MTAP 1 CC1

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Last updated 6:42 AM on 11/10/22
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121 Terms

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brain RBCs retinal cells
Carbohydrates Provide energy to the:
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sugar units found in the chain
Can be classified into 4 properties based on the number of
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Glucose, Fructose, Galactose
example of Monosaccharides
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1
Number of sugar units of monosaccharide
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Maltose, Lactose, Sucrose
example of disaccharides
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2
number of sugar units for Disaccharides
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2-10
number of sugar units for oligosaccharides
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Starch and Glycogen
examples of polysaccharides
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>10
number of sugar units for polysaccharides
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sucrose
only disaccharides that is also a non-reducing sugar.
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Monosaccharides
cannot be further hydrolyzed because they are the simplest sugar.
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glucose
only carbohydrate that could be directly use for energy.
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Embden-Meyerhof Pathway
Hexose Monophosphate Pathway
Glycogenesis
Once the glucose is transported within the cell, it can
potentially enter three pathways:
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Glucose-6-phosphate
Before entering into a pathway, glucose needs to be converted
into
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Glycogenesis
Glucose to Glycogen
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Glycogenolysis
Stored Glycogen to Glucose
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Gluconeogenesis
Synthesis of glucose from non-carbohydrate sources
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Glycolysis
Metabolism of Glucose for energy production
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Lipogenesis
Carbohydrate to fatty acids
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Insulin
Glucagon
Epinephrine
Cortisol
Growth hormone
ACTHThyroxine
Somatostatin
Regulation of Carbohydrate metabolism
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insulin and glucagon
primary hormones for carbohydrate metabolism
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INSULIN
Produce in the endocrine gland of pancreas, particularly in the β-cells of islets of Langerhans
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Decreases plasma glucose level
primary function of insulin
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Hypoglycemic agent
insulin is what kind of agent in the body?
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Increasing the transport and entry of glucose
into the muscles.
Increasing glycogenesis
Increasing lipogenesis
Increasing glycolysis
Decreasing glycogenolysis
functions of insulin
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GLUCAGON
Produced in the α-cells of islets of Langerhans
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Increasing glycogenolysis
Increasing gluconeogenesis
functions of glucagon
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Hyperglycemia
increase in the blood glucose concentration
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Hypoglycemia
decrease in the blood glucose concentration
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Type 1 Diabetes
Formerly known as “Juvenile-onset Diabetes” or “Insulin-Dependent DM”
Result from cellular-mediated autoimmune destruction of the β-cells
an absolute deficiency of insulin
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Type 1 Diabetes
Genetically related that could be triggered by an environmental factor or viral infection
Ketosis tendency
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10 to 20%
percentage of total DM cases that are type 1 DM
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Polyphagia
Polyuria
Polydipsia
what are the three P's
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Nephropathy
Neuropathy
Retinopathy
Microvascular – 3 pathy’s
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Type 2 Diabetes
Formerly known as “Non-insulin Dependent” or “Adult-onset DM”
Resistance to insulin with an insulin secretory defect
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equal or more than 6.5%
DIAGNOSTIC CRITERIA FOR DM

HbA1c
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equal or more than 126 mg/dL or 7.0 mmol/L
DIAGNOSTIC CRITERIA FOR DM
Fasting plasma glucose
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equal or more than 200 mg/dL or 11.1 mmol/L
DIAGNOSTIC CRITERIA FOR DM
Two-hour plasma glucose during an OGTT
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equal or more than 200 mg/dL or 11.1 mmol/L
DIAGNOSTIC CRITERIA FOR DM
Random plasma glucose plus symptoms of diabetes
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HbA1c, Fasting Blood Glucose, and OGTT.
considered appropriate method for DM diagnosis
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only 1
Should the patient be tested using the 3 methods to diagnose him/her
with DM?
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Gestational Diabetes Mellitus
Any degree of glucose intolerance with onset or first recognition during pregnancy.
Inability to properly metabolize glucose in GDM is usually caused by deficiency of insulin and metabolic and hormonal changes.
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Macrosomic baby
baby born in a GDM mother.
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respiratory syndrome, hypocalcemia, and hyperbilirubinemia
Macrosomic baby increased risk for?
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equal or more than 92 mg/dL or 5.1 mmol/L
DIAGNOSTIC CRITERIA FOR GDM
Fasting plasma glucose
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equal or more than 180 mg/dL or 10 mmol/L
DIAGNOSTIC CRITERIA FOR GDM
One-hour plasma glucose
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equal or more than 153 mg/dL or 8.5 mmol/L
DIAGNOSTIC CRITERIA FOR GDM
Two-hour plasma glucose
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65-50 mg/dL
Glucose level of ? considered hypoglycemic
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50-55 mg/dL
Glucose level of ? considered hypoglycemic and with symptoms
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lipids
primary sources of fuel in the body, that stabilize the cell membrane and allows transport of different molecules
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lipoprotein
Lipids require ? as their special transport
carrier
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Triglycerides
Phospholipids
Cholesterol
Cholesteryl esters
types of lipids
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TRIGLYCERIDES
Composed of 3 fatty acids attached to a glycerol backbone
Hydrophobic – water fearing and water insoluble
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12-14 hours
fasting requirement for trigly?
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PHOSPHOLIPIDS
Most abundant lipid in the body
it only contains 2 esterified fatty acids attached to a phosphate group
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hydrophobic
Fatty acid nonpolar tails are
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hydrophilic
Phosphate head group is
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CHOLESTEROL
Unsaturated steroid alcohol containing 4 rings AMPHIPHATIC
A precursor of major steroids
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OH group
part of the cholesterol that is hydrophilic
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CHOLESTERYL ESTERS
Similar to triglycerides, these are NEUTRAL lipids that are very polar, therefore are hydrophobic, hence found in the center of a lipid drop along with triglycerides
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APOPROTEIN
protein part of the lipoprotein
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CHYLOMICRONS
Largest and the least dense lipoprotein
Since they are so light, they readily float and form the CREAMY LAYER of plasma or serum
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apo-B48 apo C-3 apo lipoprotein
apo protein present in chylomicrons
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Apo B-100
Apoproteins found on the surface of VLDL is
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VERY LOW-DENSITY LIPOPROTEIN
they are the major carriers of endogenous triglyceride
They are also responsible for the turbidity of plasma but do not form
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CHYLOMICRONS
Its primary function is to deliver dietary lipids to hepatic and
peripheral cells (exogenous triglycerides)
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LOW DENSITY LIPOPROTEIN
Core is rich in cholesterol, hence considered to be the most cholesterol rich among lipoprotein
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LOW DENSITY LIPOPROTEIN
Most ATHEROGENIC
Responsible for the transport of cholesterol to the
peripheral tissues
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HIGH DENSITY LIPOROTEIN
The smallest among all lipoproteins but most dense
Place a significant role in the REVERSE CHOLESTEROL TRANSPORT, which is the transport of the excess cholesterol from the tissues back to the liver
Most ANTIATHEROGENIC lipoprotein
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DYSLIPIDEMIA
This is referred as the abnormal lipid concentrations
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LDL receptors
Patients with FH are capable of synthesizing cholesterol however there is a problem with the ?
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HYPERTRIGLYCERIDEMIA
This could also arise due to genetic abnormality resulting to Familial hypertriglyceridemia or it can be caused by other conditions secondary to other diseases
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lipoprotein lipase or Apo C-II
In Familial hypertriglyceridemia, what is the deficient component? which keeps chylomicrons from being cleared hence elevating serum triglycerides
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Familial Combined Hyperlipoproteinemia
In here, total cholesterol or the triglycerides could be elevated alone, or both are elevated
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Apoprotein B
what protein is impaired in Familial Combined Hyperlipoproteinemia
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Familial Dysbetalipoproteinemia
with the presence of apo E2/2 – which is a rare form of apo E, and iy cannot bind with hepatic A receptor therefore, impairing the uptake of VLDL and chylomicrons
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HYPOBETALIPOPROTEINEMIA
Affects LDL, VLDL and chylomicrons
A point mutation in the Apo-B resulting to Apo-B Deficiency
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Abetalipoproteinemia
Defective Apo B synthesis
VLDL, LDL and chylomicrons are not found in plasma
Defects in absorption of fat-soluble vitamins
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HYPOALPHALIPOPROTEINEMIA
Affects LDL since it contains Apo A-1
Mutation in LCAT Apo A-1 and ABCA1 Transporter gene resulting to decreased HDL
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Tangier’s Disease
Extreme form of hypoalphaproteinemia
HDL concentration is as low as 1-2 mg/dL
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PRE-ALBUMIN
Plasma protein that is reached into tryptophan.
Responsible for transporting the:
o Thyroid hormones
o Vitamin A Retinol
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Alcoholism
Chronic renal failure
Patients receiving steroids
causes of increased Pre-albumin
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Diet is deficient in protein
Reduced hepatic synthesis
causes of decreased pre-albumin
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ALBUMINS
Present in highest concentration
Responsible for the 8% of colloid osmotic pressure
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Glycated albumin
Biomarker for serum glucose pattern approx. 1 month.
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: 20 days
half-life of glycated albumin
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Dehydration
Excessive albumin infusion
causes of increase albumin
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Malnutrition and malabsorption
Liver disease
active nephrotic syndrome
Burns
Hypothyroidism
Analbuminemia
Bisalbuminemia
Hemodilution
causes of decrease albumin
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GLOBULINS
Consists of α1, α2, β, γ
Not measure but calculated.
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UREA
Major excretory product of protein metabolism
Has the highest plasma concentration
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Urea N
Today, this term is used because it is more appropriate for UREA
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Azotemia
Term for elevated urea in plasma
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Uremia
Term for very high plasma concentration of urea accompanied by kidney failure
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PRE-RENAL AZOTEMIA
Occurs due to reduced renal blood flow
Less urea filtered = less urea excreted
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Stress, fever, major illness, corticosteroid
therapy, and GI hemorrhage
Increased protein catabolism due to
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Congestive heart failure
Shock
Hemorrhage
Dehydration
High protein dietIncreased protein catabolism
symptoms for Pre-renal azotemia
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RENAL AZOTEMIA
Problem in kidneys
Decreased renal function = increase plasma urea
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Acute renal failure
Chronic renal failure
Glomerular nephritis
Tubular necrosis
examples of RENAL AZOTEMIA
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POST-RENAL AZOTEMIA
Obstruction of urine flow
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Renal calculi
Tumors of the bladder or prostate
Severe infection
examples of post-renal azotemia