Midterm Conferences Compilation

Compiled by: Drapete, RND | Tolentino, RMP | Javier, RIP | Co, DNR (do not resuscitate)

TOPICS
Cholesterol, Saturated Fat and Atherosclerosis
I. Atherosclerosis/Lipid Profile Results  Cholesterol and saturated fat – cause of atherosclerosis;
II. Lipid abnormality in alcoholism & fatty liver when increased in body, LDL is also increased.
III. Gout/Purine metabolism expt  LDL transport cholesterol to arteries and can be retained
IV. Obesity there by arterial proteoglycans and form plaques.
V. Marasmus/Kwashiorkor
 The cholesterol itself is not bad; ung paano, saan, at gaano
VI. Osteoporosis/Calcium determination
VII. Iodine deficiency (endemic goiter) kadami ung cholesterol ang magcause ng adverse effects.
Napagalaman nila na ang concentration at size ng LDL ang
Atherosclerosis magdikta ng progression ng atherosclerosis.
 Also called an atherosclerotic plaque, arterial plaque, or
plaque Non-Modifiable Risk Factors of Atherosclerosis
 Disease of large and medium-sized arteries  Age: Elderly (45 and older for men) and (55 and older for
 Characterized by endothelial dysfunction, vascular women)
inflammation, and build-up of lipids, cholesterol, calcium,  Sex: Men and postmenopausal women
and cellular debris  Genetic Disorder: Family Hypercholesterolemia
 Within the intima of the blood vessel wall - Defect in chromosome 19
 Build-up results: - Autosomal dominant – 50% chance of passing the
- Plaque formation (atheroma) mutated gene
- Vascular remodelling - This is a genetic disorder caused by a mutation in
- Acute and chronic luminal obstruction the gene for LDL receptor. The mutation prevents
- Abnormalities of blood flow synthesis of LDL receptor proteins or it can lead to
- Diminished oxygen supply formation of defective LDL receptor that cannot
 Plaque bind or ingest LDL into the liver cells. Causing
- Made of fatty substances, cholesterol, waste abnormal clearance of LDL by the liver and
products from cells, calcium, and fibrin elevated serum cholesterol levels.
- Plaque formation  Stimulates cells of artery wall
 Produce substances (accumulate in inner layer) Modifiable Risk Factors of Atherosclerosis
 Artery wall thickens (diameter reduced; blood  Smoking
flow and oxygen decreased) o Cholesterol: The toxins in tobacco smoke lower a
- Plaques can rupture, causing the sudden person's HDL level while raising levels of LDL.
formation of blood clot (thrombosis). o Hypertension: Smoking increases the risk for
 Atherosclerosis can cause: hypertension because it causes vasoconstriction.
- Heart attack – complete block in blood flow to the o Nicotine and Carbon Monoxide: The nicotine and
heart (coronary artery) carbon monoxide in cigarette smoke damage the
- Stroke – complete block in blood flow to brain endothelium, which sets the stage for the build-up
(carotid artery) of plaque.
 Can occur: arteries of neck, kidneys, thighs, and arms that o Further constricts the blood vessel thereby
will lead to kidney failure or gangrene decreasing the amount of blood flow in the tissues.
o Increases the blood’s tendency to clot by making
The Response to Vascular Injury Theory platelets stickier, increasing the risk for peripheral
artery disease.
 Mechanisms of atherogenesis remain uncertain
 Cholesterol Levels
 Response to injury theory is most widely accepted
o High levels of LDL – may cause build up in the
 Introduced by Ross in 1972
inner walls of the blood vessel
 Endothelial injury is caused by: o High total cholesterol levels – or
- Oxidized LDL cholesterol hypercholesterolemia
- Infectious agents, toxins (by-products of smoking) o High triglyceride levels - hypertriglyceridemia
- Hyperglycemia o Low levels of HDL – or hypoalphalipoproteinemia
- Hyperhomocystinemia o Impairs reverse cholesterol transport
 Circulating monocytes infiltrate the intima of the vessel wall,
and these tissue macrophages (act as scavenger cells) take  High Blood Pressure
up LDL cholesterol to form characteristic foam cell of o High blood pressure puts added force against the
atherosclerosis. These activated macrophages produce artery walls. Over time, this extra pressure can
numerous factors that are injurious to endothelium damage the arteries, making them more
 Sa madaling sabi: Endothelial injury  Cause vascular
inflammation  Fibroproliferative response (clot)
Huey Javier, RN 1 of 11
 vulnerable to the narrowing and plaque buildup
associated with atherosclerosis.
 Obesity
o Obesity, particularly abdominal (truncal) obesity  Lipid Profile
increase the risk of coronary artery disease o Blood lipid profile is a test that measures the
(atherosclerosis of the arteries that supply blood to content of the various triacylglycerol and
the heart). Abdominal cholesterol containing particles in the blood. Blood
obesity increases the risk lipid profiles are used to predict or estimate the
of other risk factor risks of development of atherosclerosis and other
atherosclerosis such as acute myocardial events such as myocardial
hypertension, diabetes infarction, unstable angina, and stroke which are
mellitus and high actually complications of atherosclerosis. For this
cholesterol levels. experiment, concentration of the following
 Physical Activity molecules, which provide the lipid profile of a
o Inactivity keeps people from reaping the benefits subject, were measured by spectrophotometric
of exercise, which burns excess fat and increases method: Total Cholesterol (TC), Triglycerides (TG),
production of nitric oxide, a chemical that Low-Density Lipoproteins (LDL), High-Density
promotes vascular health. Lipoproteins (HDL), and Very Low Density
Lipoproteins (VLDL). Lipoprotein profile provides
Complications of Atherosclerosis significant information regarding the
 Coronary Artery Disease subject/patient’s predisposition to atherosclerosis.
o Narrows or blocks the arteries of the heart Atherosclerosis is linked with high levels of
o Causes chest pain (angina), necrosis of muscles cholesterol in the blood, particularly to LDL-bound
of the heart leading to myocardial infarction and cholesterol while negatively correlated with HDL
heart failure levels.
 Peripheral Artery Disease
o Decrease or blockage of the blood flow in the
arteries of the extremities leading to decreased Chronic Alcoholism and Liver Cirrhosis
sensation of the affected part Metabolism
o Less sensitive to heat and cold, increasing your
risk of burns or frostbite.
o Can cause intermittent claudication and gangrene
 Kidney Failure
o Arteries that carry blood to the kidneys are blocked
o If atherosclerosis slows the flow of blood, chronic
kidney disease can eventually lead to end-stage
renal disease, or total kidney failure requiring
dialysis
 Aneurysm
o Plaque formation in the wall of BV that reduce
elasticity causing leakage of blood.
 Pulmonary Embolism
o All or part of a thrombus may break off and be
carried through the bloodstream as an embolus
that lodges and get into pulmonary circulation.

Role of Homocysteine Levels in the Development of

Atherosclerosis
 Homocysteine:
o Can be recycled into methionine or converted into
cysteine (with the use of B-vitamins)
o Degrades or inhibits the formation of the three
main structural components of the artery, collagen,
elastin and the proteoglycans.
o Permanently degrades cysteine disulfide bridges
and lysine amino acid residues in proteins,
gradually affecting function and structure.
o “Corrosive of long living protein”
o Increase levels promote atherosclerosis through
oxidant stress, impaired endothelial function and
induction of thrombosis.
o Increase levels activate inflammatory responses

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Affected pathways and the accumulated metabolites
1. Pyruvic Acid to Lactic Acid
 Pyruvic acid + NADH + H+  Lactic acid + NAD+
 This pathway is inhibited by low concentrations of pyruvic
acid, since it has been converted to lactic acid. The final
result may be acidosis from lactic acid build-up and
hypoglycaemia from lack of glucose synthesis
2. Synthesis of lipids
 Excess NADH may be used as a reducing agent in two
pathways: one to synthesize glycerol (from a glycolysis
intermediate) and the other to synthesize fatty acids. As a
result, heavy drinkers may initially be overweight
3, Electron Transport Chain
 The NADH may be used directly in the electron transport
chain to synthesize ATP as a source of energy. This
reaction has the direct effect of inhibiting the normal
oxidation of fats in the fatty acid spiral and citric acid cycle.
Fats may accumulate or acetyl CoA may accumulate with
the resulting production of ketone bodies
Inebriation after alcohol ingestion
 Alcohol interferes with communication between nerve cells
and all other cells, suppressing the activities of excitatory
nerve pathways and increasing the activities of inhibitory
nerve pathways.
 GABA--‐ major inhibitory neurotransmitter in the brain.
Alcohol acts primarily at the GABA receptor to facilitate its
action, thus in essence creating enhanced inhibition.
 Glutamate – major excitatory neurotransmitter in the
brain. Alcohol acts to inhibit a subset (N--‐ methyl--‐D--‐
aspartate, NMDA) of glutamate receptors thus diminishing
the excitatory actions of glutamate
Wernicke-Karsakoff encephalopathy in relation to chronic
alcohol drinkers
 Syndrome is a brain disorder involving loss of specific brain
functions caused by a thiamine deficiency
 Chronic alcoholics are at risk of developing it because of
reduced thiamine that can interfere in many cellular
functions leading to serious brain disorders
Fatty liver
 Fatty liver is caused by a combination of impaired fatty acid
oxidation and increased lipogenesis, which is thought to be
due to changes in the {NADH] / [NAD+] redox potential in
the liver.
Liver Cirrhosis
 Microsomal enzyme oxidation system (MEOS) pathway
 Inflammation incited by acetaldehyde
 Chronic alcohol exposure also activates hepatic
macrophages
 Relationship between blood and liver cells is destroyed
 Disturbed relationship between the liver and the channels
through which bile flows
Metabolic pathways affected in liver cirrhosis
 CHO metabolism
 Protein metabolism
 Lipid metabolilsm
Clinical manifestation of liver cirrhosis
 Edema, ascites, bruise formation, portal hypertension,
splenomegaly, jaundice, gallstones, hyperesterinism,
sensitivity to drugs and hepatic coma
Development of hepatic coma
 Decreased hepatic function  decreased urea synthesis 
accumulation of NH3 in blood  NH3 escapes hepatic
detoxification  NH3 in systemic circulation  Brain
Management of Hepatic Encephalopathy
 Non absorbable disaccharides
 Antibiotics
 Altering gut flora
 Increasing ammonia metabolism
 Zinc supplementation
 Flumazenil
 Dopamine agonists
Gout / Purine Metabolism Expt.
Purine Catabolic Pathway
 Purine metabolism pathway starts with α-D-Ribose 5-
phosphate then converted to Phosphoribosyl
pyrophosphate (PRPP) by the PRPP synthase. Then after
10 more enzyme-catalyzed reactions, PRPP will
then be converted to Inosine monophosphate (IMP).
 The purine base is built upon the ribose by several
amidotransferase and transformylation reactions. The
synthesis of IMP requires five moles of ATP,
 two moles of glutamine, one mole of glycine, one mole of
CO2, one mole of aspartate and two moles of formate. The
formyl moieties are carried on tetrahydrofolate (THF) in the
form of N5,N10-methenyl-THF and N10-formyl- THF.
 Two mechanisms regulate conversion of IMP to ATP
and GTP. AMP and GMP feedback-inhibit
adenylosuccinate synthase and IMP dehydrogenase,
respectively. Furthermore, conversion of IMP to
adenylsuccinate en route
 to AMP requires GTP, and conversion of xanthinylate
(XMP) to GMP requires ATP. This cross regulation
between the pathways of IMP metabolism thus serves
to decrease synthesis of one purine nucleotide when
there is a deficiency of the other nucleotide. AMP and
GMP also inhibit hypoxanthinge-guanine
phosphoribosyltransferase, which converts hypoxanthine
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 and guanine to IMP and GMP, and GMP feedback
inhibits PRPP glutamyl amidotransferase.
 AMP, a nucleotide, is now then converted to Adenine, a
nucleobase. IMP is converted to Hypoxanthine, which is a
purine derivative, then converted to x xanthine and finally to
uric acid. GMP, another nucleotide, is converted to Guanine,
a nucleobase, then converted to xanthine and finally uric
acid. From ribose-5-phosphate to the conversion of Uric acid
is called the de novo synthesis.
 Salvage pathway is the conversion of the 2 nucleobases
and one purine derivative to their respective nucleotides
which is GMP, IMP and AMP. Adenine is converted to AMP
by Adenine phosphoribosyl transferase (APRT) and PRPP.
Hypoxanthine and Guanine is converted back to IMP and
GMP respectively by hypoxanthine-guanine
phosphoribosyltransferase (HGPRT) and PRPP.
 GMP, AMP and IMP serve as feedback inhibitors of
Glutamyl amidotransferase, thereby inhibiting the formation
of 5-phosphoribosylamine. And without this, the whole de
novo synthesis pathway will not be inhibited therefore
enhancing the formation of uric acid.
Gout
Gout is a kind of arthritis that occurs when uric acid builds up in blood
and causes joint inflammation.
STAGES OF GOUT:
1. Asymptomatic Hyperuricemia



2. Acute Gout
 Hyperuricemia
 Sudden onset of intense pain and swelling
 Commonly occurs at night
 Stressful events, alcohol or drugs, or the presence of
another illness
 3 to 10 days
3. Interval or Intercritical Gout
 Does not have any symptoms
 Normal joint function
4. Chronic Tophaceous Gout
 Most disabling gout stage
 10 years
 Frequent attacks may leave over time hardened uric acid
crystal deposits called “tophi”. They get deposited in joints of
the hands, feet and elbows, even behind the ears. They
cause constant joint discomfort, inflammation and damage.
They also cause ugly joint deformities.
 Permanent damage to the affected joints and sometimes to
the kidneys
Main Causes of Gout
 Underexcretion of Uric Acid
o In the vast majority of the patients, the
hyperuricemia leading to gout is caused by
underexcretion of uric acid. Underexcretion can be
primary, due to as- yet-unidentified inherent
excretory defects or secondary to known disease
processes that affect how the kidney handles
urate, for example lactic acidosis ( lactate and
urate compete for the same renal transporter), and
to environmental factors such as the use of drugs,
for example, thiazide diuretics, or exposure to lead
(saturnine gout).
 Overproduction of Uric Acid
o A less common cause of gout is hyperuricemia
from the overproduction of uric acid. Primary
hyperuricemia is, for the most part, idiopathic
(having no known cause). However, several
identified mutations in the gene for X-linked 5-
phosphoribosyl-1-pyrophosphate (PRPP)
synthethase result in the enzyme having an
increased Vmax for the production of PRPP, a
lower Km for ribose 5-phosphate, or a decreased
sensitivity to purine nucleotides--- its allosteric
inhibitors. In each case increased availability of
PRPP increases purine production, resulting in
elevated levels of plasma uric acid. Lesch Nyhan
Syndrome also causes hyperuricemia as a result
of the decreased salvage of hypoxanthine and
guanine, and the subsequent increased availability
of PRPP. Secondary hyperuricemia is typically the
consequence of increased availability of purines,
for example, in patients with myeloproliferative
disorders or who are undergoing chemotherapy
and so have a high rate of cell turnover.
GOUT PSUEDOGOUT
More in men ages 40-60 and Equally in men and women
post menopausal women over 65 y/o
Develop quickly and reach Builds up over a number of
maximum swelling/in 12-24 hrs. days and less severe
Small joints (big toe called Multiple large joints are affected
Podagra) (knee, wrists, hip and shoulder)
calcification of cartilage in joints X-ray - calcification of joint
does not occur and plain cartilage is called
radiographs of the joints show chondrocalcinosis
distinctive submarginal erosions
with ―overhanging edge
Crystals are called Crystals are called calcium
monosodium urate crystals – pyrophosphate dihydrate
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 needle shape or spindle shape crystals – rhomboid in shape
and display negative and display positive
birefringent birefringence of crystals
DIAGOSIS: blood levels, 24 hour urine collection
GOLD STANDARD DIAGNOSIS: presence of monosodium urate
crystals in joint fluid via joint aspiration
TREATMENT:
Colchicine – reduces the inflammatory response to deposited urate
crystals and diminishes phagocytosis in joints
- inhibits lactic acid production of leukocytes
Probenecid – uricosoric agent that increases excretion of uric acid
thru blocking its reabsorption in the PCT by inhibiting the urate-anion
exchanger in proximal tubule.
Allopurinol – inhibitor of the xanthine oxidase which converts
hypoxanthine to xanthine then to uric acid
Celecoxib and Celebrex – COX 2 inhibitors
Allopurinol as an adjunct to chemotherapy
Tumor lysis syndrome is a metabolic disturbance caused by the death
of cancer cells during treatment and the release of their intracellular
components into the bloodstream. Intracellular components released
include large amounts of potassium and phosphates, along with
purine nucleic acids. Allopurinol is given 1-2 days before
chemotherapy to prevent excess uric acid.
Biochemical Basis of Obesity
Obesity
 Is a condition in which excess body fat has accumulated to
an extent that health may be negatively affected
 A prevalent nutritional disorder in prosperous countries
increasingly affecting children and young people
 An abnormal or excessive fat accumulation that presents a
risk to health (WHO)
 "Obesity" as a BMI equal to or more than 30
 Assess obesity by anatomical differences of fat deposition,
skinfold measurement, number of fat cells and body mass
index
Causes
 Is a condition in which excess body fat has accumulated to
an extent that health may be negatively affected
 A prevalent nutritional disorder in prosperous countries
increasingly affecting children and young people
 An abnormal or excessive fat accumulation that presents a
risk to health (WHO)
 "Obesity" as a BMI equal to or more than 30
 Assess obesity by anatomical differences of fat deposition,
skinfold measurement, number of fat cells and body mass
index
Types
Gynecoid/Pear Apple/Android
Excess fat on Thigh and Excess fat on the Abdomen
Buttocks
Common in women Common in men
Non-significant with Metabolic Significant correlation with
Syndrome Metabolic Syndrome
‘
Regulation of Appetite
 Appetite regulation is an immensely complex process
involving the gastrointestinal tract, many hormones, and
both the central and autonomic nervous systems
 The hypothalamus senses external stimuli mainly through a
number of hormones such as leptin, ghrelin, PYY 3-36,
orexin and cholecystokinin; all modify the hypothalamic
response.
Molecules that influence obesity
These are from the GI tract that control hunger and satiety.
Example:
 Ghrelin - secreted in between meals, an orexigenic hormone
that drives hunger
 CCk and Peptide YY (PYY)- send neural signals to
hypothalamus and terminates satiety and meals
 Neuropeptide Y (NPY), α-MSH, Dopamine, Serotonin -
Important in regulating hunger
Hormones that influence obesity
Leptin
 Plays a key role in regulating intake and energy expenditure
including appetite and metabolism
 Acts on receptor in the hypothalamus of the brain where It
inhibits appetite by:
o Counteracting effects of neuropeptide, a potent
feeding stimulant
o Counteracting effects of anandamide, potent
feeding stimulant
o -MSH, an appetite
suppressant
 obese people have unsuallly high circulating concentration
of leptin but they are resistant to the effects of leptin causing
leptin desensitization
Resistin
 Causes tissues, especially the liver to be less sensitive to
the action of insulin causing blood glucose level to rise due
to increased glycogenolysis and gluconeogenesis in the liver
 In human, It is primarily a product of macrophages, not fat
cells.
Estrogen
 Plays a role in fat distribution
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  Women of child-bearing age tend to store fat in the lower
body while men and postmenopausal women store fat
around the abdomen
Growth Hormone
 Influences the height and contributes to bone and muscle
building
 Also affects metabolism
Goals of weight management
 Induce a negative energy balance to reduce body weight
 Maintain a lower body weight over the longer term
 WEIGHT REDUCTION CAN BE ACHIEVED BY:
 PHYSICAL ACTIVITY (1)
o creates energy deficit = important component of
weight loss treatments
o Increases cardiorespiratory fitness
o Reduces the risk of cardiovascular disease
 CALORIC RESTRICTION (2)
o restrict oneself to small amounts or special kinds
of food in order to lose weight
o Effect Can be estimated Since 1lb of adipose
tissue = 3500 kcal
o Weight loss is determined primarily by energy
intake and not nutrient composition
o Ineffective over a long term for many individuals
o 90% regain the lost weight when dietary
intervention is suspended
Diet Regimen
 ATKIN’S DIET
o Low carbohydrate diet
o The body is an engine; carbs are the gas that
makes it go. Limiting carbs makes the body turn to
an alternative fuel—stored fat. So sugars and
“simple starches” like potatoes, white bread, and
rice are all but squeezed out; protein and fat like
chicken, meat, and eggs are embraced. Fat is
burned; pounds come off.
 SOUTHBEACH DIET
o Low carbohydrate
o There are good carbs and fats, and there are bad
carbs and fats. The key to weight loss is choosing
the best of each. That means lots of vegetables,
fish, eggs, low-fat dairy, lean protein like chicken
and turkey, whole grains, and nuts. South Beach is
lower in carbohydrates and higher in protein and
healthy fats
 TLC (THE LIFESTYLE CHANGE) DIET
o Low fat diet
o A heart-healthy regimen that can reduce the risk of
cardiovascular disease. The key is cutting back
sharply on fat, particularly saturated fat. Saturated
fat (think fatty meat, whole-milk dairy, and fried
foods) bumps up bad cholesterol, which increases
the risk of heart attack and stroke. That, along with
strictly limiting daily dietary cholesterol intake and
getting more fiber, can help people manage high
cholesterol, often without medication.
Pharmacological Treatment
 Sirbutamine
o Appetite suppressant
o Inhibits the reuptake of serotonin and
norepinephrine
 Orlistat
o Lipase inhibitor
o Inhibits gastric and pancreatic lipase
o Decrease breakdown of dietary fat into smaller
molecules
Surgical Treatment
 Vertical Banded Gastroplasty
o Restrictive gastric operation
o Restrict and decrease food intake
o Do not interfere with the normal digestive process
Diseases correlated with obesity
 Heart Diseases
 Lipid Problems
 Hypertension
 Type 2 Diabetes
 Dementia
 Cancer
 Polycystic Ovarian Syndrom
Marasmus and Kwashiorkor
Protein Energy Malnutrition
 A group of related disorders wherein there is cellular
imbalance between the supply of nutrients and energy and
the body's demand
Kwashiorkor
“The sickness the older child gets when
the next child is born”
 Severe deficiency more of
protein than of calories
 Common in children: 1-3 years
old
 Hallmarks of Kwashiorkor:
 Hypoalbuminemia
 Edema
 Fatty Liver
Marasmus
“Withering” ; “Anaclitic Depression”
 Severe deficiency of calories and protein
 Common in children: 0-2 years old
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 Marasmus Kwashiorkor
CHON and CHO deficiency CHON deficiency Patient’s Nutritional Status
“Wither or wasting “Sickness of the weaning”  Gomez Classification
Dry or non-edematous Wet or edematous o Assess malnutrition (1st, 2nd, 3rd degree) based on
Muscle wasting – skin and bone Edema; hypoalbuminemia; the percentage of expected weight for age
appearance; loss of weight; dry anemia; hair and skin changes;
and loose skin folds hepatomegaly
Decreased CHON, Decreased CHON;
Decreased CHO Increased CHO
Decreased Insulin Increased Insulin
Catabolism Anabolism
Increased Albumin Decreased Albumin Status Weight for Age
Normal 90-100%
Kwashiorkor Marasmus Malnutrition:
Hair Dry, Brittle, Alternated layers of 1st degree 75-89%
Depigmented non-pigmented and 2nd degree 60-74%
pigmented hair 3rd degree <60%
Face May be edematous/ Draw-in, Monkey, Overweight 101-120%
Moonface Like, wizened old Obese >120%
man face  Waterlow Classification
Skin Flaky skin Dry and lose skin o Assesses malnutrition based on wasting (%
hanging over the expected weight for height) and degree of stunting
glutei/Thigh (% expected height for age)
Body fat Diminshed Absent o For WASTING:
Muscle wasting Absent/Mild May be severe
Edema Present Absent
Hypoalbuminemia Present, may be Mild
severe
Fatty liver Present Absent
Level of Insulin Maintained Low
Level of Cortisol Normal High

Case

The 2yr old child did not receive adequate breast milk which is an Standard Stunting Wasting
essential source of CHON since he still have 4 siblings to whom the Normal >95% >90%
mother should also breastfed/take care. Even if he was breastfed, it Mild 87.5 – 87.4 % 80-90%
was insufficient since most likely the mother was already with another Moderate 80-87.4 % 70-79 %
child during the first few months of the index patient’s life. Another Severe <80% <70%
point raised was between the 2 year old and the 6mos old, the mother
will most probably breastfed/take care of the latter; that’s why it’s Mechanism behind manifestations
called “sickness of the weaning”.
 Family history
o 2yrs old with 4 siblings; youngest is 6mos old
currently being breastfed
o Lives in squatter’s area
o Father is tricycle driver with not enough earnings
 Diet
o Starchy gruel, occasionally mixed with diluted
condensed milk
 Physical examination
o Weight & height
o flaky skin; dry, brittle & depigmented hair;
distended abdomen; moderately enlarged liver,
edema on lower extremities; dry conjunctivae with
Bitot’s spot
 Laboratory Findings
o Low hemoglobin  Flaky skin (Flaky Paint Dermatosis)
o Hypoalbuminemia o Decreased collagen & keratin
o Hypoproteinemia o Similar to old paint that flakes off

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  Dry, Brittle & Depigmented Hair
o Dryness and brittleness due to decreased collagen
& keratin
o Depigmented hair due to low levels of melanin
from dopamine from tyrosine, eventually from
essential amino acid phenylalanine
o Depigmented hair, also known as flag sign,
alternating white and dark colored hair due to
fluctuating levels of CHON intake; adequate
CHON dark hair, inadequate CHON white hair
 Distended Abdomen & Edema
o Distended abdomen also known as pot belly
appearance
o Hypoalbuminemia and low levels of other plasma
CHON, decreasing oncotic pressure, so fluid is
attracted back/retained to plasma or capillary,
resulting to extravascular fluid accumulation
o Distended abdomen: fluid escapes into the
peritoneum
 Enlarged Liver
o Decreased lipoproteins and apolipoproteins
o So there will be no transporters of absorbed
dietary lipids & no regulators or cofactors for
lipoproteins, resulting to fat accumulation and
eventually hepatomegaly
o VLDL with apo B100; HDL with apo B48
 Dry Conjunctivae
o Decreased lipoproteins so there will be abnormal
lipid transport to the eyes resulting to non-
production of mucous and oil to lubricate the
conjunctiva
o Can also be due to vitamin A deficiency &
malfunctioning lacrimal glands
 Low Hemoglobin
o Decreased plasma CHON such as transferrin &
ferritin for the transport and storage of iron
o Unavailability of glycine and globin which are
CHON components for the synthesis of
haemoglobin
 Hypoproteinemia & hypoalbuminemia
o Low protein intake
Factors that contributed to the development of malnutrition
 Inadequate or lack of breast milk during first year
 Improper weaning practices
 Parents not well informed about proper nutrition
 Poor apetite, diarrhea
 Poverty, big family
Dietary Calculations
Complications of Kwashiorkor
 Even with treatment, children who have had kwashiorkor
may never reach their full growth and height potential
 If treatment comes too late, a child may have permanent
physical and mental problems
 If left untreated, the condition can lead to coma, shock, or
death
Management & Prevention
 Patient Stabilization
o Correcting fluid & electrolyte imbalances
o Infections should be treated appropriately
 Dietary Therapy
o Food should be given to patient GRADUALLY
o In order for the body to adapt by synthesizing
enzymes that can digest food; to prevent
malabsorption or diarrhea
 Discuss proper diet to the MOTHER
 Breastfeeding & family planning
Osteoporosis/Calcium Determination
Vitamin D
 Main Source: Sunlight
 At risk for Vitamin D deficiency:
o Pregnant and Breastfeeding women
o Babies and children (<5 years old)
o Elderly (>65 years old)
o People with not enough sun exposure
o Dark skin
 Maintain plasma calcium concentration
o Increased calcium absorption
o Decreased calcium excretion
o Mobilization of bone minerals
 Parathyroid and Thyroid hormones
 Inhibit interleukin production and immunoglobulin
 Modulation of cell proliferation
 Importance
o Absorption and metabolism of calcium and
phosphorous
o Immune system regulation
o Regulation of cell proliferation and differentiation
o Reduce risk of developing multiple sclerosis
o Healthy body weight
o Immune system
o Muscle function
o Cardiovascular function
o Brain development
o Lower risk of cancer
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Vitamin D Synthesis in the skin  Homeostasis is regulated through integrated hormonal
system
 2 major Ca- regulating hormones and receptors
o PTH; PTHR
o 1, 25(OH)2D; VDR
 Ionized calcium; CaR
 Decreased Ca = Inactivate CaR = Increased PTH =
Increased Tubular CA reabsorption; Increased net bone
resorption
 Increased PTH = Increased 1,25 (OH)2D = activate VDR =
increased Ca absorption; decreased PTH secretion;
increased Bone resorption
Vitamin D Metabolism
Composition of Bone
 Mainly consist of collagen fibers and inorganic bone mineral
(crystals)
 10-20% water
 60-70% bone mineral
 Matrix
o Inorganic hydroxyapatite
o Organic collagen
 Inorganic
o From carbonated hydroxyapatite
o (Ca10(PO4)6(OH)2)
 Organic
o Type 1 collagen
o Various growth factors
 Bone formation – essential process in human body
Formation and Hydroxylation of Vitamin D3 development
 Bone remodeling – life long process; resorption and
ossification

Cell Types
 Osteoblast
o Mononucleated bone – forming cells
o Near the surface of bones
o Osteoid
o Secrete alkaline phosphatase
 Osteocytes
o Osteoblasts that are no longer on the surface of
the bone
o In lacunae between lamella
o Homeostasis
 Osteoclast
o Multinucleated
o Bone resorption
o Secrete acid phosphatase
Calcium Cell Types
 5th most abundant element in the body Osteoclast -Release acids and enzymes
 A hard, dense material which forms bone and teeth that removes minerals and
 Skeletal mineralization matrix in response to signals
 Dietary Ca recommendation: 1000 to 1500mg/dL Osteoblast -Synthesizes matrix
-Deposition of new bone matrix
 Importance
(osteoid) and mineralization
o Formation of strong bones
-Control mineralization by
o Absorption and utilization of other nutrients
regulating the passage of
o Cell signaling, blood clotting
calcium and phosphate ions
o Muscle contraction, nerve function
Chondrocyte -Secretes matrix
o Send and receive NTA during communication with
other cells -Prepares matrix for
o Enzyme activation calcification
o Transport ion across cell membrane

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 Osteocyte -Osteoblast surrounded by  Calcium and vitamin D supplementation
minerals  Hormone replacement therapy (HRT)
-Dormant osteoblast in bone  Medications
matrix
Reagents
Bone Demineralization
 Ossification of bones depend on: Ca Color Reagents Ca Based Reagents
o Collagen 0.082nM o-cresolphthalein 0.51M diethylamine
o Availability of Phosphate (and calcium) complexone (OCPC) - acts as a buffer
o Removal of pyrophosphate and other inhibitors of
mineralization - Indicates Mg, Ca, Sr, Ba & 7.7mM potassium cyanide
 Osteoclast SO42-
o Lysozomal enzymes
o Tartrate – resistant acid phosphate – increased 17.2mM 8-hydroxyquinolone
concentration when bone resorption is accelerated - chelating, complex w/ metals
 Dissolution of calcium salts
 Enzymatic breakdown of organic matrix - prevents interference by Mg
 Bone collagen degradation Stabilizers and reaction
accelerator
Osteoporosis Ca + OCPC = OCPC (violet color)
 A condition in which there is a reduction of bone mass or Calcium reacts with OCPC in an alkaline medium (10pH) to form a
density purple-color that absorbs at 570nm (550-580nm)
 Bone mass decreased due to decreased bone formation
and increased resorption Iodine deficiency (Endemic Goiter)
 Typically “silent” or without symptoms and outward Iodine metabolism
manifestations  Iodine transport across thyrocytes
 Osteoporosis exists when bone density falls 2.5 SD or below  NA/I symporter
the mean o Secondary active transporter that gets its energy
from the NA-K ATPase pump
Types of Osteoporosis  Pendrin
o Carrier protein that transports Iodine to lumen
PRIMARY  Oxidation
Type 1 Type 2 Idiopathic o Iodide is oxidized to iodine by peroxidase
(Menopausal) (involutional)  Organification/Iodinification
Occurs in Associated with Unknown case o Iodine will bind to thyrosine component of the
postmenopausal normal aging thyroglobuline producing MIT and DIT
women (age 50-70) processes in both Can affect children o Enzymes
men and women and young adults as  Peroxidase and iodinase
older than age 70 well as older  Coupling
individuals o MIT+DIT = T3
Associated with Associated with hip o DIT + DIT = T4
fractures in the wrist and pelvic fractures o Enzyme:thyroid peroxidase
and in the vertebrae Thyroid hormone secretion
Secondary  Receptor mediated endocytosis
Relatively uncommon and may be due to a variety of conditions o Once TG is iodinated, it is stored in the lumen of
 Chronic renal disease the follicle, release of T3 and T4 in the blood
 Various drugs such as corticosteroids stream requires binding of TG to receptor megalin
 Endocrine disorders followed by endocytosis
 Malabsorption syndrome  Proteolysis of thyroglobulin
o Lysosomal degradation and proteolysis of TGB to
Causes of Osteoporosis release MIT, DIT
 Deiodination of MIT and DIT
 Aging
o MIT and DIT are not secreted and they are
 Medical conditions
deiodinated by zenyme deiodinase. Iodine is
 Poor diet
recycled for the synthesis of t3 and t4
 Lifestyle
 Secretion
 Genetic factors Regulation
 Alteration of levels of hormones, growth factors and
 H-H thyroid axis
cytokines
o Hypothalamus secrets TRH -> PG secretes TSH -
> TG secretes T3 and T4
Management and Treatment
 Deiodinases
 Lifestyle change (exercise, balanced diet, etc)

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 o Deiodinase 1 activates T4 to T3 or deactivates it  Thyrotropin and thyrotropin releasing hormones
o Deiodinase 2 converts T4 to T3  Myxedema/Gull’s disease
o Deiodinase 3 deactivates T4 and T3  Cretinism/Infantile Myxedema
 Wolffe-chaikoff effect
o Reduction of thyroid hormone with increased Disorders associated with iodine Deficiency
levels of iodine Goiter
 Enlarged thyroid gland
dEndemic goiter  Swelling
 Enlarged gland due to lack of iodine  Fatigue
 A type of goiter that is associated with dietary iodine  Low body temperature
deficiency  Dry skin
 Severe iron deficiency  Depression
 Impaired thyroid hormone synthesis  Shortness of breath
Myxedema
Endemic goiter as to:  Adult
 Age group affected  Skin and tissue disorder
 Adolescents at puberty  Hashimoto’s thyroiditis
 Appear at an early stage  Coarse sparse hair
 Regional distribution  Poor tolerance to cold
 Found in seawater  Low husky voice
 Mountainous areas  Dry yellowish skin
Cretinism
Clinical manifestation  Maternal iodine deficiency\
 Swelling on neck  Physically dwarfed
 Hoarseness of voice  Mentally retarded
 Difficulty in swallowing and breathing  Thick pasty skin
 Coughing  Protruding abdomen
 Wheezing  Deaf mutism

Laboratory diagnosis
 Physical exam
 Thyroid function test
 Antibody test
 Thyroid UTZ
 Radioactive iodine thyroid scan
 Biopsy

Physiologic and biochemical effects of thyroid hormones

 Cellular Activity and Heat Production
 Growth
 Carbohydrate Metabolism
 Fat Metabolism
 Plasma and Liver Fats
 Vitamins
 Basal Metabolic Rate
 Body Weight
 Cardiovascular System
 Respiration
 Gastrointestinal Motility
 Excitatory Effects on the Central Nervous System
 Function of the Muscles
 Muscle Tremor
 Sleep
 Effect on Other Endocrine Glands
 Sexual Function

Thyroid hormone Deficiency

 Hypothyroidism
 Metabolic disorder  Dany targ | Heneral Luna | Pacis
 Deficient activity and lessened secretin

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