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Foundations 1 > Week 4 Problem Concepts > Flashcards

Week 4 Problem Concepts Flashcards

1
Q

Intermediate filaments: fxn and classes

A

Fxn: resist mechanical stress (most durbale of all filaments)
Classes: nuclear lamins, keratin filaments, vimentin filaments, neurofilaments

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2
Q

Role of nuclear lamins (3)

A

found in nucleus of ALL cells. Play a role in gene expression, differentiation, cell cycle

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3
Q

Progeria: cause, symptoms

A

mutation in nuclear lamins (Lamin A). wrinkling of skin, kidney issues, MSK degeneration (Benjamin button)

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4
Q

Microtubule Fxn: 2

A

movement within cell, cilia/flagella

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5
Q

MT have a + end and - end. whats the difference?

A

(+): beta tubulin, more likely to grow

(-): alpha tubulin, more likely to shrink

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6
Q

Motor proteins associated with MT? which is used in flagella and cilia movements?

A

Dynein (move towards - end, towards centrosome/nucleus), seen in flagella and cilia

Kinesin (move toward + end, cell periphery)

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7
Q

what is the role of basa bodies?

A

serve as MT organizing center for cilia

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8
Q

dynamic instability is associated with..role

A

MT. they can grow or shrink at + end (GTP=grow, GDP=shrink), helps “search” for proteint to bind to

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9
Q

Taxol: effects? use?

A

cancer treatment; stabilizes MTs

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10
Q

B/c MT play a major role in cell division (separates chromosomes) they are often targets of….

A

cancer treatments

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11
Q

Colchicine: effects? use?

A

prevents MT polymerization; cancer treatment

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12
Q

Vinblastine: effects? use?

A

prevents MT polymerization

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13
Q

Actin is composed of…ATP bound?

A

actin monomers combined to form 2-stranded helix. free actin is ATP bound. Actin monomers in filaments are ADP bound

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14
Q

Actin filaments play a role in making what 5 structures?

A

Stress fibers, microvilli, contractile ring, lamellipodia, filopodia

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15
Q

Congential Myopathy: cause? symptoms?

A

skeletal muscle weakness caused by mutation in muscle-specific actin

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16
Q

Insulin triggers glucose uptake in what three cell types?

A

adipose, liver, muscle

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17
Q

describe insulin signaling

A

Insulin=>RTK=>IRS-1=>PI-3K=>GLUT4 containing vesicle exocytosed

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18
Q

describe the process of insulin production

A
  1. pre-proinsulin: [signal peptide-BCA]–> produced in rER
  2. proinsulin: loss of signal peptide and formation of sulfide bonds (2 between B and A, one within A) produced in rER
  3. mature insulin: Cleavage of C-peptide within vesicle
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19
Q

describe the storage form of insulin. where is this seen? when is it undone?

A

3 AB/AB dimers of insulin surrounding a Zn ion. seen in storage vesicles. undone once contents of vesicle are released

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20
Q

compare half-life of insulin vs. C-peptide

A

insulin has a short half life, but C-peptide is very stable and can be used as a measure of insulin production

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21
Q

pro-enzyme convertase and insulin: role, location

A

used to convert pro-insulin to insulin. located within vesicle

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22
Q

what is the difference between GLUT2 and GLUT4

A

GLUT4 is the only insulin sensitive glucose transporter (seen in muscle cells, liver cells, adipocytes). GLUT2 is located in Beta cells (insulin producing) of pancreas and play an important role in insulin release

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23
Q

describe the signal cascade associated with insulin release from beta cell

A
  1. Alpha and beta cells of pancreas are highly vascularized
  2. increase in blood glucose increases the amount of glucose entering beta cells through GLUT2
  3. increased glucose increased ATP
  4. ATP inactivates K channels
  5. B cell depolarizes
  6. Voltage gated calcium channels open
  7. Ca binds insulin vesicle and insulin released
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24
Q

describe insulin release over time?

A

biphasic. insulin is released in two phases: phase 1=short burst, phase 2=prolonged

(glucagon release is also biphasic)

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25
Q

In ultrasound: high f gives? low f gives?

A

high f=better resolution

low f= better depth/penetration

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26
Q

what are the four ultrasound probes? uses?

A
  • phased array: adbomen, cardiac
  • endoluminal: vaginal, oral, rectal
  • linear: superficial
  • curvilinear: abdomen
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27
Q

what is attenuation? what is the attenuation of water? air?

A

how much an object decreases a sound wave (higher attenuation = less signal)

water: 0
air: 12

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28
Q

what are the modes of US?

A
  • A mode: out dated
  • B mode: babies!
  • M mode: beach
  • Pulsed Wave Doppler
  • Color doppler: red=towards, blue=going away
  • Power doppler: tells if you have flow
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29
Q

what is the piezoelectric effect

A

this is how ultrasound works. the crystal in the US converts electrical signal to sound waves and a sound waves back to electrical signal

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30
Q

does Type I or II diabetes have a stronger familial correlation? genetic?

A

type II

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31
Q

What is the function of human leukocyte antigen (HLA) gene complex?

A

set of genes, some of which code for antigens that are presented by cells

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32
Q

which locus within the HLA complex is associated with T1DM?

A

DR locus

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33
Q

which alleles within the DR locus of HLA increase risk of T1DM? how?

A

DR3: B-cells present antigens that are targeted by antibodies

DR4: antigen present that triggers production of antibodies against insulin

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34
Q

which allele within the DR locus of HLA protects against T1DM?

A

DR2

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35
Q

what is MODY, cause? prevelance?

A

Maturity onset diabetes of the young. a type of DM (NOT T1DM or T2DM) caused by genetic defects in B cels. 1-2% of diabetes cases

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36
Q

MODY 2 cause

A

mutation in glucokinase of B-cells (increased B-cell glucose threshold)

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37
Q

MODY 1,3,4,5,6 cause

A

all caused by mutations of genes in the same pathway; delayed response to glucose uptake

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38
Q

How do you treat MODY? how does it work? is it effective?

A

treat with sulfonylureas. high effective monotherapy. Increase intracellular calcium and increases proinsulin secretion

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39
Q

what was the goal of the genome-wide association study?

A

determine if genetic differences predispose people to certain diseases

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40
Q

what did the GWA study conclude with diabetes? 2

A

> 50 SNPs identified to increase risk for diabetes (slight increase)

new genes have been associated with diabetes

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41
Q

what are 3 weaknesses of the GWA study

A

association does not mean causation

not generalizable

data collected in 1980s

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42
Q

name two genes that were ORIGINALLY identified in GWA study to increase risk of diabetes

A

TCF7L2 gene

FTO gene

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43
Q

what is the role of TCF7L2 gene? increased risk for diabetes?

A

TF in Wnt signaling; proglucagon synthesis

Homozygous carriers 2x increased risk for T2DM

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44
Q

what is the role of TFO? is it an inependent risk factor for diabetes?

A

originally thought to be an independent risk factor for diabetes. was found to be associated with obesity (a secondary risk factor for diabetes). Fxn: methylates RNA and causes preferential production of fat (epigenetic)

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45
Q

how is lifestyle associated with epigenticc; give 2 diabetes related examples

A

increase carbs: influence histone modification

stress can change methylation patterns

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46
Q

diabetes is a complex disease; what does that mean

A

diabetes is influenced by biolgical, behavioral and environmental factors

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47
Q

what causes T1DM? how common?

A

immune system destroys beta cells; less than 10% of popn with diabetes

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48
Q

what causes T2DM? how common?

A

insulin resistance and decreased insulin production. more than 90% of popn with diabetes

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49
Q

what causes gestational diabetes? how common?

A

placental hormones increase amount of glucose in blood. 3-5% of pregnant women

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50
Q

what is polydipsia?

A

thirst

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51
Q

what is polyuria?

A

frequent urination

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52
Q

what Fasting blood glucose is normal? diabetic?

A

125 mg/dL= diabetes

70-100 =normal

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53
Q

what HbA1C value is normal? diabetic?

A

normal: 6.5%

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54
Q

what is the difference between IGT and IFG

A

IGT: impaired glucose tolerance
IFT: imparired fasting glucose

both refer to a pre-diabetic state, but represent different mechanisms of insulin resistance

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55
Q

metformin: MOA

A

inhibits gluconeogenesis in liver. very effective monotherapy

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56
Q

SGLT2 inhibitors: MOA

A

prevent glucose reabsorption in kidneys

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57
Q

TZD (MOA):

A

decrease insulin resistance of skeletal muscle/fat

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58
Q

what are the two types of insulin?

A

Note: insulin should be used always in T1DM and only in special circumstances in T2DM:

Basal insulin: long acting
bolus insulin: fast acting, after meal

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59
Q

hypoglycemia is when blood glucose is below

A

Below 70 mg/dL

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60
Q

what are the diabetes ABCs

A

A: elevated A1C
B: high BP
C: Increased LDL cholesterol

all risk factors for CVDs that are associated with diabetes

61
Q

what are the vascular complications that arise in diabetes?

A

Macrovascular: heart (MI, heart failure), brain (stroke), extremities (amputations)
Microvascular: retinopathy, neuropathy, nephropathy

62
Q

Catecholamines: what are they? where are they produced?

A

NE/E

produced by adrenal gland

63
Q

what are the effects of catecholamines in skeletal muscle

A

increase: glycolysis, TG utilization
decrease: glycogen production

64
Q

what are the effects of catecholamines in liver

A

Increase: gluconeogenesis, glycogenolysis

decrease: glycogen synthesis, glycolysis, FA synthesis

65
Q

what are the effects of catecholamines in adipose

A

increase: lipolysis
decrease: TG storage

66
Q

E/NE binds what type of receptor? activates what enzyme?

A

adrenergic receptor. activates cAMP-PKA

67
Q

what explains how E can have opposing effects in liver and muscle cells?

A

In liver: PKA phosphorylates and inactivates PFK-2/F-2,6-BPase (no F-2,6-BP produced, glycolysis not active)

In muscle PKA phosphorylates and activates PFK-2. F-2,6-BP produced and glycolysis active.

68
Q

glucocorticoids: role? example? produced?

A

long-term response to stress (gene expression). Cortisol. Adrenal gland

69
Q

what are the effects of glucocorticoids in skeletal muscle?

A

increase protein degradation in peripheral muscle (increase proteasome expressions)

70
Q

what are the effects of glucocorticoids in liver cells?

A

increase gluconeogenesis and glycogen production

71
Q

what are the effects of glucocorticoids in adipose?

A

increase lipolysis

72
Q

why is ethanol bad? 4

A

ehtanol metbaolism produces an abundance of NADH, Acetyl-Coa and ATP. This high NADH/NAD+ and high ATP causes:

  • decreases glucose production (hypoglycemia)
  • increased lactate production (lactic acidosis)
  • Decreases FA oxiation (hyperlipidemia)
  • decreases glycolysis
73
Q

T2DM is characterized by hyperglycemia caused by…5

A
  1. peripheral insulin resistance
  2. progressive B-cell dysfunction
  3. hype-secretion of glucagon
  4. accelerated gastric emptying
  5. impaired incretin effect
74
Q

Incretin: produced, role,

A

hormone produced by cells of the gut. increase insulin production following a meal.

75
Q

incretin effect

A

more insulin is produced following a meal than following an IV injeciton with the same amount of glucose

76
Q

what are the insulin and glucagon levels after a meal in a person with T2DM?

A

insulin: delayed and depressed levels
glucagon: non-suppressed

77
Q

GLP-1 produced, fxn 7

A

incretin produced by L-cells of distal ileum and colon.
Fxn: increase insulin, increase size of Beta cells, suppress glucagon, enhance insulin sensitivity, slows gastric emptying, cardioprotection and neuroprotection

78
Q

GIP produced? fxN 2

A

produced by gut K-cells of duodenum and jejunum

fxn: increase insulin release, increase size of B-cells

79
Q

is GLP-1, GIP, or both a therapeutic target for T2DM?

A

only GLP-1, GIP levels are not typically altered in T2DM

80
Q

incretins are degraded by?

A

DPP-4

81
Q

Exenatide (Byetta) fxn, how do you admin?

A

GLP-1 receptor agonist, 2x daily injections

82
Q

Liraglutide fxn, how do you admin?

A

modified synthetic GLP-1, 1x daily injected

83
Q

Vildagliptin/sitagliptin fxn, how do you admin

A

DPP4 inhibitors (1x daily ingestion)

84
Q

when blood glucose decreases, what is the normal progression of events in CRH?

A

glucagon–>E/NE–>Cortisol/Growth hormone

85
Q

what are the four CRH? overall role?

A

Glucagon, Catecholamines, Glucocorticoids, Growth Hormones. Increase blood glucose levels

86
Q

in T1DM>5 years what is lost completely?

A

Glucagon response

87
Q

what is hypoglycemia induced autonomic failure

A

E/NE response decreased after recurring hypoglycemia; after glucagon response is lost E/NE becomes new line of defense

88
Q

what causes Diabetic Ketoacidosis

A

Hyperglycemia and ketonemia (increased ketones in blood). Body cant use glucose even though it is present. FA oxidation occurs and ketone bodies accumulate. Excess ketones and glucose causes increase in urine volume. Further concentration of ketones in body,

89
Q

what are the physical findings of DKA

A

tachycardia, dehydration, respiratory distress, coma, abdominal tenderness

90
Q

DKA is a characteristic of what type of DM?

A

T1DM; although it can be triggered in T2DM

91
Q

what is acanthosis nigricans? what is it an indication of? cause

A

darkening of skin fold as a result of INSULIN RESISTANCE (insulin binds IGF receptor and stimulates keratinocyte growth). High risk for developing T2DM

92
Q 
rank the order of these: 
insulin resistance 
impaired glucose tolerance
T2DM
increased plasma glucose
A

Normal–> increased plasma glucose–>insulin resistance–>impaired glucose tolerance–>T2DM

93
Q

A patient was just diagnosed with polycystic ovary syndrome; what are they at an increased risk of?

A

increased risk of insulin resistance and therefore T2DM

94
Q

how is cushing’s syndrome associated with an increased risk for diabetes

A

excess cortisol; glucose levels raised too high–>insulin resistance–>T2DM

95
Q

how is acromegaly associated with an increased risk for diabetes?

A

excess GH; blood glucose chronically elevated

96
Q

Diabetes Prevention Program: setup, findings

A

3 pre-diabetes groups; placebo, metformin, lifestyle change

Lifestyle change>metformin>placebo in preventing T2DM

(1kg weight loss correlated with 16% reduction in incidence of T2DM)

97
Q

The DPP found that metformin was only useful in individuals with…

A

BMI>35

98
Q

Look AHEAD study: setup, findings

A

will intensive lifestyle intervention (lose 7-10% of weight by diet, exercise, pillls) reduce the incidence of cerebrovascular/cardiovascular event.

ILI group had better ABCs

99
Q

FInnish Diabetes Prevention study findings

A

individualized advice is more effective than generalized diet instructions for preventing T2DM

100
Q

what is the legacy effect?

A

early glucose control (diet, exercise, lifestyle changes) will have a lasting postive impact

101
Q

what are the physical activity recommendations for adults?

A

30 min PA/day ~5 days/wk

102
Q

role of nodal cilia

A

motile cilia that plays role in L+R asymmetry during embryo development

103
Q

Primary Ciliary Dyskensia: cause, results in (3)

A

auto rece disorder caused by Loss of dynein (essential in motile cilia). Loss of mucociliary escalator, immotile sperm, and situs inversus (NOT caused by loss of primary cilia)

104
Q

Autosomal Dominant Polycystic kidney Disease (ADPKD); cause, results in

A

loss of polycystin proteins essential for primary cilia (non-motile;used for mechanoreceptors)

large cystic kidneys

105
Q

Cell Adhesion Molecules invovled in cell-cell connecitons

A

Cadherin and Integrin

106
Q

Cadherin; role, intracellular domain, extracellular domain

A

cell-cell interaction; intracellular=associate with cetenins; extracellular domain=calcium dependent

107
Q

General structure/fxn of cell-cell CAMs

A

transmembrane proteins that link interior of cell to ECM or other cells

108
Q

intergrins; role,

A

cell-cell and cell-ECM binding, mechanoreceptors

109
Q

cell jxns of lateral domain (in order from apical to basal)

A

Zonula Occludens (tight jxn), Zonula Adherin (intermediate jxn), Macula Adherin (Desmosome), Gap Jxn

110
Q

Role of Zonula Occludens; important proteins

A

separate apical and basal domains.

Occludin, claudin

111
Q

Role of Zonula Adherens; important proteins

A

anchor adjacent cells; cadherins, catenins, actin

112
Q

role of Macula Adherens; important proteins

A

resist shearing force (spot welds);

desmoglein, desmocolin (Cadherin), desmoplakin, plakoglobin, keratin

113
Q

Role of gap jxn; important protieins

A

cell-cell communication

connexin and connexons

114
Q

types of basal domain jxns

A

focal adhesions, hemidesmisomes

115
Q

focal adhesion; role, proteins

A

link cytoplasmic actin and the ECM, relay signals from ECM to cell

integrins, fibronectin, collagen, laminin

116
Q

hemidesmisomes; role, proteins

A

anchors basal PM to basal lamina

BP230, Type XVII collagen, Type VII collagen, integrins

117
Q

Pemphigus Vulgaris: cause, blister type, nikolsky sign

A
  • skin disorder; body creates antibody against desmogleins (desmosome); loss of lateral domain but basal domain still attached to BM
  • flaccid (easily popped) blisters
  • Nikolsky sign +
118
Q

Bullous Pemphigoid: cause, blister type, nikolsky sign

A
  • skin disorder; body creates antibodies against BP230 or collagen XVII (hemidesmosomes); basal domain lost (epidermis and dermis separated)
  • tense blister (not easily popped)
  • nikolsky -
119
Q

Dystrophic Epidermolysis Bullosa: cause, symptoms

A
  • Group of inherited diseases resulting from mutated basal domain (inherited defect in collagen VII); epidermis and dermis separated,
  • Skin literally falls off, esophageal symptoms as well
120
Q

what is alpha-phase of drug distribution, beta-phase?

A

alpha: sharp decline in plasma drug concentration due to plasma protein/tissues binding drug

beta phase: gradual loss of drug from metabolism and excretion

121
Q

phase of drug metabolism

A

phase I: Cytochrome P450 (ER membrane of liver cells); oxidation, hydrolysis, reducction

phase II: addition of larger group that make the drug more polar and easily excreted

122
Q

Vd eqn

A

Vd=amount of drug given/[plasma drug]

123
Q

what eqn relates t(1/2), Vd, and CL

A

t(1/2)=(.693(Vd))/CL

124
Q

what eqn relates k, CL and Vd

A

k=CL/Vd

125
Q

what four processes (performed on a drug) occurs when we take in a drug?

A

ADME

Absorption, Distribution, Metabolism, Excretion

126
Q

what is Css in regard to drug accumulation

A

the steady state concentration of a drug accomplished when rate of intake=rate of elimination

127
Q

for an IV: relate Css and rate of admin, Clearance

A

Css directly proportional to rate of admin, inversely proportional to CL

128
Q

what factors will alter the time to reach a Css

A

factors that alter t(1/2) such as altering clearance or metabolism of a drug. rate of infusion will NOT change the TIME to reach Css

129
Q

for oral admin drugs relate Css and frequency of dose, dose interval, dose of drug, CL, fraction of drug absorbed

A

directly proportional: frequency of drug, dose of drug, fraction of drug absorbed

Inversely proportional: CL, dose interval

130
Q

what are the three functions of sER

A

lipid synthesis (steroid hormones in adrenal cortex), calcium storage (muscle cells), detoxification (Cyt P450 in sER membrane of liver cells)

131
Q

the sER of liver aids in detox of what two substances (high yield)

A

ethanol, barbiturates

132
Q

Role of CYP2C9 detoxes what? 3

A

hydroxylates drugs such as warfarin, phenytoin (anticonvulsant), tolbutamide (insulin release stimulator)

133
Q

Warfarin; complication, genes involved, is screening required

A

3% of people have bleeding during first month. VKORC1 gene (drug target of warfarin) and CYP2C9 gene (Cyto P450 that metabolizes warfarin). FDA does not require screening

134
Q

CYP2D6 metabolizes what 4

A

Anti-psychotic, antidepressants, metoprolol (decrease BP), tamoxifen (anti-cancer pro-drug)

135
Q

CYP2D6 inhibited by (4)

A

coke, prozac, paxil, protease inhibitors

136
Q

metabolizer groups of CYP2D6

A

poor metabolizer (LOF), intermediate metabolizer, efficient metabolizer, utrarapid metabolizer (*2xn=increase copy number)

137
Q

what is the active from of the pro-drug tamoxifen

A

endoxifen

138
Q

three people; one is UM, one is PM, one is IM. each take same dose of tamoxifen, who has the most benefit

A

UM because there is more active from of the drug

139
Q

for non pro-drugs how should you augment dose for individuals who are UM, PM

A

UM: increase dose
PM: decrease dose

140
Q

does FDA require genetic screening prior to Tamoxifen use?

A

no

141
Q

G6PD def has a higher risk for ADRs when taking? genetic screen?

A

rasburicase, uricemia, primaquin, dapsone

genetic screen is recommended

142
Q

HLA-B*1502 has a higher risk for ADRs (steven-johnson syndrome) when taking? genetic screen?

A

carbamazepine; screen recommended

143
Q

HLA-B*5701 has increase risk for ADRs when taking? genetic scree?

A

abacavir. screen recommended

144
Q

TPMT-deficient have increased risk of ADRs when taking? screen?

A

azathiorprine

screen recommended

145
Q

role of TPMT

A

phase II inactivation of thiopurines (immuno-suppresant). if thiopurines accumulate leukopenia occurs (drop in plasma WBCs)

146
Q

Imatinib has increased efficacy in… screen?

A

C-KIT-positive GI tumors. Screen required

147
Q

Maravicor has increased efficacy in….screen?

A

treating CCR5-tropic HIV-1

screeen required

148
Q

Trastuzumab has increased efficacy in….screen?

A

treating HER-2 positive breast cancer. screen required

149
Q

Pre-diabetes values for A1C and Fasting Blood Glucose

A

A1C: 5.7-6.5%
FBG: 100-125 mg/dL

Foundations 1 (65 decks)

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