Week 3 Problem Concepts Flashcards
Fxn and Location of Simple Squamous Epithelium
Diffusion! located: alveoli, bowman’s capsule, endothelium
Fxn (3) and Location of Simple Cuboidal Epithelium (3)
Absorption, Secretion, minimal protection. Location: small ducts of exocrine glands, thyroid follicles, kidney tubules
Function (1) and location (1) of Simple columnar Epithelium
Function: absorption
location: GI tract
Function (3) and location (2) of pseudostratified epithelium
Fxn: absorption, secretion, transport
Location: vas deferens/epididymis, bronchial tree
function and location of stratified squamous epithelium
Protection
Skin (keratinized), vagina, oral cavity, esophagus
function (2) and location (2) of stratified cuboidal epithelium AND stratified columnar epithelium
Protection and conduit
large ducts exocrine glands, anorectal jxn
function and location of transitional epithelium
distension
bladder
holocrine secretions
A mode of exocrine secretion in which the cell dies and releases its contents
apocrine secretions
a mode of exocrine secretion in which a cell releases a vesicle with its contents
merocrine secretions
a mode of exocrine secretion in which a cell exocytoses its contents (most common)
what type of exocrine gland is a eccrine sweat gland? secretion type?
multicellular, simple coiled tubular (serous secretions)
what type of exocrine gland is the intestinal gland? secretion?
multicellular, simple tubular, mucus secretions
what type of exocrine gland is the pancreatic gland? secretion type?
mutlicelllar, compound acinar, serous secretions
what four steps should you follow prior to taking vital signs?
wash your hands, introduce yourself and verify patient, tell the patient about the procedure and ask if they have any questions, ask if the patient has done anything (meds, exercise, pain) that will alter vitals
what is an apical pulse?
listen to the pulse with stethescope
what is a peripheral pulse
palpate or feel the pulse
what is eosin? what does it reveal?
an acidic dye that binds to positively charged molecules (cytoplasm, collagen, muscle fibers)
what is hemtoxyln dye? what does it reveal?
a basic dye that binds to negatively charged molecules. DNA/RNA. Hematoxylin and Eosin (H&E) are commonly used together
epidermis: composition, originates?
keratinized stratified squamous epithelium. originates from ectoderm
dermis: composition, originates?
composed of connective tissue, mesoderm
what are the layers of the dermis?
superficial: papillary layer, loose areolar connective tissue
deep: reticular layer, dense irregular connective tissue
what is connective tissue?
cells in an ECM
what is the ECM
ground substance and protein fibers
what are the types of connective tissue?
Specialized: Bone, cartilage, blood
Connective tissue proper:
dense: regular, irregular
loose: reticular, areolar, adipose
how do you calculate the incidence rate?
Incidence/sum of disease-FREE person time
what is disease free person time? how can it be measured?
the amount of time (in years) that each subject was without a disease. You can either add up the total years (most exact), you can average the number of people and multiply by years (500,000 people 1 yr), or you can average the number of years and multiply by people (100 people2.5 yrs)
what is the relationship between prevalence and incidence?
P=(incidence)(duration)
which AA is a precursor for heme?
Gly
how do you calculate nitrogen balance? what are the three nitrogen balance terms?
Nitrogen balance= Nitrogen consumed-nitrogen excreted
positive nitrogen balance, negative nitrogen balance, nitrogen equilibrium
what is cachexi? symptoms? treatment?
a hyper-catabolic state in which protein and AA (Gln) are degraded (negative nitrogen balance). Symptoms: weight loss, seen in cancer renal disease and burns.
Treat: anabolic steroids
what is Phenylkeonuria (PKU) caused by? (2)
lack of Phe Hydroxylase which results in no Tyr being formed OR a lack of phe hydroxylase cofactor (tetrahydrobiopterin)
why is PKU a problem. how can you treat it?
Tyr becomes essential AA, Phe metabolites accumulate (neurotoxic).
Treat: supplement Tyr, avoid Phe (artificial sweeteners)
what is the cause of homocystinuria? treatment?
Recall: Met gives rise to homocysteine. Homocysteine and Ser combine to form Cystathionine via Cystathionine Synthetase. Cystathionine is converted to Cys via cystathionase.
Homocystinura (an accumulation of homocystine) is caused by a defect in Cystathionine synthetase
Treat: decrease Met, supplement Cys
why is homocysteine accumulation bad?
disrupts collagen cross-linking (stroke, heart attack), Cys becomes essential
what is the cause of Acute lymphatic leukemia?
most common cause of childhood cancer! Asn not produced in WBCs due to a defect in Asn synthetase (Asp–>Asn via Asn Synthetase)
what is the treatment for Acute Lymphatic Leukemia
Provide body with L-Asparaginase which converts Asn to Asp. this will kill the defective cells as their only source (diet) of Asn will deplete
what is chemical score of a protein?
compares the AA content of a test protein to an egg protein. (CS=(mg AA/g test)/(mg AA/g egg protein))x100. The AA with the lowest % is reported as the CS of that protein
what is the protein digestivility corrected AA score?
similar to CS, but instead of egg use the requirement for a 2-5 yr old. then you multiply the lowest score (not percentage) by the protein digestibility. PDCAAS=((mg AA/g test)/(mg AA/g requirement))–>figure our which AA is the lowes–>multiply by digestibility
what is the biological value of a protein?
tells you how much of a protein is retained in the body
=(N diet-(N urine-N0 urine)-(N poop-N0 poop))/(Ndiet-(Npoop-N0 poop))
what is net protein utilization?
similar to BV but the denominator is only N diet
what is the protein efficiency ratio?
weight gain over a period/total weight of protein ingested over that period
how do you calculate protein digestibility?
(N diet-(Npoop-N0poop))/Ndiet
what are PEM disorders?
Protein Energy Metabolism Disorders
what are the two PEM disorders discussed?
Kwashiorkor disease:
Marasmus disease
what is Kwashiorkor disases?
PEM disorder caused by severe protein deficiency. Often seen when a second baby is born and the older child is no longer given breast milk (in developing countries)
what is marasmus disease?
PEM disorder. Protein-calorie malnutrition (less severe than kwashiorkor but with a more starved appearance)
what is an available vs. unavailable carb?
available: carb we can use (starch)
unavailable: carb we cant digest (cellulose)
what are the three main lipids in our diet?
sterols, phospholipids, gylcerides
what are the essential FAs?
omega 6 (linoleic acid) and omega 3 (linolenic acid)
what are the three behavior treatments related to classical conditioning?
aversive conditioning, systematic desensitization, exposure w/o learning incompatible response
what is the DRI? goal? what are the values?
Daily dietary reference intake for groups of people.
Goal is to prevent nutrient deficiencies AND prevent over-nutrition (RDA only prevents deficiencies)
Values; estimated average requirement, tolerable upper intake level, atequate intake
what is the estimated average requirement? EAR
requirements that meet needs of 50% of a group (this is the average in which RDA values are based)
what is the upper tolerable intake level?
UL: the highest nutrient intake w/o adverse effects
what is adequate intake?
somewhere between RDA and UL (amount to sustain good health)
what are four hormones that regulate appetite? they all act on what?
Leptin, orexin, PYY, ghrelin. all act on the hypothalamus
what is the role of leptin? produced? long or short term?
produced in SubQ adipose. decrease appetite, increases energy expenditure (increase lipid oxidation and lipolysis), long
what is role of ghrelin? produced? long or short?
stimulates appetite when you think about a meal and releases hormones. produced in stomach. short
what is role of PYY? produced? long or short
produced in intestines. decrease appetite and slow movement of food in gut. short
what is role of orexin? produced? long or short?
increase appetite, decrease REM, increase wakefulness. Produced in lateral pituitary. short
define metabolic syndrome
a group of conditions (increase BP, increase visceral fat, increase cholesterol, increase glucose) that act together to increase risk of CVD, obesity and diabetes
what is the role of white adipose tissue?
storage of triglycerides, insulate/protect body, endocrine fxn
role of LPL and HSL?
LPL: stores FFAs in adipose
HSL: liberated FFAs from adipose
what are adipokines?
endorcine hormones produced by adipocytes
what are the main adipokines?
leptin, adiponectin, IL-6, angiotensinogen
role of adiponectin, main site of production.
this is a good adipokine, anti-atherosclerotic, increases glucose uptake, insreases insulin sensitivity (breakdown of FFAs)
produced in visceral, decreased production in obesity
role of IL-6, produced?
recurit macrophages, visceral
role of angiotensinogen? produced
signals RAS to increase BP, visceral
define obesity
a chronic low grade inflammatory state due to increased size of adipocytes and icreased macrophages
describe adipose dysfuncrion
a hyper-secretory state of adipose tissue caused by increased visceral adipose tissue.
what occurs as adipocytes enlarge?
Increase release of bad adipokines–>release FFAs–>recruit macrophages–>macrophages invade and release TNF-a–>TNF-A increases FFAs, cylce repeats.
Insulin nomrally suppresses what?
inhibits FFA release (inhibit HSL) and promotes FFA storage (promotes LPL)
Insulin is suppressed by what?
FFAs, TNF-alpha
what is the RQ of carbs, protien, lipids?
carbs: 1.0
protein: 0.8
lipids: 0.7
what is BMR (basal metabolic rate) for men and women?
men: 1.0 kcal/hour/kg
women: 0.9 kcal/hour/kg
what is active form of Vit D? how is it produced?
Calcitriol. Pro-vitamin activated with light to form Vit D3. Vit D3 undergoes two hydroxylation events (in liver then in kidney) an form calcitrol. Vitamin D3 also obtained from diet.
what is the role of calcitrol
stimulated by PTH to increase Ca absorption in intestines
how does Vit D defic manifest in adults? kids?
adults: osteoporosis
kids: rickets
Vit D toxicity?
hypercalemia, calcium deposits in heart and kidney
Vitamin A active forms?
Retinol, retinoic acid
fxns 2, of Vit A
Retinol: visoin
retinoic acid: gene expression–>proliferation and differentiation
Vit A def conditions (3)?
Night blindness, skin lesions, Xerophthalmia: blindness (gross eye abnormalities)
how does retinol work?
trans retinal binds opsin (forming rhodopsin complex), when light strikes retinol it becomes all cis
Vitamin E fxn:
anti-oxidant for PUFA, no major fxn. often used in lotions and oils to increase shelf life
Vit K funciton
coagulation and bone growth
how does Vit K work?
important cofactor for carboxylation reactions. once carboxylated, the proteins bind calcium
What is VKDB
Vit K deficiency bleeding: seen in newborns with sterile guts
where is VIt K obtained?
gut bacteria (50%), diet (50%)
B1 AKA
Thiamin
B2 AKA
Riboflavin
B3 AKA
Niacin
B7 AKA
Biotin
B9 AKA
Folic Acid
What are teh B vitamins?
B1, B2, B3, B5, B6, B7, B9, B12
what is the active from of B1
TPP
fuxn of thiamin?
B1: important cofactor for metabolic enzymes (PDH complex, PP pathway)
thiamin def should be correlated with…
Berberi Disease (decrease in NS fxn)
Riboflavin function?
B2: converted to FAD and FMN (easily destroyed by light (conjugated))
Function of Niacin
B3: converted to NAD and NADP (can be made from Try)
Niacin Defic
Pellegra: 3 D’s: dermatitis, dementia, diarrhea
B5 fxn
CoA precursor
B6 important role?
PLP is a coenzyme for >100 enzymes. W/o B6 all AA essential
Biotin role?
B7: conenzyme in carboxylation reactions (pyruvate carboxylase, propionyl-CoA carboxylase)
Folic acid role?
B9, functions in single carbon transfer reactions (AA, purine, thymidine synthesis)
B12 role
Met (coenzyme for Met synthetase), needs Tranport (IF) to get into blood
Vitamin C AKA
ascorbic acid
Ascorbic Acid role
anti-oxidant, aids in hydroxylaiton (important in collagen)
Vit C def?
scurvy: failure to cross-link collagen
Important vitamins?
Zn, Fe, Se, I
importance of Zn
essential in fxn of enzymes and TFs
importance of Se
forms selenoproteins that play a role in preventing oxidative damage, disulfide bond homeostasis and thyroid hormone metabolism
Se defic?
Keshan Disease
Arsenate Poisoning
“ate Pi” Arsenate is incorporated with G3P instead of Pi causing a loss of 1,3BPG and therefore a loss of ATP (1,3BPG–>3 PG produces ATP)
Aresnite Poisoning
PDH complex is inhibited, pyruvate accumulates
Lactic acidosis? cause?
buildup of lactate that decreases pH. can be caused by lack of O2, Pyruvate buildup, increase in NADH/NAD ratio
What is Chronic Hemolytic Anemia? what are two causes
Anemia cuased by excessive hemolysis. Seen in G6PD and PK deficiency of RBCs (causes morphology changes that and hemolysis by spleen)
what occurs in Pyruvate Carboxylase Defic?
pyruvate accumulates (lactic acidosis), hypoglycemia, decrease in myelin sheath, decrease in neurotransmitter. Mainly due to a decrease in oxaloacetate being produced, an important precursor in many reactions
how can you treat PC defic? (3)
biotin, glucose, citrate
PDH Defic results in?
lactic acidosis, decrease Acetyl-CoA, decreased ATP
how does dichloroacetate treat PDH defic?
inhibits the kinase that deactivates PDH
What does CN poisoning do?
blocks complex IV of ETC (binds iron), massive lactic acidosis
what does rhodanase do?
liver enzyme that detoxifies CN in our diet
what does MERRF stand for
Myoclonic Epilepsy and Ragged Red Fiber Disease
MERRF cause? presents as?
mtDNA mutation DNA that codes for tRNALys. Muscle twitching, clumps of diseased mito appear (stain red)
Leber’s Optin Neuropathy cause? symptoms?
mutation in complex I of ETC. Acute blindness due to degeneration of optic nerve
Leber’s Optic Neuropathy treatment
Idebenone: bypass Complex I of ETC
MCAD Defic cause? results in? triggered?
cant break down MCFA. results in hypoketonic, hypoglycemic. tirggered by prolonged fasting.
MCAD treatment
avoid fasting, high carb dier
CPT II defic
CPT II transports FA into mito. Rhabdomylosis: muscle breakdown and release of Mb
Jamaican Vomiting Syndrome. Cause? effect?
eating unripe akee fruit. produces MCPA which inhibits FA oxidation
Propionly CoA Carboxylase Def cause? result?
cant break down odd chain FA. organic acidemia
Peroxisomes breakdown what 2 FAs?
VLCFA, branched FA
why is accumulation of VLCFA and Branched FA bad?
neurotoxic
X-linked adrenoleukodystrophy cause?
cant transport VLCFA
Zellweger syndrome cause
no peroxisomes produced
Adult refsum disease
branched FA accumulates due to loss of alpha-oxidation
how is nitrogen removed from AA?
- Amino transferase move amino from AA to alpha-ketogluterate to form Glu
- Glu can either give up the ammonia or make other AA
- Ammonia is carried by Ala or Gln in the blood
- LIver detoxifies Ammonia into urea using urea cycle (5 enzymes, 3ATP)
what is hyperammonemia? why is it bad? cause?
Increased blood ammonia, bad because ammonia can cross blood-brain barrier and cause coma/death, caused by liver defect
Congenital Hyperammonemia: cause? occurs when?
defective urea cycle enzyme (present at birth). the earlier enzymes will have a greater impact (CPSI). occurs after birth becuase urea cycle not present in utero
Acquired heyperammonemia: cause
liver damage (alcoholic, hep, fatty liver disease)
what is hepatic encephalopathy
loss of brain fxn as a result of liver damage. Seen in half of individuals with acquired liver damage
what are some treatments (2) for hyperammonemia?
decrease protein (supplement essential AA), find alternate pathway (Na Benzoate or Na Phenylbutyrate can comples with AA and make them readily excreted)
