Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Foundations 1 > 8/28/17 > Flashcards

8/28/17 Flashcards

1
Q

Insulin, GLUT-4, and Glucose Uptake

A

Insulin binds to its receptor and causes signaling via IRS-1 and PI3K

GLUT4 fuses with PM and does facilitated transport

GLUT4 found in skeletal/cardiac muscle and adipose tissue, brain has glucose transporter that doesn’t rely on insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Post-translational modifications of insulin

A
  1. Start as preproinsulin, put in lumen of rough ER by signal peptide
  2. Signal peptidase removes the signal peptide as enter rough ER, makes proinsulin (inactive)
  3. Folding of the disulfide bond formation (between A and B chain) occurs in the rER, sent to Golgi and then sent to secretory vesicles
  4. Cleavage of C chain occurs in secretory vesicles by prohormone convertase, C peptide and insulin secreted together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Insulin Structure

A

1°: A chain shorter than B chain and also has an intrachain disulfide bond, has two interchain disulfide bonds

2°: Chain A has 2 alpha helices connected by disulfide bond, Chain B is an alpha helix

3°: A and B chains are perpendicular to each other

4°: six insulin molecules arranged around Zn ions surrounded by His

Storage form for secretory vesicles that dissociates into monomeric active forms after secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Insulin Secretion

A

Glucose enter beta cells via GLUT2

Glycolysis and ATP generation increase

ATP inhibits plasma membrane K+ channels, altered membrane potential opens voltage-gated Ca2+ channels

Incoming Ca2+ triggers export of storage granules by exocytosis

Biphasic Insulin Release
Rapid/transient insulin secretion at first by vesicles close to the PM and then a delayed but more sustained release of insulin

Second phase of release requires monomeric GTPases and vesicles movement by rearrangement of actin cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glucagon structure

A

Simple alpha helix

Made as a preprohormone that has the signal peptide cleaved in the rER

Prohormone contains peptides for several hormones like GLP-1, cut by tissue-specific prohormone convertases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glucagon Secretion

A

Not entirely clear

Low Glu triggers voltage-gated Ca2+ channels to let Ca2+ in the cell, expcytosis of glucagon vesicles

Biphasic release since two pools of glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effects of malnutrition during pregnancy

A 
Glucose-insulin disorders
Cardiovascular disease
Renal dysfunction 
Airway disease
Breast cancer 
Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Kidney Hypertension from uterus

A

Insult to fetus like malnutrition, lack of protein, or glucocorticoid exposure slows tissue growth and leads to lower cell number

Nephrons have a higher glomerular filtration rate per cell to compensate and focal glomerulosclerosis occurs (leads to scarring and death)

Sodium builds up in blood and get high blood pressure

Adaptations as a fetus become maladaptive as an adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mid Brain

A

Develops first and fast

Emotional outbursts: fear, anxiety, impulsive, stressed, reactive

When get emotional they use all 5 senses and remember the experiences with long term memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Front Brain

A

Develops slowly

Calculating

Plans ahead, thinks fast, multitasks, logical, organized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prefrontal Cortex

A

Emotions: managing frustrations, modulating emotions

Activation, focus, effort, memory, action

Not fully developed until young adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HPA Axis

A

Plays a role in response to stress

Stress: any real or perceived threat to homeostasis

Hypothalamus releases Corticotropin-releasing factor (CRF) to anterior pituitary, which releases adrenocorticotropic hormone to the adrenal cortex

Adrenal cortex releases cortisol, a glucocorticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How children can avoid toxic stress from Adverse Childhood Events

A

Social and Emotional Buffers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 Executive Functions for Learning Something

A

Self-Control: ignore distractions, control emotions, stay focused

Working Memory: remember and connect, manipulate info, perform multiple steps

Flexible Thinking: switch perspectives, assess different strategies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Scaffolding

A

Adult support throughout everyday routines: highly responsive, encouraging, interactive, and playful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Intermediate Filament

A

Rope-like structures that can withstand mechanical stress

Toughest and most durable

Act as desmosomes and form nuclear lamina

Alpha helices that bundle in opposite directions, have no structural polarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Classes of intermediate Filaments

A
  1. Keratin filaments: each type of epithelial cell has its own type of keratin filament
  2. Vimentin and vimentin-related filaments: connective tissue, muscle cells, and glial cells
  3. Neurofilaments: in nerve cells
  4. Nuclear lamins: in all animal cells, provide support and also involved in nuclear organization, cell cycle regulation, and gene expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Defective Intermediate Filaments

A
  1. Epidermolysis Bullosa Simokex: skin blistering after little mechanical stress, mutation in the skin-specific keratin gene
  2. Progeria: the nuclear lamina on he inside of the nuclear membrane is defective

Can’t provide support so get misshapen nucleus that affects chromatin organization, cell division, and gene expression

Age prematurely so have hair loss, wrinkles, CV/kidney problems, die in teens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Microtubules

A

Hollow, rigid rods that are like RR tracks for vesicles, organelles, and other things

Made of alpha and beta tubulin stacked on top of each other, 13 parallel chains called protofilaments

Beta end is plus end, polymerize faster
Alpha end is minus end, polymerize slower

Grow out of centrosome that has 2 perpendicular centrioles, gamma tubule is a matrix protein that acts as a nucleation site

Found in cilia (lung epithelium) and the centrioles are called basal bodies, also do mitotic spindle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Microtubule Dynamic Instability

A

Like fisherman, will stop growing if not bind to specific proteins or cellular components

Alpha/beta tubule dimers added to plus end if have GTP bound

GTP becomes hydrolyzed to GDP, GDP-tubulin not bind to stuff as well so will depolymerize

GTP cap if add GTP tubulin faster than hydrolyze to GDP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Microtubule drugs

A

Prevent polymerization or stabilize so can’t shrink, used for tumor cells with rapid cell division

Taxol: stabilize microtubules

Colchicine, Vinblastine: prevent polymerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Microtubule transport

A

Used in nerve cells with long axons, motor proteins direct cargo movement

Kinesins: walk toward plus end (cell periphery)
Dyneins: walk toward minus end (centrosome)
Different kind of each, tail binds specific cargo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cilia and Flagella

A

Cilia in respiratory tract to move mucus, sperm have flagella

9 + 2 array with 9 doublets outside and 2 singles inside, use dyneins

Cilia in inner ear (used for sensory input) and in respiratory tract

Are stable, no dynamic instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Actin Filaments

A

Create cell shape and movement, regulated by many different types of proteins

Polymerization of actin monomers into two stranded helix

Has cleft for ATP, can be hydrolyzed to ADP to create depolymerization

Faster growing plus end and slower minus end but can grow/shrink at both ends, do treadmilling, less rapid rate of change compared to microtubules

Stress bundles, contractile ring for dividing cells, transient cellular projections, microvilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Microvilli

A

Made of actin filaments

Small intestines and kidney tubules

Non-motile, increase surface area of the cell membrane to improve absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cell Migration via Actin

A

Lamellipodia: broad thin sheets that have dense actin network

Filopdia: long stiff finger-like projections with parallel actin filaments

Plus ends oriented towards PM that pushes the membrane outward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Myosin II

A

Muscle Cell: 2 myosin II can associate tail to tail to form myosin thick filament, create muscle contraction

Non-muscle Cell: double myosin II facing opposite direction walks the head along actin filament towards plus end to create cell contraction

Creates stress fibers- regulate cell shape, cell division, migration, and sensing of mechanical stress

Regulated by Rho GTPases (monomeric G protein from Ras family) that create downstream signaling to do stuff like filopedia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Congenital Myopathy

A

Skeletal muscle weakness that can be neonatal life threatening to mild muscle weakness in adults

No cure

Mutations in the actin cytoskeleton, can be a number of ways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ultrasound propagation

A

Use pulse echo technique, utilizes a crystal

Duty factor: how much the ultrasound is actually on
Pulsed wave: 1% or 0.01
Continuous wave: 100% or 1.0

30
Q

Velocity and Attenuation of Ultrasound by different media

A

Velocity: air slowest at 330, tissues are middle and 1500, bone fastest at 4080

Attenuation: water lowest at 0, tissues middle at 1, bone at 5, air highest at 12

31
Q

Scanning planes and field edges for ultrasound

A

Sagittal: divides body into left and right
Coronal: divides body into front and back
Transverse: divides body into top and bottom

Near field: closest to probe
Far field: furthest from probe
Leading edge: closest to indicator mark
Receding edge: furthest side from indicator

32
Q

Grayscale colors for ultrasound

A

Black (Anechoic): fluid like blood or bile

Gray (Hypoechoic): soft tissue and solid organs, includes muscle

White (Hyperechoic): air, bone, dense fascia, includes diaphragm

33
Q

Ultrasound Modes

A

A Mode: amplitude, used rarely and in ophtho

B Mode: brightness, common

M Mode: motion, displays anatomy over time

34
Q

Medical vs Surgical Asepsis

A

Asepsis: the state of being free from pathogenic microorganisms

Medical asepsis: clean technique to reduce /prevent spread of pathogens like hand washing, glove use, and cough etiquette

Surgical asepsis: sterile technique, practices to eliminate all microorganisms from an area, used for invasive procedures

35
Q

Principles of Sterile Technique

A 
Never turn back on sterile field
Don't reach over sterile field
Can become non-sterile if prolonged exposure to air
Moisture contaminates sterile field
Skin not sterile
Check package sterility
Consider not sterile when in doubt
Items in sterile field must be sterile
One inch border around sterile field is nonsterile
Anything below waist is not sterile
36
Q

SGLT2 Inhibitors

A

Sodium Glucose Co-Transporter 2

SGLT2 normally reabsorbs 90% of the glucose that is filtered by the kidney, located in the proximal convoluted tubule

SGLT2 Inhibitors prevent reabsorption, glycosuria, lose weight

37
Q

Hypoglycemia

A

Glucose less than 70

Rule of 15: have 15g of carbs and check back in 15 mins, repeat if necessary

Causes: missed meal, too much exercise or insulin

Severe hypoglycemia associated with higher CV mortality and cognitive dysfunction

38
Q

Macrovascular Diabetes Complications

A

Most common cause of diabetes death

Include coronary artery disease, cerebrovascular disease, and complications of peripheral vascular disease

Heart: myocardial infarction (heart attack), heart failure (heart pump failure)

Brain: stroke, cognitive impairment

Extremities: ulcers, amputations, aneurysms

39
Q

Microvascular Complications of Diabetes

A

Eye: retinopathy, cataracts, glaucoma that can lead to blindness

Kidney: neuropathy like macro/microalbuminuria that can lead to kidney failure

Nerves: peripheral/autonomic neuropathy that can lead to amputation

All can lead to disability or death

40
Q

3 key junctions in metabolism

A

Glucose-6 phosphate: can lead to glycogen, pyruvate, or ribose 5-phosphate

Pyruvate: can lead to oxaloacetate, alanine, or lactate

Acetyl CoA: FAs, CO2, and ketone bodies

41
Q

Common Characteristics in Metabolic Regulation

A

Allosteric Interactions: PFK1 is stimulated by fructose 2,6 bisphosphate

Covalent Modification: phosphorylation of glycogen synthase inhibits the formation of glycogen

Adjustment of Enzyme Levels: glucagon induces expression of PEP carboxykinase, glucagon triggers gluconeogenesis of oxaloacetate into PEP

Compartmentation: transport of FAs into mitochondria for degradation

Metabolic specialization of organs

42
Q

Glycogen Break Down

A
  1. Glucagon (in the liver only) or epinephrine (via a beta receptor) binds to a G protein receptor, activates adenylate cyclase to make cAMP
  2. cAMP activates PKA
  3. PKA activates phosphorylase kinase
  4. Phosphorylase kinase converts inactive glycogen phosphorylase b to active glycogen phosphorylase a
  5. PKA inactivates glycogen synthase by phosphorylation
  6. Glycogen is degraded to Glu 1-phosphate
43
Q

Effect of catecholamines on different body areas

Epinephrine

A

Released by kidneys upon sympathetic NS signals, get acute response

  1. Muscle-
    Greatly increased: glycolysis, glycogenolysis
    Slight Increase: gluconeogenesis
    Moderate decrease: glycogen synthesis

Liver-
Greatly increased: glycogenolysis
Slight increase: gluconeogenesis
Slight decrease: glycolysis, FA synthesis

Adipose tissue-
Greatly increased: Lipolysis
Slight decrease: triglyceride utilization

44
Q

Fructose 2,6-bisphosphate

A

Fructose 2,6-bisphosphate activates PFK1 in liver and muscle to promote glycolysis

PFK2 makes it, different isoform for muscle and liver

Epinephrine causes PKA-cAMP to phosphorylate each isoform

Phosphorylation stimulates Fructose 2,6-bisphosphate in the muscle to turn on glycolysis, inactivates liver isoform to stop making Fructose 2,6-bisphosphate

45
Q

Effect of glucocorticoids on different body areas

Cortisol

A

Chronic stress causes corticotropin-releasing factor in the hypothalamus to be released, leads to glucocorticoids in the adrenal cortex to be released

Regulates gene expression, takes hours or days

  1. Muscle: Protein degradation in peripheral tissues slightly increased
  2. Liver: gluconeogenesis and glycogen synthesis slightly increased
  3. Adipose tissue: lipolysis and expression of lipase slightly increased
46
Q

Ethanol Metabolism

A

Alcohol Dehydrogenase System- occurs in cytoplasm of the liver

Ethanol to acetaldehyde to acetate, use NAD+

Microsomal Ethanol-Oxidizing System: used for large amounts of alcohol

Use O2 and NADPH to convert ethanol to acetaldehyde, which feeds back to cytoplasm for further detox

47
Q

Effect of Alcohol on Liver Metabolism

A

Alcohol metabolism makes large quantities of acetyl-CoA, NADH, and ATP

TCA cycle inhibited by high ATP and NADH levels, glycolysis inhibited at PFK1 and PDH

FA oxidation impaired by NAD+ depletion

Gluconeogenesis inhibited cuz high NADH:NAD+ ratio drives lactate dehydrogenase towards lactate and malate dehydrogenase towards malate instead of pyruvate and oxaloacetate

Alcohol precipitates hypoglycemia

48
Q

Health Requirements for Adults

A

25-45 kcal/kg for adult male, 25-35 for girls

Fewer kcal needed as we age, young people have the highest

Avoid chronic diseases, do prudent diet

49
Q

Nutrition Requirements for Infants

A

Feed every 2-3 hours, double birth weight by 4 months, height by one year

Breast milk is better than bottle, low in protein and high in fats (good for babies though), higher conc. of immune components and growth factors, reduce illness

108 kcal/kg for first 6 months, want 7% calories from protein (half of adult amount), higher fats and avoid ketosis, less carbs than adult

Supplement with iron for first year and folate/B12 for first 6 months

Wean at one year

50
Q

Nutrition for Lactating Moms

A

Normal healthy diet

Takes about 750 kcal to make milk each day

Take in polyunsaturated fats

Slight increase in protein

51
Q

Nutrition for Toddlers

A

Picky eaters, developing healthy habits is crucial for later in life, less appetite since less growth so make eat

70-90 kcal/kg, want ideal growth specified by WHO not CDC, after 2 keep fat intake like adults, less protein and more carbs than adults, fluids since dehydrate faster than adults

Iron (anemia a big problem), zinc, and calcium are important

52
Q

Iron deficiency and anemia symptoms (stages II and III)

A

Impaired body temp regulation so always cold, decreased immune function, sensitivity to light, pica, koilonychia (spoon nails), angular stomatitis (lesions around mouth), up susceptibility to lead poisoning

53
Q

Nutrition for Childhood

A

Need nutrient dense foods, but needs vary greatly

Energy to ensure growth and spare protein degradation but not allow excess weight gain

Energy intake similar to an adult

Monitor calcium, iron, zinc, and vitamin D

54
Q

Nutrition for Adolescence

A

47-65 kcal/kg with males needing more

Calcium important for acquiring bone mass, Vitamin D is crucial

Iron important for deposition of lean muscle mass and iron lost during menses

Folic Acid important for lean body mass and females of reproductive age

55
Q

Nutrition for Old People

A

Lose lean mass, more sedentary

BMR declines so need slightly less calories

Vitamin C, B6, and B12 deficiency are common

Nutrients for repair/maintenance: A, D, Fe, Ca, and protein

Fiber and poly fats help fight disease

Exercise helps with cancer and CV probsq

56
Q

Effects of Insulin

A

Anabolic hormone

Protein synthesis, glycogen synthesis, lipogenesis
Inhibits the catabolism of each of these

57
Q

Role of FFA in Hyperglycemia

A

Adipose tissue insulin resistance leads to increased lipolysis and FFA mobilization as a result

FFA mobilization creates muscle insulin resistance by increasing FFA oxidation, causing lower glucose utilization

FFA mobilization creates liver insulin resistance by increasing FFA oxidation, increasing gluconeogenesis

Creates hyperglycemia

58
Q

Mechanism of insulin resistance

A

Primary mechanism not known but probably a combo of genetics, obesity, cytokines, and FFAs

Insulin receptor levels and tyrosine kinase activity in skeletal muscle are reduced, most likely to hyperinsulinemia and not primary defect

Post receptor defects in insulin regulated phosphorylation and dephosphorylation play a predominant role

59
Q

Insulin receptor and insulin signal transduction

A

Insulin binds to receptor tyrosine kinase

Interacts with IRS and Shc proteins for cell growth, protein synthesis, glycogen synthesis, and glucose transport

PI-3 kinase and the Cbl pathway promote translocation of intracellular vesicles with GLUT4 transporters to the PM

60
Q

Clinical Features of Insulin Resistance

A

Central/android obesity

Acanthosis nigricans: hyperpigmentation and velvety plaques, high insulin levels bind to IGF receptors to stimulate growth of keratinocytes/dermal fibroblasts, can be painful and smelly, goes away with weight loss

Metabolic syndrome

Associated with Hypertension and dyslipidemia

61
Q

Progression of Insulin Levels and beta cell mass before Diabetes

A

Insulin Secretion initially increases to maintain normal glucose levels, mild secretory defect initially

Eventually insulin secretory defect progresses to inadequate insulin secretion

Beta cell mass decreases by 50% when diagnosed, amyloid deposit in islet cells, elevation of FFAs (lipotoxicity) may worsen islet function

62
Q

Incretin

A

Gut hormones released from intestine in response to ingestion of food like glucose, need sufficiently high conc. to stimulate release of insulin, release of insulin in response to physiological levels of the hormone occurs only when glucose levels are elevated (Glu-dependent)

Glucagon-like Peptide 1 (GLP-1) and Gastric Inhibitory Peptide (GIP), both rapidly metabolized by dipeptidyl peptidase-4 (DPP-4)

Both stimulate insulin response from beta cells in glucose-dependent manner

GLP-1 inhibits gastric emptying, reduces food intake, and inhibits glucagon Secretion from alpha cells in glucose-dependent manner unlike GIP

Reduced incretin effect in diabetics

63
Q

Drug Induced Diabetes

A

Glucocorticoids

Steroids

Immunosuppressants

Niacin

HAART

Atypical antipsychotics

Diazoxide

64
Q

Polycystic Ovary Syndrome

A

Insulin resistance

Obesity

Irregular menses

Reduced fertility

Hyperandrogenism (guy hair patterns)

65
Q

Gestational Diabetes

A

Due to placental hormones (human placenta lactogen) which promotes insulin resistance through various mechanisms to increase nutrient supply to growing fetus

Higher risk for subsequent diabetes

66
Q

Stress Hyperglycemia

A

Critically ill, ICU, burn victims

May or may not be reversible

Increased cortisol, catecholamines, glucagon, growth hormones, gluconeogenesis, and glycogenolysis

Underlying insulin resistance a contributing factor

67
Q

Cushing’s Syndrome and Acromegaly

A

Cushing’s: excess cortisol
Associated with Central obesity, diabetes, Hypertension, muscle wasting

Acromegaly: excess growth hormone
Associated with Diabetes, Hypertension, sleep apnea

68
Q

Type II Treatment

A

Entry A1C <7.5%: monotherapy, metformin

Entry A1C >7.5%: dual therapy, metformin plus another drug

Entry A1C >9%: dual or triple therapy if no symptoms, insulin and other agents if symptoms

69
Q

DPP-4 Inhibitors (Gliptin Family)

A

Inhibit the enzyme DPP-4 that breaks down GLP-1 and GIP

Both incretins have an insulintropic effect leading to clearance of glucose from bloodstream

Incretins stay in system from 12 hours to several days

Lower A1C levels and do weight loss

70
Q

How to Assess a Type II patient

A

Start with basics and don’t overwhelm

Assess their resources and support system

Make initial weight loss goal of 5-10%

Give education: starting new meds, nutrition counseling like what a carb is

Short term follow up with reachable short term goals

Foundations 1 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions