21 April 2009

Hyperventilation



Hyperventilation
Powerpoint presentation by:Pat Confer


What is Hyperventilation?

* Hyperventilation (hyperpnea) or over breathing is a type of breathing in which breaths are taken at a faster rate or breaths become much deeper than normal.


Physiology of Hyperventilation

* Increases in the breathing rate results in more carbon dioxide withdraw from the blood.
* During this carbonic acid levels lower in the blood and raise the pH value of the blood.
* This decrease in CO2 is known as hypocapnia
* Low levels of carbon CO2 cause blood vessels to constrict resulting in a number of different consequences.


Symptoms of Hyperventilation

* shortness of breath, belching, bloating, dry mouth, weakness, numbness and tingling in your arms or around your mouth, muscle spasms in hands and feet, chest pain, various lung diseases, palpitations
* dizziness or lightheadedness, confusion, sleep disturbances, stroke

Causes of Hyperventilation

* Anxiety and nervousness
* stress
* panic attack
* stimulant use
* lung disease such as asthma, chronic obstructive pulmonary disease(COPD), or pulmonary embolism (blood clot in the lung)

Causes continued

* infection such as pneumonia or sepsis
* cardiac disease such as congestive heart failure or heart attack
* severe pain
* bleeding
* drugs (such as an aspirin overdose)
* pregnancy
* ketoacidosis and similar medical conditions

Psychology of Hyperventilation

* Often brought upon by stress and/or anxiety
* Often seen in cases of anxiety disorders. Such disorders include:
o panic disorder
o generalized anxiety disorder
o specific phobia
o social phobia
o acute stress disorder

Psychology Continued

* Hyperventilation is also associated with different other anxiety disorders classified by the DMS-IV
o adjustment disorders with anxious features
o anxiety disorders due to general medical conditions
o substance-induced anxiety disorders
o residual category of anxiety disorder not otherwise specified

Fight or Flight

* Hyperventilation can be seen as a fight or flight response.
* It is possible that this biological response is an effort by the body to prepare for flight or fight
* The increase of O2 in the blood coupled with the decrease of CO2 in the blood would allow for better muscular response.

Anticipatory Response

* It is hypothesized that hyperventilation onset occurs before the stimulus.
* Thus hyperventilation can be seen as an anticipatory response in which the brain anticipates the undesired stimulus and prepares the body for that stimulus.
* Comparable to the flight or fight response.

The Fear Cycle

Immediate Treatment

* Relaxation techniques
* Breathing into a paper bag is not recommended
* Doctors will often perform tests to determine whether hyperventilation is psychological or physiological
* Tests include
o Arterial blood sample
o Chest x-ray
o Ventilation/perfusion scan
o Chest CT scan
o ECG

Spirometers

* Devices used to determine lung functioning
* Comes in several different varieties.
* A spirometer measures both the amount of air expelled and how quickly the air was expelled from the lungs.
* Spirometers display a volume-time curve.
* Results are compared to the average expected in someone of the same age, height, sex, and race, according to the National Heart, Lung, and Blood Institute (NHLBI)

References
Hyperventilation.ppt

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Bioactive Lipids: Membrane Sphingolipids And Gangliosides



Bioactive Lipids: Membrane Sphingolipids And Gangliosides
Powerpoint presentation by:Michael A. Collins, Ph.D.

Four major phospholipids in mammalian cell membranes
Structure of a ceramide (N-acylsphingosine)
Structure of sphingomyelin
Sphingosine

SPHINGOMYELIN-CERAMIDE-SPHINGOSINE BIOCHEMISTRY

Model of dynamics of membrane raft constituents and organization
Membrane raft-containing neutral and acid sphingomyelinases (SMase) activation and regulation in signal transduction
sphingomyelin
cerebrosides
and sulfatide(s)
Sphingolipidoses are lysosomal storage diseases with inherited defects in sphingolipid (SL) catabolism
Key points:
Structures of common sphingolipids
Sphingolipidoses are lysosomal storage diseases with inherited defects in sphingolipid (SL) catabolism: GANGLIOSIDOSES

Sphingolipids.ppt

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Thyroid Hormone



THYROID HORMONE
powerpoint presentation by: D. C. MIKULECKY
PROFESSOR OF PHYSIOLOGY

THE THYROID GLAND

* OVER TRACHEA
* TWO LARGE LATERAL LOBES CONNECTED BY AN ISTHMUS
* 15 to 20 g
* FUNCTIONAL UNIT IS THE FOLLICLE: EPITHELIAL CELLS AROUND A HOLLOW VESSICLE FILLED WITH THYROGLOBULIN

THE THYROID HORMONES

* THYROGLOBULIN: STORAGE FORM BINDS HORMONES
* TETRAIODOTHYRONINE
* TRIIODOTHYRONINE
* IODINE REQUIRED FROM DIETARY INTAKE

THYROID HORMONES
THYROID HORMONE SYNTHESIS

* DEPENDENT ON IODINE (IODINE PUMP CONCENTRATES IODINE IN CELLS)
* DEPENDENT ON TYROSINE
* PARTIALLY SYNTHESIZED (THYROGLOBULIN) EXTRACELLULARLY AT LUMINAL SURFACE OF FOLLICULAR CELLS AND STORED IN FOLLICULAR LUMEN

EFFECTS OF IODINE

* DURING IODINE DEFICIENCY, HORMONE SYNTHESIS IS IMPAIRED
* EXCESS IODINE ALSO INHIBITS SYSNTHESIS

THYROID HORMONE SECRETION

* WITH TSH STIMULATION, ENDOCYTOSIS BRINGS THE THYROGLOBIN BACK INTO FOLLICULAR CELLS
* THYROGLOBULIN IS DEGRADED TO T3 AND T4

THYROID HORMONE’S EFFECTS

* METABOLIC RATE: INCREASED BMR
* CALOROGENIC: INCREASED HEAT PRODUCTION(OXIDATIVE METABOLISM)
* SYMPATHOMIMETIC: FLIGHT OR FIGHT
* CARDIOVASCULAR:INCREASES RESPONSIVENESS OF HEART
* GROWTH: ESSENTIAL FOR NORMAL GROWTH OF SKELETAL SYSTEM (PERMISSIVE OR SYNERGYSTIC WITH GH, INSULIN-LIKE GROWTH FACTOR), CNS, ANS
* NERVOUS SYSTEM:DEVELOPMENT AND ADULT ACTIVITY

METABOLIC EFFECTS OF THYROID HORMONE

* CALOROGENIC EFFECT: INFLUENCES TOLERENCE TO COLD, AVAILABILITY OF ATP
* CARBOHYDRATE METABOLISM: INCREASED GLUCOSE ABSORPTION FROM GUT,GLCOGENOLYSIS, GLUCONEOGENESIS, GLUCOSE OXIDATION.
* LIPID METABOLISM: LIPOGENESIS IN ADIPOCYTES, IN COORDIMNATION WITH BLOOD GLUCOSE LEVELS

CONTROL OF FUEL METABOLISM

* GLYCOGENESIS
* GLYCOGENOLYSIS
* GLUCONEOGENESIS
* PROTEIN SYNTHESIS
* PROTEIN DEGRADATION
* FAT SYNTHESIS
* FAT BREAKDOWN


GLYCOGENESIS

* GLYCOGEN IS A BRANCHED POLYMER OF GLUCOSE STORED IN THE LIVER AND MUSCLE CELLS
* SYNTHESIS IS BY SEPARATE PATHWAY FROM BREAKDOWN
* HIGHLY REGULATED BY INSULIN

GLYCOGENOLYSIS

* BREAKDOWN OF GLYCOGEN STORES INTO GLUCOSE
* REGULATES BLOOD GLUCOSE BETWEEN MEALS
* HOMONALLY CONTROLLED (GLUCAGON, EPINEHRINE, NOREPINEPHRINE AND CLUCOCORTICOIDS) AMPLIFIED BY THYROID HORMONE

GLUCONEOGENESIS

* PRECURSORS ARE 3 AND 4 CARBON COMPOUNDS
* VIA FRUCTOSE PHOSPHATE
* GLUCAGON CONTROLLED AIDED BY THYROID HORMONE
* MAIN PRECURSOR ALANINE AND OTHER AA


PROTEIN DEGRADATION

* USUALLY BALANCED BY SYNTHESIS
* NO ENERGY STORES IN FORM OF PROTEIN
* CAN BE ENHANCED BY GLUCAGON AND THYROID HORMONES LEADING TO GLUCONEOGENESIS

THYROID HORMONE EFFECTS ON NITROGEN METABOLISM

* ENHANCES BOTH SYNTHESIS AND DEGRADATION OF PROTEINS
* EXCESS HORMONE PROMOTES DEGREDATION

FAT SYNTHESIS

* GLUCOSE - FATTY ACID CYCLE
* FATTY ACIDS PRODUCED CONSTANTLY IN ADIPOSE TISSUE.
* BECOME FFA OR BECOME TRIGLYCERIDES DEPENDING ON -GLYCEROL PHOSPHATE FROM GLUCOSE OXIDATION
* NEED OPTIMAL AMOUNTS OF THYROID HORMONE

GLUCOSE - FATTY ACID CYCLE

THYROID AND TEMPERATURE REGULATION

* T3 IS THE DOMINANT FORM INVOLVED
* EXPOSURE TO COLD CAUSES T4 CONVERSION TO T3 .
* PROMOTES CALOROGENIC EFFECT (LONG TERM COLD ADAPTATION)
* SHORT TERM EFFECTS DUE TO SYMPATHETIC MIMETIC EFFECTS AND THE SHIVERING RESPONSE OF MUSCLES

REGULATION OF THYROID SECRETION
EFFECTS OF TSH
TSH MODE OF ACTION
ABNORMALITIES OF THYROID FUNCTION
THYROID HORMONE.ppt

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