For medical students, especially for early clinical exposure , it will help preclinical medical students. It gives details of about seven case reports in carbohydrate metabolism. MBBS students can use the information for theory exam also.
For medical students , it will help. Especially for preclinical students, as early clinical exposure, it will be very useful. Even for theory exam, it will help.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
For medical students , it will help. Especially for preclinical students, as early clinical exposure, it will be very useful. Even for theory exam, it will help.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
this presentation will give an insight to various clinical manifestations and their approach to diabetes and its complication. it will help medical students to understand the basics of diabetes.
Lecture on DKA in pregnancy - presented at JGH Obstetrics & Gynaecology Teaching Jan 2020. Fictional details have been used to anonymise any resemblance to persons living or passed.
pediatrics emergency, hypoglycemia of infancy.
Glucose level can drop if:
There is too much insulin in the blood (hyperinsulinism). Insulin is a hormone that pulls glucose from the blood.
The baby is not producing enough glucose.
The baby's body is using more glucose than is being produced.
The baby is not able to feed enough to keep glucose level up.
Extra cellular matrix is recently being explored in connection with cancer , metastases and autoimmune disorders. It is prepared for the benefit of both UG and PG medical and dental students.
Various neurotransmitters, mechanism of action and their physiological functions are explained and is useful for ug and pg students of medicine, neurology, psychiatry branches.
Porphyrias are difficult to diagnose . Here it is comprehensively explained to aid making diagnosis of porphyrias easier for the benefit of medical students and practitioners.
Renal function tests are very useful for effective clinical evaluation of renal failure for effective management. So it is useful for medical and allied professional students and clinical practitioners.
Test for pancreatic and intestinal functions are very important for clinical evaluation gastro intestinal disorders . So it will e useful for medical and allied professional students and practitioners.
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
Students of medical and allied subjects must be exposed to the concept of monoclonal antibodies for the efficient practice of clinical and laboratory medicine.
Concepts of acid base balance and its disorders are very important for practice of medicine.It is for the benefit of medical and students of allied fields.
Coronary heart disease due to atherosclerotic process is the major cause of death.Lipids have been implicated for enhanced atherosclerosis. The major lipids involved are triacy glycerol and cholesterol which are transported in the plasma by lipoproteins. So a better understanding of lipid transport and its abnormalities is essential for medical and health professional students.
Water and electrolyte balance is clinically very important topic . It will be very useful for both UG and PG medical students. Efforts are made to explain basic concepts clearly.
It gives basic things regarding urinalysis and will be very useful for medical students, house surgeons, laboratory technicians and postgraduates in medicine.
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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.
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.
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
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
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
2. Case 1
2 years old male child brought by parents with complaints of
yellowish discoloration of eyes intermittently from 3 months of
age, passing dark yellow urine with abdominal swelling.
Given exclusive breastfeeding. Baby developed yellowish
discoloration of conjunctiva at 3 months of age.
No clay colored stool or staining of diapers.
Parents – Consanguineous marriage
Had convulsion at 1 year of age.
Delayed milestones
3. Conscious, Mild pallor +HR-110/min Icterus +/-
RR-32/min. No cyanosis, clubbing, koilonychia.
A rounded doll's face, fatty cheeks, and a protuberant
abdomen
No lymphadenopathy CVS- Normal R/S – Normal
CNS – child was conscious, lethargic
Hb – 10.5 g/dl TLC – 8,800 Platelets – 3.1 lakhs
PT – 12.6
Urine – Glucose negative, Ketones - positive
6. Liver biopsy
Glucose – 6-phosphatase activity assay-liver tissue
Management
Dietary therapy
Fequent meals with high carbohydrate content, including
night feeds.
Uncooked cornstarch, multivitamins, vitamin D, and
calcium supplements
To limit the intake of sucrose, fructose, and galactose-
containing products.
Regular follow-ups to monitor for long-term complications
Iiver transplant
7. Diagnosis - Von Gierke’s disease
Key features
Fasting hypoglycemia
Hepatomegaly
Hyperlipidemia
Hyperuricemia
Ketoacidosis
Doll like facies with chubby cheeks
History of seizures ( hypoglycemic)
Glucose 6-phosphatase deficiency
Dietary therapy
Liver transplant
8. Autosomal recessive
An annual incidence of about 1/100,000 live births
Common Glycogen storage disease – Type 1 GSD – Von
Gierke’s
Glucose 6-phosphatase deficiency
Complications- Renal dysfunction , osteoporosis, and
gout
9. Case 2
A 22-year old student presented with complaints of
abdominal pain, bloating and diarrhea, after taking
cheese sandwich, and coffee with milk.
He had abdominal cramping soon after eating .
After approximately 1 hour of consuming milk, he also
developed excessive bloating and diarrhea. No fever
.No vomiting
He had similar complaints 7-8 days back also.
10. No pallor, cyanosis, or edema.
Blood pressure, 122/78 mm hg; pulse, 74/min,
regular; respiratory rate, 16/min.
Auscultation of the chest revealed clear lung
fields, and normal cardiac findings.
However, abdominal examination revealed
mild tenderness and generalized distension;
bowel sounds were increased
( borborygmi).
11. A fecal occult blood test and stool culture was
negative.
Stool Benedict’s test – positive
Stool acidity test - positive
Complete blood count (CBC), erythrocyte
sedimentation rate (ESR), lipid profile, and liver
function tests and thyroid function tests, were
normal.
12. Diagnosis – Lactose intolerence
Lactase deficiency
( Congenital /Acquired)
Treatment
Lactase capsules can be given along with
the intake of milk products
Avoiding milk and dairy products
13. Case 3
A 10-year-old boy presented with a history of lethargy, weight loss,
polydipsia, and polyuria for 2 weeks.
His past medical history included nocturnal enuresis.
Not on regular medications.
His weight at presentation was 56.6 kg.
Blood glucose was found to be raised - 770 mg/dl
Venous blood gas revealed a pH of 7.380 (7.35–7.45), bicarbonate 21.3 (21–
28) mmol/L, and base deficit of 3.3 (2 to +3) mmol/L.
HbA1c - 11%
His urine ketones were found to be negative.
urine glucose- ++++
14. hemoglobin of 13 (11–14) g/dl, white blood cell count of 8100, and
platelet count of 2.7 lakhs.
His serum sodium was 127 (136–145) mmol/L.
His renal function tests, liver function tests, and thyroid profile were
normal.
Positive islet cell antibodies
Glutamic acid decarboxylase antibodies were higher than 2000 (<5) U/ml.
Diagnosis
A case of type 1 diabetes mellitus of recent onset
without Diabetic Ketoacidosis (DKA)
A regime of subcutaneous insulin injections and
health education given.
15. Case 4
A 5-year-old boy came with a chief complaint of pale
and fatigue.
No family history of hemolytic anemia or parental
consanguinity.
He appeared icteric and with severe anemia.
He consumed fava beans twelve hours prior to the
onset of the symptoms
HR- 110/min RR- 22/min
Anemic, no cyanosis, no clubbing, no edema
16. Hb 4.9 g/dl
Total bilirubin 6.17 mg/dl, indirect bilirubin 5.49 mg/dl
AST – 34 u/l, ALT- 27 U/l, ALP – 74 U/l
Serum LDH - 742 U/l ( child- 60-170, adult – 140-280)
Patient was transfused with Packed Red Cells
Hb became 9.2 g/dl and total bilirubin 0.2 mg/dl.
The blood smear result -Hemolytic anemia and bacterial
infection.
The level of G6PD was - 5.1 U/gr Hb (10.0-14.2 U/g of Hb).
17. Diagnosis - G6PD deficiency
G6PD – generates NADPH+H which helps in the
regeneration of reduced glutathione
Glutathione protects RBC from oxidative stress
G6PD deficiency results in RBC hemolysis due to
oxidative stress.
Reduced protection against oxidative stress is due to
poor availability of reduced glutathione and triggers.
18. • Glucose-6-phosphate dehydrogenase (G6PD)
deficiency - the most common inherited disorder of
red blood cell metabolism
• It can cause hemolysis in the presence of triggers
• X-linked disorder affecting males and homozygous
females
• Incidence is higher in certain ethnic groups (eg, people
with African, Mediterranean, or Asian ancestry).
• Triggers - infections), drugs (eg, salicylates, sulfa drugs,
antimalarial drugs ), fava beans) cause oxidative stress.
19. • Investigations
• Peripheral smear and G6PD assay
• False negative G6PD assays are possible
during acute hemolysis- due to loss of
vulnerable G6PD deficient RBCs.
• Hence repeat testing after several weeks if
initial G6PD assay is negative.
• Treatment
• Avoidance of triggers
• Supportive therapy and blood transfusion
20. Case 5
A 37-year-old woman came with complaints of
repeated nausea and vomiting after the administration
of fruits, sucrose, or fructose foods.
A lifelong history of aversion to sweets was revealed.
After being forced to eat fruits at the age of three, she
showed symptoms of nausea, vomiting, and visual
disturbance.
In adulthood, after one sip of a beverage, nausea,
vomiting, and diarrhea occurred.
Two hours later, she presented with a cold sweat and
faintness.
21. She had no family history of liver or genetic disease
Her height was 160 cm and her weight was 50.2 kg).
Her physical examination was normal; no
hepatomegaly or splenomegaly was found.
Laboratory findings
White blood cell count was 8,460/mm3
Hemoglobin 14.1 g/dL, platelet 261,000 /mm3,
Calcium 8.8 mg/dL, phosphorus 3.5 mg/dL,
Glucose 96 mg/dL, uric acid 3.0 mg/dL,
22. Total cholesterol 180 mg/dL
Total protein 7.5 g/dL, albumin 4.5 g/dL,
Total bilirubin 0.7 mg/dL,
Alkaline phosphatase 61 IU/L,
Aspartate aminotransferase 19 IU/L,
Alanine aminotransferase 16 IU/L,
Blood urea nitrogen 12 mg/dL, creatinine 0.49
mg/dL,
Prothrombin time 13 secs ( 10-14)
Liver ultrasonography showed normal size, shape,
and echotexture without focal lesions.
23. Diagnosis – Hereditary fructose intolerance- HFI
HFI was suspected, and gene analysis of aldolase B dobe
HFI has an estimated incidence of 1:18,000 to 1:31,000.
HFI is caused by a mutation in aldolase B, which results in the
accumulation of F 1-P.
Symptoms usually manifest as nausea, vomiting, and aversion
to fructose-containing foods.
Prolonged fructose ingestion may cause liver and renal failure.
Physical examination might reveal hepatomegaly and jaundice
24. Depletion of phosphate due to trapping as
Fructose -1-Phosphate
Depletion of phosphate due to the phosphorylation
of fructose.
Hypophosphatemia, hyperuricemia,
hypermagnesemia, hypoglycemia, and acidosis after
fructose loading.
Glycogenolysis , gluconeogenesis could not proceed
Hence administration of glucagon does not correct
hypoglycemia
25. Case 6
A known diabetic on insulin therapy who was
a shop keeper about 54 years old, got fainted
and became semiconscious.
How will you proceed with the case?
26. Possibilities
1. Hypoglycemia
2. Severe hyperglycemia
First we have to give the patient 10% Dextrose
intravenously.
Since hypoglycemia is more dangerous than
hyperglycemia
27. Since the patient is on insulin, due to busy hours of
business in the morning, he would have forgotten
taking food after insulin injection . It would have
caused hypoglycemia.
or
Due to uncontrolled diabetes mellitus , he would
have become semiconscious.
Investigations
Plasma glucose – 37 mg/dl
Urine glucose – negative
Urine ketones – negative
Hypoglycemia
28. Plasma glucose - 610 mg/dl
Plasma ketones- 3.2 mmol/l ( less than 1.5
mmol/l, 1.6 – 3.0 –repeat test after 2 to 4
hours)
Urine glucose - 4+
Urine ketones - 4+
Uncontrolled diabetes mellitus
29. Case 7
A 4-month-old, male infant was normally delivered at full
term (40 weeks of gestational age) as a first son to non-
consanguineous mother.
He started breast-feeding on his third day of life.
Two days later, he developed poor feeding and vomiting.
Then he developed jaundice and jaundice progressed .
Baby and mother were Rh positive only.
Infant developed hepatosplenomegaly.
31. Metabolic screening
Ferric chloride test- PKU- negative
Dinitro phenyl hydrazine test- alpha keto acids- negative
Cyanide nitroprusside test- negative ( Sulphur amino acids)
Cetyl trimethyl ammonium bromide test –
for mucopolysaccharides-Negative
Rothera’s test - negative
Benedict test - ++ ( but no black precipitate)
Urine glucose – negative ( Glucose strip)
Aminoacids metabolic defects are ruled out.
32. Stopping milk improved jaundice.
Soya milk feeding improved the condition and he started taking feed
normally.
In case of lactose intolerance, liver is not affected , no jaundice but
diarrhea will be there. So it is ruled out.
No sugar was given . Hence hereditary fructose intolerance is ruled out.
Probable diagnosis- Galactosemia
Investigations
Galactose -1-phosphate uridyl trasferase (GALT) assay in RBCs.
Molecular analysis of GALT gene.
The treatment of galactosemia
The elimination of galactose and galactose-containing foods, that results in
in complete recovery
33. Galactosemia - inherited metabolic disorder
Deficiency of the enzyme galactose-1-
phosphate uridyltransferase
Prevalence -1 in 30,000 and 1 in 60,000 births
Clinical presentations characterized by severe
liver involvement
It may progress to fatal liver failure
Cataract may be present