This document discusses congestive heart failure (CHF) and its nutrition management. Myocardial infarction can weaken the heart, limiting its ability to pump blood and removing fluid from the body. This causes a build up of fluid in the extremities and lungs. Nutrition is also impaired as the heart and lungs work harder to pump more fluid. Treatment includes diuretics to reduce fluid load and strengthen the heart. Nutrition therapy aims to reduce cardiac workload by limiting sodium and fluid intake to reduce fluid retention, and providing nutrient-dense foods and supplements if needed to support nutrition and weight status. Close monitoring is needed when providing nutrition support to avoid worsening heart failure.
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Body Fluid and Compartments | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Body Fluid and Compartments | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
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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.
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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
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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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1. Lecture 6b
10 Feb. 2014
Congestive heart failure
Class activity-what is the best approach to avoiding
CHF
2. Pathology
Myocardial infarction can lead to chronic or
congestive heart failure
-a weakened heart does not pump sufficient
blood to the kidneys
-hence kidneys’ ability to filter blood and
produce urine is reduced
-decreased urine production results in more
water being retained in the blood
3. Pathology
Myocardial infarction can lead to chronic or
congestive heart failure
-weakened heart can not keep up with water
load returning to heart and fluid backs up in
the extremities and in lungs
-heart becomes even more weakened because
it tries to pump more fluid
-ultimately the heart is overwhelmed by the
fluid load and quits
4. CHF and Nutrition status
-build up of fluid causes heart and lungs to work
harder
-when the heart and lungs work harder they
require more energy
-yet that extra energy is not available because fluid
build up impairs cardiac and pulmonary function
5. CHF and Nutrition status
- since blood flow and oxygen delivery are
critical to the processes of digestion,
absorption and transport and energy release
the extra energy required for the heart and
lungs is not there
- therefore heart and lungs cannot keep up
and there is heart failure and ultimately
flooding of the lungs
-all above limits energy and protein intake
6. CHF and Nutrition status
-oral intake may be limited by anorexia, taste
sensitivity, intolerance to food odours,
physical exhaustion, low sodium diet
-weight loss may go unnoticed due to oedema
since oedema masks weight loss
-consequently PEM can occur – in this case
PEM is called cardiac cachexia
7. Treatment of CHF
-treatment consists of diuretics (reduce fluid
load) and glycosides (strengthen cardiac
intropy)
-with this combination strong chance of
potassium deficiency (why?) and constipation
constipation can stress heart
8. Nutrition therapy for CHF
-increase potassium by eating potassium rich
foods if potassium deficient
-if overweight –lose weight- why?
-aims are to reduce or restore nutrition status
and to reduce cardiac work
9. Nutrition therapy for CHF
-reduce fluid and sodium intake- remember
body in CHF is having trouble keeping up
with the water load
-sodium increases the water load and
ultimately the blood pressure
10. Nutrition therapy for CHF
reduce fluid and sodium intake- remember body in
CHF is having trouble keeping up with the water
load
-as blood pressure increases the risk of kidney
failure increases
-if kidney failure occurs then fluid retention
will shut down the body
-dialysis is an option but not nearly as
good as properly functioning kidneys
11. Nutrition therapy for CHF
reduce fluid and sodium intake- remember body in
CHF is having trouble keeping up with the water
load
-patient gets high nutrient density foods-get
energy and protein with less fluid
-heart healthy diet described in previous
lectures is appropriate to ensure that there is
a reduced risk of heart attack or subsequent
heart attack
12. Nutrition therapy for CHF
-a healthier heart is critical to being able to meet
the demands of increased water load
-max 2000 mg sodium per day
-if recurrent or persistent fluid retention then no
more than 2 litres of fluid/day
-adequate fibre
-no alcohol
13. Nutrition therapy for CHF
-carbohydrate requirement is dictated by the
presence of hyperglycemia-
- possible reasons for hyperglycemia
-if supplements are required then nutrient dense
liquids are the first choice
14. Nutrition therapy for CHF
-if patient does not want to eat then duodenal
feeding can be initiated
-feedings begin slowly (30 ml/hour) and then
are increased gradually
-fluid and electrolyte status must be carefully
monitored
why?
15. Nutrition therapy for CHF
-if patient does not want to eat then duodenal
feeding can be initiated
-overly aggressive nutritional support can
worsen CHF resulting in pulmonary edema
-2 kcal/ml and moderate to low sodium
-continuous nasogastric feeding can result in
loss of body weight (fluid) loss and lean body
mass increase without compromising cardiac
status
16. Nutrition therapy for CHF
if oral and tube feeding fail then parenteral feeding
is instituted
-as with nasogastric- therapy begins slowly
-1500 ml per day to start
-cachetic patient as low as 600 ml/day –why?
-central venous pressure, pulse rate, arterial
blood pressure and urine output are tracked
as fluid input increases
17. Nutrition therapy for CHF
-at the first sign of nutritional inadequacy, enteral
or parenteral therapy should begin as progression
of nutritional inadequacy is slow and nutritional
goals take longer to obtain