8/23/17 Flashcards
Classical conditioning
Neutral stimulus (CS) paired with unconditioned stimulus (UCS)
UCS elicits a natural response (UCR)
Eventually CS will elicit a conditioned response (CR), which is often similar to the UCR
Operant Conditioning
Learning due to environmental contingencies of reward and punishment
Positive reinforcement: applying rewards makes behavior more likely to occur
Negative reinforcement: withdrawing aversive consequences makes behavior more likely to occur
Punishment: applying aversive consequences makes behavior less likely to occur
Extinction: withdrawing positive consequences makes behavior less likely to occur
Challenges of Operant Conditioning
Shaping: progress, not perfection
Frequency of consequences (at least for positive reinforcement): continuous reinforcement to acquire, intermittent reinforcement to maintain (fading reinforcement)
Timing of consequences: close temporal link between behavior and consequence
Clarity of consequences
Clinical Application of Operant Conditioning
Feeding disorder of infancy or early childhood
Counts of Disease Frequency
Can’t be compared since can be from pop. of different sizes
Good if single count is useful for public health (Ebola) or for allocating resources
Ratio for Disease Frequency
Shows the relative size of two values/groups
Proportion of Disease Frequency
Ratio in which the numerator is a subset of the denominator
Rate of Disease Frequency
Like proportion but during some period of time
Contain counts of disease frequency, size of pop. at risk, and a time period
Incidence
Cumulative incidence
Incidence rate (density)
Frequency of new cases over time period, measures the appearance of diseases
Cumulative: risk of getting a disease, usually used in fixed pop. but most dynamic so bad measure # new cases / # originally at risk (over certain time)
Rate: # of new cases / sum of disease free person-time over a certain time period
Point prevalence vs. Period prevalence
Point: # of existing cases / total pop. At a specific point in time
Period: (# of existing cases + # of cases that occur during the interval) / pop. at midpoint of interval or the average pop. size
Both are proportions
Relationship between prevalence and incidence
Prevalence is similar to incidence * disease duration (P=ID)
I~P if short disease duration
Prevalence higher than incidence if chronic disease
Measure incidence if care about etiology
Protein turnover
Total flux through protein synthesis and degradation
Conversion of AA pool into protein and breakdown of protein into the free AA pool
AA precursors for N-containing compounds
Cys to taurine to bile salts
Tyr to thyroid hormones, melanin, catecholamines (NE, epi, dopamine)
Gly to heme, purines, creatine, bile salts
Nitrogen balance
Nitrogen ingested - nitrogen excreted
At eq.: you intake 100 mg/kg/day of nitrogen or 600 protein
Positive: anabolic state to build mass, plateaus, normal growth, athletes, increased protein translation from free AA pool
Cachexia
Negative nitrogen balance that accompanies chronic diseases like cancer, renal diseases, severe burns, and septicemia
Rapid weight loss of 5-20%, high catabolic state that leads to muscle loss
Need nutritional supplementation since normal nitrogen diet is still negative nitrogen balance, also use stimulation of anabolism through steroids
Protein turnover accelerated from inflammatory process
Reductive amination
Glutamate-dehydrogenase with any aminotransferase can form any non-essential AA except Tyr/Cys given the proper alpha-keto acid and ammonia source
Phenylketonuria
Phe is converted to Tyr by phenylalanine hydroxylase
PKU has mutated Phe hydroxylase or enzymes in tetrahydrobiopterin (it’s cofactor)
Avoid Phe in diet and supplement with Tyr, avoid aspartame
Homocystinuria
Recessive, deficiency in gene for cystathionine beta-synthase
Accumulate homocysteine and Met
Free sulfhydrl of of homocysteine disrupts collagen cross linking and leads to premature atherosclerosis, strokes, heart stacks, vascular disease, ectopia lentis, and mental retardation
Avoid Met in diet and supplement with Cys
Cys becomes conditionally essential
Cystathioninuria
Recessive, Cys becomes essential AA
Cystathionine accumulates, is more benign since Met and homocysteine levels are more normal
Asparagine synthetase
Requires ATP
Adds NH2 to Asp to make Asn, also Gln becomes Glu by losing an NH2
Acute lymphonic leukemia
Accumulate immature lymphocytes in blood, they lack aspargine synthetase and Asn becomes an essential AA
L-asparaginase hydrolyzed Asn to Asp in the plasma conc. and deprive lymphoblasts only source of Asn, lymphoblasts do apoptosis
Most abundant AA in plasm
Gln which is made by glutamine synthetase from Glu
AA absorption
Active transport that requires Na+ in the small intestines
Transporters:
- Small neutral
- Large neutral
- Basic
- Acidic
- Proline
AA imbalance even if get min cuz competition at transporters
Go to liver via hepatic portal vein and then transported in the blood
Essential AA
PVT TIM HALL
Arg and His are not as essential
Can’t be made in human body and need from diet
Conditional essential AA if have like PKU
Protein Quality
Biological Value:
Measures the percentage of absorbed AAs retained for protein synthesis (during growth)
Depends on dietary N, urinary N, and fecal N (with endogenous values for the last two)
Net Protein Utilization:
Like BV but neglects absorption
Protein Efficiency Ratio:
No chemical analysis
Weight gain/weight of protein ingested during period of time
Digestibility:
Percentage of nitrogen absorbed, only fecal and no urinary
Chemical Score:
Mg of essential AA in test / mg in egg
Protein Digestibility Corrected AA Score:
Like chemical Score but use rigorous requirements needed for a 2-5 year old, takes digestion into account
Kwashiorkor
Marasmus
Kwashiorkor: Severe protein deficiency, when stop breast feeding first born, occurs within days to weeks
Edema and distended abdomen, mental apathy, pigmentation changes, muscle wasting, high mortality
Marasmus: protein energy malnutrition over the course of months or a year, wasting of fat and muscles but mentally alert
Benefits of fiber in diet
- Reduce incidence of hemorrhoid, cardiovascular disease, hyperlipidemia, and diverticulitis
- Promote weight loss since feel full
- Stimulate peristalsis and prevent constipation
- Remove cholesterol and sterols from feces
- Help promote glycemic control and reduce hyperlipidemia for diabetics
Glycemic index and glycemic load
Index: classifies carbs based on ability to raise blood sugar, use glucose as reference
Load: index * amount of carbs in grams / 100
High index/load associated with type II diabetes
Types of Carbs and Fiber
Available: can be digested and absorbed for use calorically or to make other metabolic products
Basic mono and disaccharides plus stack, glycogen, and dextrins
Unavailable: largely indigestible, provide bulk in diet and help wth elimination
Insoluble like cellulose or soluble like pectins, oatmeal, and bananas
Dietary fiber: remains after breakdown in digestive tract
Crude fiber: remains after acid and alkaline digestion of food, smaller than dietary fiber
Added fiber: isolated nondigestible carbs that are added to food for good physiological benefits
Essential FA deficiency
Can’t make a double bind at omega-3 or-6 so need from diet
Occurs in children, dermatitis, alopecia, growth retardation
Linoleic (18:2 w6) > linolenic (18:3 w3) > arachidonic (20:4 w6) help treat
Characteristics of trans FA
Higher melting point
Increase LDL/HDL ratio
Inhibits desaturase which helps make arachidonic acid (precursor of prostaglandin)
Increase shelf life of foods
Present in fried foods
Daily recommended intake of macronutrients
Carbs: 45-65%
Fat: 20-35%
Protein: 10-35%
Proteins have sparing effects where like high Cys spares lower Met since Met makes Cys and lower that conversion, complementary proteins have essential AAs when combined like beans and wheat
Have at least 2 fish per week for omega-3 FA
Heart contraction
HR set by sinoatrial node, located in right atrium and discharges without control from the brain
Both atria contract, electrical impulse travels through atria to the atrioventricular node
EKG Prep
Position the patient: make supine, head flat or no more than 45°, position can alter EKG so note any changes if not supine
Skin prep: use alcohol pad to de-fat where put electrodes, gently abrade skin with gauze, improve conduction and reduce noise
If oily/soiled skin- wash with soap/water and dry first, briskly rub with alcohol
If diaphoretic (sweaty)- dry with cloth first
If hairy- separate hairs or clip, try not to shave
Lead Electrode Placement: one for each limb, six for chest, make sure attached right and sticky
Chest Leads for an EKG
V1: 4th intercostal space, right eternal border
V2: 4th ICS, left sternal border
V3: equidistant between V2 and V4
V4: 5th ICS at the midclavicular line
V5: at the horizontal level to V4 at the anterior axillary line
V6: horizontal level to V4 at the midaxillary line
Find 4th ICS by finding Angle of Louis at 2nd rib, count down to 4th intercostal
Limb Electrode Placement
Arms: below elbow and between wrist on lower forearm
Legs: below knee and between ankle, lower leg
Placed on fleshy areas and same position for same type of limb
3 Troubleshooting Issues for an EKG
- Electrical interference: closely jagged lines from too many electronics or improper grounding
Fix: turn off all nonessential electronics and lights, check to ensure wires stent twisted, possibly switch rooms
- Wandering baseline: bad electrode connection or exaggerated respiratory movements makes the waveform go up/down during tracing
Fix: check that electrodes are in the right spot and the skin isn’t oily/sweaty, have patient breath in and out and hold breath while run EKG
- Somatic or muscle tremor: lines spiking and running close together, over shorter period of time than electrical interference, skeletal muscle movements like chills or Parkinson’s
Fix: cover patient if chilled, position patient’s hands under hips to quiet movement, try higher limb lead placement if movement not that exaggerated
