Week 3 Problem Concepts Flashcards
1
Q
Fxn and Location of Simple Squamous Epithelium
A
Diffusion! located: alveoli, bowman’s capsule, endothelium
2
Q
Fxn (3) and Location of Simple Cuboidal Epithelium (3)
A
Absorption, Secretion, minimal protection. Location: small ducts of exocrine glands, thyroid follicles, kidney tubules
3
Q
Function (1) and location (1) of Simple columnar Epithelium
A
Function: absorption
location: GI tract
4
Q
Function (3) and location (2) of pseudostratified epithelium
A
Fxn: absorption, secretion, transport
Location: vas deferens/epididymis, bronchial tree
5
Q
function and location of stratified squamous epithelium
A
Protection
Skin (keratinized), vagina, oral cavity, esophagus
6
Q
function (2) and location (2) of stratified cuboidal epithelium AND stratified columnar epithelium
A
Protection and conduit
large ducts exocrine glands, anorectal jxn
7
Q
function and location of transitional epithelium
A
distension
bladder
8
Q
holocrine secretions
A
A mode of exocrine secretion in which the cell dies and releases its contents
9
Q
apocrine secretions
A
a mode of exocrine secretion in which a cell releases a vesicle with its contents
10
Q
merocrine secretions
A
a mode of exocrine secretion in which a cell exocytoses its contents (most common)
11
Q
what type of exocrine gland is a eccrine sweat gland? secretion type?
A
multicellular, simple coiled tubular (serous secretions)
12
Q
what type of exocrine gland is the intestinal gland? secretion?
A
multicellular, simple tubular, mucus secretions
13
Q
what type of exocrine gland is the pancreatic gland? secretion type?
A
mutlicelllar, compound acinar, serous secretions
14
Q
what four steps should you follow prior to taking vital signs?
A
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
15
Q
what is an apical pulse?
A
listen to the pulse with stethescope
16
Q
what is a peripheral pulse
A
palpate or feel the pulse
17
Q
what is eosin? what does it reveal?
A
an acidic dye that binds to positively charged molecules (cytoplasm, collagen, muscle fibers)
18
Q
what is hemtoxyln dye? what does it reveal?
A
a basic dye that binds to negatively charged molecules. DNA/RNA. Hematoxylin and Eosin (H&E) are commonly used together
19
Q
epidermis: composition, originates?
A
keratinized stratified squamous epithelium. originates from ectoderm
20
Q
dermis: composition, originates?
A
composed of connective tissue, mesoderm
21
Q
what are the layers of the dermis?
A
superficial: papillary layer, loose areolar connective tissue
deep: reticular layer, dense irregular connective tissue
22
Q
what is connective tissue?
A
cells in an ECM
23
Q
what is the ECM
A
ground substance and protein fibers
24
Q
what are the types of connective tissue?
A
Specialized: Bone, cartilage, blood
Connective tissue proper:
dense: regular, irregular
loose: reticular, areolar, adipose
25
how do you calculate the incidence rate?
Incidence/sum of disease-FREE person time
26
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 people*2.5 yrs)
27
what is the relationship between prevalence and incidence?
P=(incidence)(duration)
28
which AA is a precursor for heme?
Gly
29
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
30
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
31
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)
32
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)
33
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
34
why is homocysteine accumulation bad?
disrupts collagen cross-linking (stroke, heart attack), Cys becomes essential
35
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)
36
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
37
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
38
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
39
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))
40
what is net protein utilization?
similar to BV but the denominator is only N diet
41
what is the protein efficiency ratio?
weight gain over a period/total weight of protein ingested over that period
42
how do you calculate protein digestibility?
(N diet-(Npoop-N0poop))/Ndiet
43
what are PEM disorders?
Protein Energy Metabolism Disorders
44
what are the two PEM disorders discussed?
Kwashiorkor disease:
Marasmus disease
45
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)
46
what is marasmus disease?
PEM disorder. Protein-calorie malnutrition (less severe than kwashiorkor but with a more starved appearance)
47
what is an available vs. unavailable carb?
available: carb we can use (starch)
unavailable: carb we cant digest (cellulose)
48
what are the three main lipids in our diet?
sterols, phospholipids, gylcerides
49
what are the essential FAs?
omega 6 (linoleic acid) and omega 3 (linolenic acid)
50
what are the three behavior treatments related to classical conditioning?
aversive conditioning, systematic desensitization, exposure w/o learning incompatible response
51
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
52
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)
53
what is the upper tolerable intake level?
UL: the highest nutrient intake w/o adverse effects
54
what is adequate intake?
somewhere between RDA and UL (amount to sustain good health)
55
what are four hormones that regulate appetite? they all act on what?
Leptin, orexin, PYY, ghrelin. all act on the hypothalamus
56
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
57
what is role of ghrelin? produced? long or short?
stimulates appetite when you think about a meal and releases hormones. produced in stomach. short
58
what is role of PYY? produced? long or short
produced in intestines. decrease appetite and slow movement of food in gut. short
59
what is role of orexin? produced? long or short?
increase appetite, decrease REM, increase wakefulness. Produced in lateral pituitary. short
60
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
61
what is the role of white adipose tissue?
storage of triglycerides, insulate/protect body, endocrine fxn
62
role of LPL and HSL?
LPL: stores FFAs in adipose
HSL: liberated FFAs from adipose
63
what are adipokines?
endorcine hormones produced by adipocytes
64
what are the main adipokines?
leptin, adiponectin, IL-6, angiotensinogen
65
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
66
role of IL-6, produced?
recurit macrophages, visceral
67
role of angiotensinogen? produced
signals RAS to increase BP, visceral
68
define obesity
a chronic low grade inflammatory state due to increased size of adipocytes and icreased macrophages
69
describe adipose dysfuncrion
a hyper-secretory state of adipose tissue caused by increased visceral adipose tissue.
70
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.
71
Insulin nomrally suppresses what?
inhibits FFA release (inhibit HSL) and promotes FFA storage (promotes LPL)
72
Insulin is suppressed by what?
FFAs, TNF-alpha
73
what is the RQ of carbs, protien, lipids?
carbs: 1.0
protein: 0.8
lipids: 0.7
74
what is BMR (basal metabolic rate) for men and women?
men: 1.0 kcal/hour/kg
women: 0.9 kcal/hour/kg
75
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.
76
what is the role of calcitrol
stimulated by PTH to increase Ca absorption in intestines
77
how does Vit D defic manifest in adults? kids?
adults: osteoporosis
kids: rickets
78
Vit D toxicity?
hypercalemia, calcium deposits in heart and kidney
79
Vitamin A active forms?
Retinol, retinoic acid
80
fxns 2, of Vit A
Retinol: visoin
| retinoic acid: gene expression-->proliferation and differentiation
81
Vit A def conditions (3)?
Night blindness, skin lesions, Xerophthalmia: blindness (gross eye abnormalities)
82
how does retinol work?
trans retinal binds opsin (forming rhodopsin complex), when light strikes retinol it becomes all cis
83
Vitamin E fxn:
anti-oxidant for PUFA, no major fxn. often used in lotions and oils to increase shelf life
84
Vit K funciton
coagulation and bone growth
85
how does Vit K work?
important cofactor for carboxylation reactions. once carboxylated, the proteins bind calcium
86
What is VKDB
Vit K deficiency bleeding: seen in newborns with sterile guts
87
where is VIt K obtained?
gut bacteria (50%), diet (50%)
88
B1 AKA
Thiamin
89
B2 AKA
Riboflavin
90
B3 AKA
Niacin
91
B7 AKA
Biotin
92
B9 AKA
Folic Acid
93
What are teh B vitamins?
B1, B2, B3, B5, B6, B7, B9, B12
94
what is the active from of B1
TPP
95
fuxn of thiamin?
B1: important cofactor for metabolic enzymes (PDH complex, PP pathway)
96
thiamin def should be correlated with...
Berberi Disease (decrease in NS fxn)
97
Riboflavin function?
B2: converted to FAD and FMN (easily destroyed by light (conjugated))
98
Function of Niacin
B3: converted to NAD and NADP (can be made from Try)
99
Niacin Defic
Pellegra: 3 D's: dermatitis, dementia, diarrhea
100
B5 fxn
CoA precursor
101
B6 important role?
PLP is a coenzyme for >100 enzymes. W/o B6 all AA essential
102
Biotin role?
B7: conenzyme in carboxylation reactions (pyruvate carboxylase, propionyl-CoA carboxylase)
103
Folic acid role?
B9, functions in single carbon transfer reactions (AA, purine, thymidine synthesis)
104
B12 role
Met (coenzyme for Met synthetase), needs Tranport (IF) to get into blood
105
Vitamin C AKA
ascorbic acid
106
Ascorbic Acid role
anti-oxidant, aids in hydroxylaiton (important in collagen)
107
Vit C def?
scurvy: failure to cross-link collagen
108
Important vitamins?
Zn, Fe, Se, I
109
importance of Zn
essential in fxn of enzymes and TFs
110
importance of Se
forms selenoproteins that play a role in preventing oxidative damage, disulfide bond homeostasis and thyroid hormone metabolism
111
Se defic?
Keshan Disease
112
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)
113
Aresnite Poisoning
PDH complex is inhibited, pyruvate accumulates
114
Lactic acidosis? cause?
buildup of lactate that decreases pH. can be caused by lack of O2, Pyruvate buildup, increase in NADH/NAD ratio
115
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)
116
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
117
how can you treat PC defic? (3)
biotin, glucose, citrate
118
PDH Defic results in?
lactic acidosis, decrease Acetyl-CoA, decreased ATP
119
how does dichloroacetate treat PDH defic?
inhibits the kinase that deactivates PDH
120
What does CN poisoning do?
blocks complex IV of ETC (binds iron), massive lactic acidosis
121
what does rhodanase do?
liver enzyme that detoxifies CN in our diet
122
what does MERRF stand for
Myoclonic Epilepsy and Ragged Red Fiber Disease
123
MERRF cause? presents as?
mtDNA mutation DNA that codes for tRNALys. Muscle twitching, clumps of diseased mito appear (stain red)
124
Leber's Optin Neuropathy cause? symptoms?
mutation in complex I of ETC. Acute blindness due to degeneration of optic nerve
125
Leber's Optic Neuropathy treatment
Idebenone: bypass Complex I of ETC
126
MCAD Defic cause? results in? triggered?
cant break down MCFA. results in hypoketonic, hypoglycemic. tirggered by prolonged fasting.
127
MCAD treatment
avoid fasting, high carb dier
128
CPT II defic
CPT II transports FA into mito. Rhabdomylosis: muscle breakdown and release of Mb
129
Jamaican Vomiting Syndrome. Cause? effect?
eating unripe akee fruit. produces MCPA which inhibits FA oxidation
130
Propionly CoA Carboxylase Def cause? result?
cant break down odd chain FA. organic acidemia
131
Peroxisomes breakdown what 2 FAs?
VLCFA, branched FA
132
why is accumulation of VLCFA and Branched FA bad?
neurotoxic
133
X-linked adrenoleukodystrophy cause?
cant transport VLCFA
134
Zellweger syndrome cause
no peroxisomes produced
135
Adult refsum disease
branched FA accumulates due to loss of alpha-oxidation
136
how is nitrogen removed from AA?
1. Amino transferase move amino from AA to alpha-ketogluterate to form Glu
2. Glu can either give up the ammonia or make other AA
3. Ammonia is carried by Ala or Gln in the blood
4. LIver detoxifies Ammonia into urea using urea cycle (5 enzymes, 3ATP)
137
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
138
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
139
Acquired heyperammonemia: cause
liver damage (alcoholic, hep, fatty liver disease)
140
what is hepatic encephalopathy
loss of brain fxn as a result of liver damage. Seen in half of individuals with acquired liver damage
141
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)
