micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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.
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
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.
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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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
3. Applications of ABG
o To document respiratory failure and assess
its severity
o To monitor patients on ventilators and
assist in weaning
o To assess acid base imbalance in critical
illness
o To assess response to therapeutic
interventions and mechanical ventilation
o To assess pre-op patients
4. ABG – Procedure and Precautions
Where to place -- the options
Radial
Dorsalis Pedis
Femoral
Brachial
5. Technical Errors
Excessive Heparin
Ideally : Pre-heparinised ABG syringes
Syringe FLUSHED with 0.5ml 1:1000 Heparin &
emptied
DO NOT LEAVE EXCESSIVE HEPARIN IN
THE SYRINGE
HEPARIN DILUTIONAL HCO3
-
EFFECT pCO2
7. Technical Errors
Risk of alteration of results with:
1) size of syringe/needle
2) vol of sample
Syringes must have > 50% blood
Use only 3ml or less syringe
25% lower values if 1 ml sample taken in 10 ml
syringe (0.25 ml heparin in needle)
8. Technical Errors
Air Bubbles
pO2 150 mm Hg & pCO2 0 mm Hg
Contact with AIR BUBBLES
pO2 & pCO2
Seal syringe immediately after sampling
Body Temperature
Affects values of pCO2 and HCO3
- only
ABG Analyser controlled for Normal Body
temperatures
9. Technical Errors
WBC Counts
0.01 ml O2 consumed/dL/min
Marked increase in high TLC/plt counts : pO2
Chilling / immediate analysis
ABG Syringe must be transported earliest via COLD
CHAIN
Change/10 min Uniced 370C Iced 40C
pH 0.01 0.001
pCO2 1 mm Hg 0.1 mm Hg
pO2 0.1% 0.01%
10. ABG Equipment
3 electrode system that measures
three fundamental variables - pO2,
pCO2 and pH
All others parameters such as HCO3
-
computed by software using standard
formulae
13. Assessment Of Gas exchange
PaO2 vs SpO2
Alveolar-arterial O2 gradient
PaO2/FiO2 ratio
PaCO2
14. Determinants of PaO2
PaO2 is dependant upon Age, FiO2, Patm
• PaO2 = 109 - 0.4 (Age)
• Alveolar Gas Equation:
• PAO2= (PB- PH20) x FiO2- pCO2/R
As Age the expected PaO2
As FiO2 the expected PaO2
15. Hypoxemia
o Normal PaO2 : 95 – 100 mm Hg
o Mild Hypoxemia : PaO2 60 – 80 mm Hg
o Moderate Hypoxemia : PaO2 40 – 60 mm Hg
– tachycardia, hypertension, cool extremities
o Severe Hypoxemia : PaO2 < 40 mm Hg –
severe arrhythmias, brain injury, death
16. Alveolar-arterial O2 gradient
o P(A-a)O2 is the alveolar-arterial difference in
partial pressure of oxygen
o PAO2 = 150 – PaCO2/RQ
o Normal range : 5 - 25 mm Hg (increases with
age)
o Increase P(A-a)O2 : lung parenchymal disease
17. PaO2 / FiO2 ratio
Inspired Air FiO2 = 21%
PiO2 = 150 mmHg
PalvO2 = 100 mmHg
PaO2 = 90 mmHg
O2
CO2
18. Berlin criteria for ARDS severity
PaO2 / FiO2 ratio Inference
200 - 300 mm Hg Mild ARDS
100 - 200 mm Hg Moderate ARDS
< 100 mm Hg Severe ARDS
ARDS is characterized by an acute onset within 1 week, bilateral
radiographic pulmonary infiltrates, respiratory failure not fully
explained by heart failure or volume overload, and a PaO2/FiO2
ratio < 300 mm Hg
19. Hypercapnia
o PaCO2 is directly proportional to CO2
production and inversely proportional to
alveolar ventilation
o Normal PaCO2 is 35 – 45 mm Hg
27. Renal Regulation
Kidneys control the acid-base balance by excreting
either a basic or an acidic urine
• Excretion of HCO3
-
• Regeneration of HCO3
-
with excretion of H+
28. Excretion of excess H+ & generation of new
HCO3
- : The Ammonia Buffer System
• In chronic acidosis, the dominant mechanism
of acid eliminated excretion of NH4
+
GLUTAMINE
HCO3
- NH3
REABSORBED NH3 + H+ NH4
+
EXCRETED
29. Response…
Bicarbonate Buffer System
• Acts in few seconds
Respiratory Regulation
• Starts within minutes good response by 2hrs,
complete by 12-24 hrs
Renal Regulation
• Starts after few hrs, complete by 5-7 days
31. Simple Acid-Base Disorders
Simple acid-base disorder – a
single primary process of acidosis
or alkalosis with or without
compensation
32. Compensation…
The body always tries to normalize the pH so…
pCO2 and HCO3
- rise & fall together in simple
disorders
Compensation never overcorrects the pH
Lack of compensation in an appropriate time
defines a 2nd disorder
Require normally functioning lungs and kidneys
34. Disorder Compensatory response
Respiratory acidosis
Acute ↑ HCO3
– 1 mEq/L per 10 mm Hg ↑ pCO2
Chronic ↑ HCO3
– 3.5 mEq/L per 10 mm Hg ↑ pCO2
Respiratory alkalosis
Acute ↓ HCO3
– 2 mEq/L per 10 mm Hg ↓ pCO2
Chronic ↓ HCO3
– 5 mEq/L per 10 mm Hg ↓ pCO2
Metabolic acidosis ↓ pCO2 1.3 mm Hg per 1 mEq/L ↓ HCO3
–
(Limit of CO2 is 10 mm Hg)
Metabolic alkalosis ↑ pCO2 0.7 mm Hg per 1 mEq/L ↑ HCO3
–
(Limit of CO2 is 55 mm Hg)
35. Mixed Acid-base Disorders
Presence of more than one acid base
disorder simultaneously
Clues to a mixed disorder:
o Normal pH with abnormal HCO3
- or pCO2
o pCO2 and HCO3
- move in opposite directions
o pH changes in an opposite direction for a
known primary disorder
36. Anion Gap
AG = [Na+
] - [Cl-
+HCO3
-
]
• Elevated anion gap represents
metabolic acidosis
• Normal value: 12 ± 4 mEq/L
• Major unmeasured anions
– albumin
– phosphates
– sulfates
– organic anions
38. Increased Anion Gap
o Diabetic Ketoacidosis
o Chronic Kidney Disease
o Lactic Acidosis
o Alcoholic Ketoacidosis
o Aspirin Poisoning
o Methanol Poisoning
o Ethylene Glycol Poisoning
o Starvation
Normal Anion Gap
o Diarrhea
o Renal Tubular Acidosis
o Addisons Disease
o Carbonic Anhydrase
Inhibitors
39. Delta Gap
o The difference between patient’s AG & normal AG
o The coexistence of 2 metabolic acid-base
disorders may be apparent
Delta gap = Anion gap – 12
Delta Gap + HCO3
- = 22-26 mEq/l
If >26, consider additional metabolic alkalosis
If <22, consider additional non AG metabolic acidosis