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OSU Foundations 1 > Week 4 > Flashcards

Week 4 Flashcards

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1
Q

Pancreatic cells by mass Blood flow

A

Mostly acinar(exocrine). Islet cells(endocrine) are: 60-80% beta (insulin) 10-20% alpha (glucagon) 5% gamma (somatostatin) <1% PP-cells Beta cells take up over ten percent of blood flow despite only being 2% of mass

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2
Q

Insulin pathway in regular cell

A

Insulin binds predimerized tyrosine kinase receptor-> IRS-1 -> PI3K -> stimulate fusion of vesicles with GLUT4 receptors

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3
Q

Insulin processing

A

Made as a single long peptide with signal,A,C,B (preproinsulin) Signal brings to rER where the signal is then cleaved by signal peptidases and the protein is folded and cysteine bonds formed. (Proinsulin) The protein is then transported into a secretory vesicle through the Golgi apparatus. Inside the secretory vesicle, prohormone convertases cleave off the middle C-chain to form insulin and the c-chain.

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4
Q

C-protein assays

A

Used to determine levels of insulin production in pancreas.

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5
Q

Insulin structure

A

Shorter A chain with two alpha helices is bonded to longer B chain with one alpha helix by two cysteine bonds. A third cysteine bond links the A chain to itself.

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6
Q

Zinc insulin complex

A

Zinc complexes with histidines on B chain of six insulins to condense insulin within the secretory vesicle. Upon secretion the monomers are released from the complex. Poor insulin secretion and diabetes resulted in mice that were deficient for zinc ion transporters in beta cells.

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7
Q

Insulin release from beta cells.

A

Sugar goes through GLUT 2 transporter -> up ATP production from glycolysis -> inhibit K+ channel -> up membrane potential -> open voltage gated Ca2+ channel -> influx of ca2+ and secretion of insulin

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8
Q

Biphasic nature of insulin/glucagon release

A

Two types of vesicles. Ones that can fuse quickly, and ones that fuse more slowly. Results in an initial spike (5min) and then a slower more constant release (100 min)

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9
Q

Glucagon function and release pathway

A

Increase blood sugar. Release pathway is less well studied but results in influx of Ca2+ that leads to biphasic secretion of vesicles.

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10
Q

Glucagon structure and processing

A

Single chain with an alpha helix. Made as a preprohormone that can be cleaved into different forms depending on what cells it’s being expressed in. Glucagon in the pancreas.

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11
Q

Intermediate filaments function and structure

A

Rope like structures that help cells endure mechanical stress. Form desmosomes. Coiled dimers that complex into 8 sets of tetramers that stack end to end. Non-polar structure.

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12
Q

4 major classes of intermediate filaments

A

Keratin filaments in epithelial cells Neurofilaments in nerve cells Nuclear lamins (all cells) Vimentin filaments in glial/muscle cells and connective tissue

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13
Q

Progeria

A

Defective nuclear lamina lead to misshapen nucleus. This leads to defects in chromatin organization, cell division, and gene expression. Symptoms include premature aging, limited growth, hair loss, wrinkling of skin, musculoskeletal degeneration, cardiovascular/kidney problems. Symptoms start in early months and typically live to early teens.

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14
Q

Microtubules Structure and function

A

Rigid rods that act as tracks for movement of cell components Alpha beta dimers grow out of MTOC (centrosomes/centrioles) and reach out toward cell periphery. Alpha(negative) end is towards MTOC while beta (positive) end grows towards periphery. Beta end is easily polymerized/depolymerized (dynamic instability) allows searching for binding partner. Binds when GTP is attached, unbind when GTP is hydrolyzed to GDP. Forms cilia, mitotic spindles for movement of cellular components.

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15
Q

Drugs that target microtubules

A

Taxol- stabilizes polymer Colchicine- prevents tubulin polymerization Vinblastine- prevents tubulin polymerization

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16
Q

Microtubule motor proteins

A

Kinesin-> moves toward positive beta end (cell periphery) Dynein -> moves toward negative alpha end (MTOC) also cause movement in cilia and flagella

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17
Q

Actin structure and function. Binding proteins.

A

Long flexible filaments of monomers. Polar in nature. Can form stable projections like villi, transient projections , contractile rings (mitosis), and contractive bundles. Unlike microtubules, can shrink or grow at both ends (sometimes results in treadmilling) Binding proteins can create many different patterns and arrangements of actin filaments.

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18
Q

Role of actin in cell migration

A

Actin forms lamellipodium (flat sheets) and filopodium(long fingers) in direction of migration. These structures increase surface area for attachment, and can then pull in direction of migration.

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19
Q

Actin motor protein

A

Myosin, walks in positive direction

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20
Q

Congenital myopathy

A

Dysfunction in muscle specific actin/associated regulators. Major symptom is hypotonia No cure or drug treatments available.

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21
Q

Carolina Abecedarian study

A

Quality pre-school vs no quality pre-school. Those with QPS resulted in much stronger social skills, academic success, and better health including no incidence of metabolic syndrome.

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22
Q

Dutch famine study

A

Famine in 1944-45 resulted in children with low birth weight, brain damage, high obesity as well as many chronic diseases later in life.

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23
Q

Focal Glomerulosclerosis

A

Low protein to mice at kidney critical point of gestation. Decrease in total nephrons -> increase in stress for individual nephrons (up GFR)-> scarring -> necrosis -> sodium increase -> essential hypertension

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24
Q

Epigenetic control mechanisms And measurement of

A

Cytosine methylation, histone mods(Acetylation, methylation, ubiquitination), miRNA changes Gene arrays can measure expression

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25
European/African bee experiment
Witch young and bee gene expression switched to match colony they grew up in
26
Development after birth brain, sensory-motor, size, terrible twos, etc.
After birth 60% of metabolism may be used in brain development. Play or sensory motor exploration is essential for early development. Brain doubles in size by first year nd triples by second. More synapses in two year brain than adult. Adult strengthens some but loses many. Amygdala develops before executive function (frontal cortex) in two year old resulting in terrible twos.
27
Acute mild stress vs. chronic traumatic Lickers groomers experiment.
One can be good for development while the other can be very damaging. Traumatic is anything that the child views as overwhelming. Malnutrition, illness, neglect. Results in social withdrawal, early death, chronic disease, emotional and behavioral problems. Lickers/groomers- supportive rat moms produced healthier, more social kids.
28
HPS axis
Hypothalamus-\> ant pit-\> adrenal cortex In charge of stress response.
29
3 colors of ultrasound
Black= fluid or artifact from white spot Grey= soft tissue White = hard tissue (bone, air, pericardium)
30
4 screen directions of ultrasound
Top= shallow Bottom= deep Left= indicator side (leading edge) Right = receding edge
31
5 motions of ultrasound
Slide= translate along indicator axis Rock= rotate along indicator axis Sweep= translate perp to indicator Fan= rotate perp to indicator Rotate= about vertical axis
32
Doppler shift
Use frequency shift in ultrasound to determine velocity of object Can create a color plot where red is toward probe and blue is away from probe
33
Pulsed wave ultrasound
Look at Doppler shift at certain depth in tissue by windowing reflection times. Produces delta wavelength vs. time plot. Tall peaks will be systole while shorter peaks will be diastole.
34
Continuous wave Doppler
Hook up to speaker and listen to reflections. Intermittent whooshing for arteries, low continuous for veins.
35
Amplitude mode Brightness mode Motion mode
Amplitude vs depth plot Typical ultrasound mode Displays anatomy over time
36
IAIM of ultrasound
Indication, acquisition, interpretation, medical decision making Acquisition- identify patient, and position as necessary, selection nd motion of probe
37
Probe selection
low f = poor resolution high penetration (curvilinear) High f= high resolution and low penetration (linear/standard)
38
Morrisons pouch
Space between kidney and liver. Normally no fluid, but trauma victims may show some fluid (blood) here.
39
Progression of TIIDM
Peripheral insulin resistance -\> progressive beta cell dysfunction -\> hypersecretion of glucagon-\> accelerated gastric emptying-\> impaired incretin effect\*\*\*\*\*
40
Incretin GLP-1 When/where secretion? What effects?
Following oral ingestion, GLP-1 is secreted from L-cells of ileum/colon. Starts as proglucagon. Stimulate glucose dependent insulin response. Suppress glucagon Glucose dependently. (Glucose dependence lowers risk of hypoglycemia) slow gastric emptying(weight loss), and reduce blood glucose spike. Increases cardio protection. Long term: improved insulin sensitivity, increased beta cell mas and function.
41
GIP When/where secretion? What effects?
Starts as proGIP in jejunem, secreted after eating. Triggers glucose dependent insulin release. And beta cell proliferation. Less prolific than GLP-1, and not. Therapeutic target.
42
DPP-4
Produces inactivation of GLP-1 via enzymatic cleavage. DPP-4 inhibitors can help to increase incretin effect in GI tract. Taken orally to increase effectiveness of incretin and incretin mimetics. Vildagliptin, sitagliptin. Side effects are pancreatitis and infection. (Mild side effects compared to other drugs)
43
Incretin mimetics
Subcutaneous administration(protein) that have many of the same effects as GLP-1. Weight loss, lower risk of hypoglycemia, inhibition of gastric emptying, weight loss. And improvement of CV health. Available in once weekly extended release Side effect is nausea, pancreatitis, renal stress(clearance), medullary thyroid cancer(mild side effects compared to other drugs)
44
Counter regulatory hormones
Work against insulin action. Raise blood glucose in response to hypoglycemia. Stimulate glycogenolysis, gluconeogenesis, lipolysis, ketogenesis. GLucagon, cortisol, growth hormone, epinephrine
45
Normal Hypoglycemic response
Decrease insulin to increase blood sugar Glucagon increases hepatic glucose production Adrenal glands secrete epinephrine to signal hepatic glucose production to decrease insulin secretion. Body releases cortisol and growth hormone for long lasting glucose upright
46
Impaired CRH response
Glucagon response lost first, epinephrine becomes main defense against hypoglycemia. Epinephrine response gets blunted after recurring hypoglycemic episodes. (Hypoglycemia associated autonomic failure) Less common in TIIDM Prevention of hypoglycemia can rescue impaired CRH in TIDM
47
Diabetic ketoacidosis
Body cannot use glucose as a fuel source, fat breakdown produces ketones. Insulin no longer able to send signals to inhibit transport of fatty acids into mitochondria. Insulin deficiency prevents glucose from entering cell -\>intracellular starvation -\>excess of CRH -\> ketoacidosis Characterized by hyperglycemia(cortisol, epinephrine) and ketonemia(glucagon), ketones/glucose cleared in urine and dehydration (osmotic diuresis from increased glucose)results. Free fatty acids converted to ketoacidosis in glucagon response. Nausea, vomiting, dehydration, abdominal pain, shortness of breath, tachycardia
48
PFK-1
Phosphofructokinase-1, rate limiting step in glycolysis. Inhibited by ATP, activated by AMP, F26BP.
49
PFK-2
Makes F26BP or converts it back to F6P (F26BPase action) depending on phosphorylation (PKA, PrPase2A). Phosphatase slows glycolysis, kinase ups glycolysis through up F26BP. In liver, glucagon and Ep Activate F26BPase. Insulin activates PPFK-2. In muscle F6P regulates activity of PFK-2/F26BPase
50
Glycogen synthase
Inactivate by PKA to allow glycogenolysis. PKA is activated by glucagon and epinephrine (in liver)
51
Catecholamines
Epinephrine, norepinephrine Stimulate fast response to stress. Breakdown of glycogen, fatty acids to increase blood sugar and fatty acids available for use in muscle. Increase O2 through hyperventilation. In muscle, stimulate glycolysis, glycogenolysis, triglyceride utilization. Lower glycogen synth. In liver, lower glycolysis, glycogen synth, up glycogenolysis and gluconeogen.
52
Glucocorticoids
From adrenal cortex, regulate gene expression for long term changes. Increase lipolysis in adipose Increase protein degradation in muscle Increase gluconeogen and glycogen synth in liver
53
Alcohol metabolism Where is it happening? Through what processes? What does it inhibit?
Ethanol can enter cells via simple diffusion and travel through blood (lipid and water soluble) . Diluted and slowed in GI by addition of food. Processed by both the alcohol dehydrogenase system and microsolmal ethanol oxidizing system (CytP450) Large levels of acetyl-CoA, NADH, ATP inhibit glucose metabolism (PFK, PDH) Depletion of NAD inhibits beta oxidation. TCA inhibited by ATP, NADH. NADH allows oxphos to continue Gluconeogen is inhibited by NADH, drives lactic acidosis. Hypoglycemia
54
Adulthood diet attributes and circumstances
Typically focused on career, little time for cooking/planning. Exploration of diet fads, supplements. 25-35 kcal/kg 5-9 servings of fruit/veggies Fats=30% (\<10% saturated)
55
Hot state and cold state decision making
Impulsive vs logical
56
Pregnancy nutritional requirements
Infant mortality is increased by a number of factors, many of these risk factors can be reduced by improving mother nutrition. Folate is a big one
57
Infancy nutrition attributes and circumstances
Breast is best Double weight in first year and triple by second year Mother must increase nutrition to produce high quality milk Breast milk has right mix -isosmotic, low protein content (better for gut), high fat content (development of sight, cognition, neural function), minerals are protein bound. Also contains immunity and growth factors
58
infancy macro breakdown
108kcal/kg for first 6 months 55% of Cal from fats 7% protein 38% carbs Fe, D, B12, F supplements,
59
Toddler nutrition attributes and macro breakdown
Picky eating starts. Here is where healthy eating habits are developed. 70-90 kcal/kg 5-20%protein 25-35% fats 45-65% carbs Fe, Zn, Ca supplementation
60
Lead anemia How and what symptoms?
Lead ties up iron, leading to iron deficiency/anemia Koilonychia (spoon nails) Pica (eating ice, starch, clay) Lesions around mouth Impaired temp. Regulation Impaired immune function
61
Childhood nutrition
70-90 kcal/kg 45-65% carbs 25-35% fat 10-30% protein Ca, Fe, D, Zn concerns
62
Adolescence nutrition
Puberty (big changes), meal skipping and irregular snacking common. 47-65 kcal/kg Ca, Fe, B9, D intakes are crucial 45-65% carbs 25-35% fat 10-30% protein
63
Senior/elderly nutrition
Often time of declining health, anxiety, and depression Diet must be more nutrient dense to get all nutrients within 20-35kcal/kg limit. A,D, Fe, Ca, protein concerns Strong evidence for health benefits through exercise
64
3 types of diabetes Cause and symptoms
Type 1- 10% immune system destroys beta cells. Sudden onset with weight loss. Treated with insulin. Type 2- 90% insulin resistance and decreased production. Gradual onset in obese people, weight gain, sometimes no symptoms. Pills/insulin Gestational-3-5% insulin resistance caused by pregnancy. Increased risk for type 2 afterwards
65
Progression of Type 2 diabetes
Beta cell function slowly decreases. First treated with sensitizers then later on insulin injections. Typically present with insulin deficiency and resistance. Hyperglycemia itself exacerbates insulin resistance/beta cell function
66
Diagnosis of DM
Fasting blood glucose above 125 mg/dL(100-125=preDM) Random BG \>200 mg/dl A1c \> 6.5% (5.7-6.5=preDM) Oral glucose tolerance test \>200mg/dL (140-199 = preDM)
67
Chronic vs acute symptoms of DM
Chronic: frequent urination, thirst, blurry vision, fatigue, hunger, weight loss Acute: dizziness, confusion, vomiting, ab pain
68
Diabetes testing
Should be triggered for anyone with BMI \> 25 and any other risk factor (essentially any obese person) In absence of criteria, over 45 years Blood pressure/ weight- each visit A1c- quarterly Eye/foot/lipid profile-yearly
69
ABC’s of Diabetes
A1c Blood pressure LDL Cholesterol
70
Metformin
Decreases gluconeogen. Starting medication for all patients. High efficacy with low risk. Some weight loss, can cause lactic acidosis.
71
SGLT2
Inhibitors Blocks reabsorption in proximal tubule. Glucoseuria, weight loss, low risk of hypoglycemia, lowers blood pressure, and uric acid lowering must hydrate well and have good kidney function, can cause genital infections(sugar in urethra)
72
Insulin
Only used in severe conditions: Type I, pregnancy, acute illness, intolerance to other therapies, uncontrolled DM, high A1c, ketosis, etc.
73
Basal vs. bolus insulin
Long vs. short acting
74
Hypoglycemia rule of 15 Detriments
15 grams of glucose/carbs every 15 minutes until blood glucose rises over 70 Risk of injury/death, CV mortality, cognitive dysfunction, recurrent can limit ability to manage diabetes.
75
Diabetes complications
Metabolic injury to both large and small vessels Large: stroke, heart attack, aneurysms, ulcers Small: neuropathy, nephropathy, retinopathy
76
IGT and IFG
Impaired glucose tolerance and Impaired fasting glucose. Strong predicters of Diabetes risk.
77
Diabetes prevention programs
Metformin combined with weight loss 5-10% typically. Also tend to look at A1c as a marker. Lifestyle intervention effective at any BMI, metformin more effective at high BMI. Reversal/delay of diabetes most strongly correlated with weight loss, not method of weight loss.
78
Macronutrient breakdown of diabetes diet interventions
No correlation with glycemic control or CV health!!! Better to pick something comfortable for patient so that they stick to it. Fat quality more important than quantity . High fiber intake = good
79
Sulphonylureas
Similar function to insulin. Lower blood sugar
80
Adherence vs. compliance
Compliance= present, checks boxes, but not necessarily fully engaged Adherent=fully engaged in process Less than 10% 100% adherent
81
White coat compliance
Increase use of medication 1-2 days before appointment. A form of intentional non-adherence.
82
Health belief model
Adherence depends on patients beliefs about suceptibility, severity, benefits, barriers, cues
83
Social cognitive theory
Interaction between behavior, personal factors, and external environment Skill building and self advocacy are major interventions
84
Transtheoretical model
Stages of change. Recognizing stage and providing support and resource accordingly. Precontemplation, contemplation, preparation, action, maintenance
85
Acanthosis Nigricans
Hyperpigmented plaques in body folds due to keratin containing epithelium. High circulating levels of insulin cause growth of keratinocytes. Salicylic or retinoic acid to reduce lesions. Reversible with weight loss. Accutane can help, but will come back once drug is stopped.
86
Amyloid deposits in beta cells
Result of increased insulin secretion. Amylin is peptide that is co-secreted with insulin.
87
Diabetes genetics
Type 2 does display some heritability, more likely to do with environement.
88
Glucocorticoid drug effect on diabetes
Can make management of blood glucose more difficult.
89
Drug induced diabetes
Can be from steroids, glucocorticoids, niacin, antipsychotics
90
Endocrine disorders associated with diabetes
Cushing’s -hypercortisolism Acromegaly-excess growth hormone
91
Polycystic ovary syndrome
Hormonal disorder. Enlarged ovaries with cysts at sides. Associated with obesity, insulin resistance, irregular menses, reduced fertility
92
Gestational diabetes
Placenta hormones promote insulin resistance to promote nutrient delivery to fetus. No known diabetes history, although family history may be present. Have aa higher risk for DM in future
93
Stress hyperglycemia
Associated with critical illness/injury. My have underlying insulin resistance, but illness/injury should be treated first before determination. Better control of this is associated with better prognosis and decreased mortality rate
94
Gametogenesis
Formation of sperm or eggs. Spermatogenesis begins at puberty. Oogenesis begins before birth, halts, starts again at puberty
95
Spontaneous abortion prevalence
Thought to be 1/3 of all pregnancies 14-15% of known conceptions
96
Process of Fertilization
Sperm penetrates corona radiate of egg. When sperm penetrates zona pellucida, chem rxn takes place to make it impermeable to other sperm. Fusion of sperm and locate membrane forms zygote
97
Week 1 travel of oocyte and zygote through Fallopian tube
Oocyte is released into Fallopian tube from ovary. Sperm finds oocyte in fallopian tube and forms zygote. Compaction-zygote divides into smaller cells without total growth -2, 4, 8 cell stages-\> morula (solid ball) Morula Then forms into hollow ball called blastocyst -blastocyst consists of the inner portion of a thickened border(embryoblast) and a thinner border that reaches all the way around (trophoblast) -transition to blastocyst happens as zygote leaves Fallopian tube
98
Implantation of blastocyst in uterine wall
Embryoblast end of blastocyst implants in wall and tissue. Blastocyst differentiates: Syncytiotrophoblast- trophoblast cells that directly embed in uterine wall Cytotrophoblast- outer portion of blastocyst Epiblast- middle layer of embryoblast cells (will differentiate into germ cell layers) Hypoblast- inner most layer of embryoblast
99
Ectopic pregnancy
Implantation of zygote at abnormal site. Abnormal vasculature that develops in response to abnormal implantation sister is susceptible to rupture and can be life threatening to mother. Ovarian-in ovaries Tubal-may be at ampullar(bend) or isthmus (along straightaway) Cornual- at transition of tube to uterus Abdominal and cervical also possible
100
Week 2 embryonic development
Amniotic cavity= expanding cavity formed by growing epiblast Hypoblast expands around inner surface of cytotrophoblast to form heusers membrane. Extraembryonic mesoderm tissue expands to fill blastocyst cavity between heusers membrane and cytotrophoblast- chorionic cavity forms in the middle of the extraembryonic mesoderm Primary yolk sac forms between heusers membrane and hypoblast Sac splits into two to form definitive yolks sac and leave some remnants of the primary yolk sac Yolk sac is integral in early germ cell differentiation, nutrition, and early hematopoesis
101
Week 3 embryonic gstrulation
3 germ(trilaminar) layers ectoderm, mesoderm, and endoderm. Primitive streak forms as a thickening of midsagittal embryo at bilaminar disc. Epiblast cells enter bilaminar disc through primitive streak to form mesoderm and endoderm. At this point, remaining epiblast becomes ectoderm.
102
Germ layer formations
Ectoderm=epidermis and nervous system Mesoderm=muscle, heart Endoderm=epithelial linings, liver, pancreas
103
Formation of notochord
Invagination of primitive streak (ectoderm)around week 3. Notocordal process moves cranial. Hollow Notocordal process fuses with endoderm and then reseparates to form solid notocord around day 20
104
Neuralation
Thickening of ectoderm forms neural plate above notochord. Neural plate invaginates to form neural groove and neural crests Neural folds fuse together to pinch off neural tube. Neural crest forms between neural tube and now fused ectoderm
105
Neural tube closure
Neural tube first closes at center and proceeds both cranially and causally. Cranial and Caudal neuropores are remaining openings on either end of the tube. Neurpores close on days 25 and 27 respectively. Defects in this process can result in spina bifida and anencephaly
106
Mesoderm differentiation
Medially to laterally: paraxial mesoderm (somites), intermediate mesoderm (urogenital), and lateral plate (splits into two layers)
107
Body folding
Folding of embryo in cylinder like shape Occurs in both Sagittal (cranial/caudal) and horizontal (lateral) planes. Three layers fold together to form fetus inside amnion. come together at umbilicus
108
Diabetes symptoms
Chronic- thirst, fatigue, hunger, frequent urination, weight loss, blurry vision Emergency— vomiting, nausea, dizziness, abdominal pain, confusion

OSU Foundations 1 (6 decks)

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