are detected with nitroprusside tests, while serum ketones can be detected with either a nitroprusside test or by direct assay of beta-hydroxybutyrate levels. Direct assay of beta-hydroxybutyrate levels is preferred, particularly for monitoring response to therapy.
Na+ should be corrected for hyperglycemia (for each 100 mg/dL glucose >100 mg/dL, add 2.0 mEq to sodium value for corrected serum sodium value
The choice of replacement fluid (isotonic or one-half isotonic saline) depends upon the state of hydration, corrected sodium concentration, dose of KCl, blood pressure, and a clinical assessment of overall volume status.
Repeat arterial blood gases are unnecessary during the treatment of DKA; venous pH, which is approximately 0.03 units lower than arterial pH , is adequate to assess the response to therapy and avoids the pain and potential complications associated with repeated arterial punctures.