25 May 2009

CALCIUM METABOLISM



CALCIUM METABOLISM

CALCIUM METABOLISM
* PHYSIOLOGY OF CALCIUM METABOLISM
* HYPERCALCEMIA
* HYPOCALCEMIA
* METABOLIC BONE DISEASES

CALCIUM PHYSIOLOGY: BLOOD CALCIUM

* BLOOD CALCIUM IS TIGHTLY REGULATED
o PRINCIPLE ORGAN SYSTEMS
o HORMONES
o INTEGRATED PHYSIOLOGY OF ORGAN SYSTEMS AND HORMONES MAINTAIN BLOOD CALCIUM

CALCIUM PHYSIOLOGY: BLOOD CALCIUM

* CALCIUM FLUX INTO AND OUT OF BLOOD
CALCIUM HOMEOSTASIS
DIETARY CALCIUM
INTESTINAL ABSORPTION
ORGAN PHYSIOLOGY
ENDOCRINE PHYSIOLOGY
DIETARY HABITS,
SUPPLEMENTS
BLOOD CALCIUM
BONE
KIDNEYS
URINE


VITAMIN D PHYSIOLOGY
VITAMIN D SYNTHESIS
TISSUE-SPECIFIC VITAMIN D RESPONSES
VITAMIN D MECHANISM OF ACTION: VITAMIN D RECEPTOR
VITAMIN D REPCEPTOR: TRANSCRIPTIONAL REGULATION
VITAMIN D MECHANISM OF ACTION
VITAMIN D RESPONSIVE GENE
TRANSCRIPTION START SITE
FUNCTION OF VITAMIN D
PARATHYROID HORMONE (PTH) PHYSIOLOGY
CALCIUM, PTH, AND VITAMIN D FEEDBACK LOOPS
CALCIUM FEEDBACK TO REGULATE PTH SECRETION
CALCIUM SENSING RECEPTOR: CLINICOPATHOLOGIC CORRELATES
PTH RECEPTOR CLINICOPATHOLOGIC CORRELATES
ORGAN PHYSIOLOGY AND CALCIUM METABOLISM
GI PHYSIOLOGY
RENAL PHYSIOLOGY
BONE PHYSIOLOGY
MEASUREMENT OF BONE TURNOVER
HYPERCALCEMIA: SIGNS AND SYMPTOMS
CAUSES OF HYPERCALCEMIA
PRIMARY HYPERPARATHYROIDISM
TREATMENT OF PRIMARY HYPERPARATHYROIDISM
HYPERVITAMINOSIS D
HYPERVITAMINOSIS D: CLINICAL CHARACTERISTICS
NON-HORMONAL HYPERCALCEMIA
RENAL FAILURE-ASSOCIATED HYPERCALCEMIA
DRUG-INDUCED HYPERCALCEMIA
HYPOCALCEMIA: SIGNS AND SYMPTOMS
CAUSES OF HYPOCALCEMIA
HYPOCALCEMIA: HYPOPARATHYROIDISM
HYPOPARATHYROIDISM: TREATMENT
HYPOPARATHYROIDISM: TREATMENT SUMMARY
HYPOCALCEMIA: HYPOVITAMINOSIS D
DEFECTIVE VITAMIN D FUNCTION
NON-PARATHYROID HYPOCALCEMIA: SECONDARY HYPERPARATHYROIDISM
HYPERPARATHYROIDISM: PRIMARY vs. SECONDARY
SECONDARY HYPERPARATHYROIDISM
RICKETS AND OSTEOMALACIA
RICKETS AND OSTEOMALACIA: CLINICAL MANIFESTATIONS
RICKETS AND OSTEOMALACIA: CAUSES

CALCIUM METABOLISM.ppt

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Vitamin Deficiency Disorders



Vitamin Deficiency Disorders
By:Abdelaziz Elamin, MD, PhD, FRCPCH
Professor of Child Health, College of Medicine
Sultan Qaboos University, Muscat, Oman

BACKGROUND

* Vitamins are organic substances that are essential for several enzymatic functions in human metabolism
* Thiamine was discovered in 1912 & was thought to be a vital amine compound & thus the term vitamin was invented

VITAMINS
* Vitamins are classified according to solubility into fat soluble & water soluble.
* 13 vitamins are known, 4 fat soluble (KEDA) & 9 water soluble (C, Folate & the B group).

VITAMIN A
* Vitamin A is a generic term for many related compounds.
* Retinol (alcohol), Retinal (aldehyde) are often called preformed vitamin A. Retinal can be converted by the body to retinoic acid which is known to affect gene transcription.
* Body can convert b-carotene to retinol, thus called provitamin A.

FUNCTIONS
* Vision: integrity of eye & formation of rodopsin necessary for dark adaptation.
* Regulation of gene expression: vital to cell differentiation & physiologic processes
* Growth & development
* Immunity: important for activation of T lymphocyte, maturation of WBC & integrity of physiological barrier.

Nutrient Interactions
* Zinc deficiency interfere with vitamin A metabolism in several ways:
o It decreases the synthesis of retinol binding protein, which transports retinol to tissues.
o It decreases the activity of the enzyme retinyl palmitate, which is necessary for release of retinol from the liver.
o Zn is needed for the enzyme that convert retinol into retinal.
* Iron & vitamin A.
o Vitamin A deficiency may exacerbate IDF
o Vitamin A supplementation improves iron status among children & pregnant women.
o Combining vitamin A with iron controls IDA more quickly & effectively than using iron alone.

VITAMIN A UNITS
* 1 mg of retinol = 6 mg of b-carotene.
* 3 mg of retinol = 10 international units of vitamin A.
* 100 mg carrots contain 10 mg of b-carotene.

Recommended Allowance
Papaya
Fish & meet
Apricot
Milk & cheese
Spinach
Butter
Cantaloupe
Egg
Carrots
Liver & kidney
Sweet potato
Cod liver oil
Plant Foods
Animal Foods
RICH DIETARY SOURCES

Vitamin A deficiency
* Deficiency of vitamin A leads to:
o Night blindness & xerophthalmia
o Growth retardation
o Acquired immune deficiency
o Keritinization of epithelia in RT, GIT & UT with increased risk of RTI, malabsorption & UTI.

THERAPEUTIC USES
* Vitamin A deficiency
* Boosting immunity of infants
* Skin disorders
* Acute promyelotic leukemia
* Cancer prevention (lung & breast)

TOXICITY
* Vitamin A in excess leads to:
o Dermatitis with xanthosis cutis
o Hepatosplenomegaly
o Bone pain & increased risk of fracture
o Pseudotumor Cerebri

VITAMIN D
* Vitamin D comprises a group of sterols; the most important of which are cholecalciferol (vitamin D3) & ergosterol (vitamin D2).
* Humans & animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol.
* Cholesterol is converted to 7-dehydro-cholesterol (7DC), which is a precursor of vitamin D3.
* Exposure to the ultraviolet rays in the sunlight convert 7DC to cholecalciferol.
* Vitamin D3 is metabolically inactive until it is hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol.
* 1,25 DHC acts as a hormone rather than a vitamin endocrine & paracrine properties.

FUNCTIONS
* Calcium metabolism: vitamin D enhances ca absorption in the gut & renal tubules.
* Cell differentiation: particularly of collagen & skin epithelium
* Immunity: important for Cell Mediated Immunity & coordination of the immune response.

Vitamin D deficiency
* Deficiency of vitamin D leads to:
o Rickets in small children.
o Osteomalacia
o Osteoporosis

GROUPS AT RISK
* Infants
* Elderly
* Dark skinned
* Covered women
* Kidney failure patients
* Patients with chronic liver disease
* Fat malabsorption disorders
* Genetic types of rickets
* Patients on anticonvulsant drugs

Sources of Vitamin D
* Sunlight is the most important source
* Fish liver oil
* Fish & sea food (herring & salmon)
* Eggs
* Plants do not contain vitamin D3

THERAPEUTIC USES
* Rickets & Osteomalacia
* Osteoporosis
* Psoriasis
* Cancer prevention (prostate & colorectal)
* Autoimmune diseases

TOXICITY
* Hypervitaminosis D
causes hypercalcemia, which manifest as:
o Nausea & vomiting
o Excessive thirst & polyuria
o Severe itching
o Joint & muscle pains
o Disorientation & coma.
RICKETS

Vitamin Deficiency Disorders.ppt

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Disorders of Sodium and Potassium Metabolism



Disorders of Sodium and Potassium Metabolism

Outline
* Review of sodium and potassium metabolism
* Paradigm for analyzing pathophysiology
* Abnormalities of potassium balance
* Abnormalities of sodium and water balance
* Example cases

Major Mediators of Sodium and Water Balance
* Angiotensin II
* Aldosterone
* Antidiuretic hormone (ADH)

Renin-Angiotensin-Aldosterone Axis

Angiotensin II
Aldosterone
Role of ADH (antidiuretic hormone)
Overview of Biochemical Homeostasis
Overview of Potassium Balance
Etiologies of Hyperkalemia
Excessive Dietary Intake
Decreased Urinary Excretion
Internal Redistribution
Etiologies of Hypokalemia
Poor Intake
Increased Urinary Excretion
Increased GI Losses
Diarrhea
Laxative abuse
Vomiting / NG drainage

Increased Transcutaneous Losses
Transmembrane Shift
Overview of Sodium Balance
Etiologies of Hyponatremia
Poor Intake of Sodium
Increased Urinary Loss of Sodium
Increased GI Loss of Sodium (Fluid loss must be followed by repletion with free water).
Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water).
Excessive Intake of Water (1° polydipsia)
Decreased Urinary Excretion of Water
Transmembrane Shift of Water
Primary Sodium Loss
Primary Water Excess
Etiologies of Hypernatremia
Primary Sodium Excess
Excess Intake of Sodium
Decreased Urinary Excretion of Sodium
Primary Water Loss
Poor Intake of Water
Increased Urinary Loss of Water
Increased GI Loss of Water
Increased Transcutaneous Loss of Water
Transmembrane Shift of Water (most often due to rapid production of intracellular lactate)

4 Case studies

Disorders of Sodium and Potassium Metabolism.ppt

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