Exam 1 Flashcards
(121 cards)
1
Q
Components of cytoskeleton
A
Microtubules, Microfilaments, Intermediate filaments
2
Q
Microtubules
A
Largest cytoskeletal component --> Cell shape Transport of secretory vesicles Rigidity of cilia and flagella Mitotic spindle
3
Q
Kinesin
A
Proximal –> Distal
4
Q
Dynein
A
Distal –> Proximal
5
Q
Microfilaments
A
Smallest cytoskeletal element
Actin and myosin (contractile)
Enhance cell structure and stability
6
Q
Myofibroblasts
A
Contain actin, important in wound closure
7
Q
Intermediate Filaments
A
Cytoskeletal component that provides resistance to externally applied cell stress (e.g. shear)
e.g. Neurofilaments, keratin
8
Q
Cytoplasm
A
Everything inside cell except nucleus
9
Q
Cytosol
A
Liquid portion filling cell (mostly H2O)
10
Q
Endoplasmic Reticulum function
A
Protein and lipid production
11
Q
Rough ER
A
Synthesizes proteins for secretion and internal membrane support
Synthesizes lipids for new membranes
12
Q
Free ribosomes of ER (within cytosol)
A
Produce proteins for internal cell use only
13
Q
Smooth ER
A
“Packaging and discharge” - forms buds that are sent to Golgi
Transports proteins
Synthesizes lipid hormones
Detoxification
14
Q
Golgi
A
Receives and sends out vesicles
Raw materials processed into finished product
Sorts finished product to final destination
15
Q
Lysosomes
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Sacs of hydrolytic enzymes
Paired with phagocytosis
16
Q
Peroxisomes
A
Contain oxidative enzymes –> H202
Also contain catalase to break down H202
17
Q
Vaults
A
Transporters from nucleus –> cytoplasm?
Possibly sequester CA drugs, rendering them ineffective
18
Q
Components of Plasma Membrane
A
Lipids (phospholipids and cholesterol), proteins, CHO
19
Q
CHO in plasma membrane
A
Markers of cell ID, allows like cells to find each other
Only on outer membrane, anchored to proteins or lipids
20
Q
Components of Extracellular Matrix
A
Collagen, elastin, fibronectin
21
Q
ECM disorders
A
Emphysema: Elastin destruction
Ehlers-Danlos: Collagen dz
22
Q
Desmosomes
A
Hold cells together, found in tissues subject to stress
23
Q
Tight junctions
A
Block passage between cells
e.g. blood brain barrier
24
Q
Gap Junctions
A
Facilitate passage between cells
e.g. cardiac cells
25
Osmotic pressure
Pulls H2O into cell
| AKA oncotic, colloid pressure
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Hydrostatic pressure
Pushes H2O out of cell
27
3 properties of receptors
Specificity
Competition
Saturation
28
Cholesterol function in membrane
Provides stability of membrane while allowing pliability
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Extracellular Matrix function
Structural connection from cell to cell
30
Immediate energy sources
ATP-->ADP + Pi
ADP +Creatine phosphate
Adenylate kinase system
^Small quantities readily available in cytoplasm
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Intermediate energy source
Glycolysis
| glucose --> 2 ATP + 2 pyruvate
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Long term energy source
Oxidative Metabolism
| Uses byproducts from glycolysis
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What drives source of ATP?
Intensity of activity
34
Glycolysis
Breakdown of 6C chain to 2, 3C chains
Directly --> 2 ATP
Produces byproducts (NADH and pyruvate) used in oxidative metabolism
Pyruvate --> lactate in anaerobic condition
35
NADH
"energy escort" - escorts H to MT for oxidative metabolism
| Anaerobic: NADH degraded
36
Oxidative Metabolism
Permits metabolism of CHO, proteins, and fats
Oxidation of pyruvate through Krebs/TCA cycle
--> 15 ATP per pyruvate (30 total)
--> 12/ 2 C unit of lipid
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Steps of Oxidative Metabolism
3C pyruvate --> 2C acetic acid
Acetic acid + CoA --> Acetyl CoA
Acetyl CoA--> MT --> 15 ATP
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Lipid (Fat) Metabolism
Must be oxidative
Begins at site of fat
Costs 2 ATP to raise energy level of fatty acid to enter MT
---> Large quantities of ATP
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Review Steps of Lipid Metabolism
There are 7
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"Mobilization" Step of Lipid metabolism
Breakdown of lipid to FFA
Inhibited by increased insulin, blood glucose levels
Stimulated by degreased blood glucose, increased sympathetic stimulation
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Carnitine
Transports energized fatty acid into MT
42
Beta oxidation
Breaking off 2C units from fatty acid to enter Krebs cycle
| Each cleavage of 2C unit --> 5 ATP
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CHO vs. lipid metabolism
CHO produces ATP more quickly and can produce ATP anaerobically. Lipids produce more ATP
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Lipid vs. CHO metabolism at low intensity
60% lipid, 40% CHO
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Lipid vs. CHO metabolism at moderate intensity
50/50%
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Lipid vs. CHO metabolism at around 65%
CHO becomes primary source of energy
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"Off Label" Prescriptions
Prescriptions for drug for use other than it's approved purpose
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Threshold dose
Smallest dose that will elicit a response
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Plateau/ Ceiling effect/ Maximal efficacy
Further increase in dose will not increase response
50
Potency
A more potent drug requires a lower dose to produce the same effect
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Median effective dose (ED50)
Dose at which 50% of population responds to drug in specified manner
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Median toxic dose (TD50)
Dose at which 50% of population exhibits adverse effects
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Therapeutic Index
Assesses relative safety of drug
TI = TD50/ED50
Larger TI = Safer drug
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Pharmacokinetics
What the body does to the drug
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Pharmacodynamics
What the drug does to the body
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Enteral Administration
Oral, Sublingual, Buccal, Rectal
Oral: First pass effect
Rectal: Poor absorption
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Parenteral
Inhalation, Injection, Topical, Transdermal
Topical: Poor absorption - local treatment
Transdermal: High absorption
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Bioavailability
% of administered amount of drug that reaches blood stream
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Storage of drugs
Fat (primary source b/c many drugs are lipid soluble)
Muscle
Bone
Organs (liver, kidney)
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Biotransformation
Drug changed to inactive or less active metabolite while still in body
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Excretion of drugs
Primarily lungs, also GI tract
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#1 factor affecting response and metabolism of drug
Genetics
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3 Types of extracellular receptors for drugs
Channels, enzyme linked, G-protein linked
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Agonist vs. Antagonist
Agonist binds and --> Change (Has affinity and efficacy)
Antagonist binds and --> NO change (Has affinity and no efficacy)
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Competitive Antagonist
Has equal affinity to receptor as agonist, binding is reversible
--> Whichever compound is in higher concentration will rule
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Noncompetitive antagonist
Forms a strong permanent bond to receptor (for life of receptor protein)
Increasing levels of agonist does not displace antagonist
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Receptor desensitization
Temporary period of decreased receptor responsiveness
| Temporary decrease in functional receptors
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Receptor downregulation
Prolonged, permanent decrease in number of receptors, decrease in responsiveness
Only reversed when receptor is replaced
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Receptor Supersensitivity
Increased receptor sensitivity following decreased stimulation
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Lipophilic hormones
Bind directly to target cell nucleus to influence production of new proteins
Circulate in blood bound to proteins
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Lipophobic hormones
Bind to surface membrane to activate 2nd messenger systems and affect activity of existing proteins
Circulate freely in plasma
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Tropic glands
Glands that regulate other endocrine glands
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Anterior Pituitary
Glandular tissue
Linked to hypothalamus via vascular pathway
Produces and secretes 6 hormones
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Posterior Pituitary
Neural tissue
Linked to hypothalamus via neural pathway
Stores and releases 2 hormones (vasopressin and oxytocin) - these are produced in hypothalamus
75
Vasopressin
AKA ADH
| Increases H2O retention; BP regulation
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Oxytocin
Uterine contractions, milk ejections
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Hypothalamus
Endocrine and ANS control center
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Follicular cells form follicle enclosing:
Colloid - mostly thyroglobulin (Tg)
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Parafollicular cells produce
Calcitonin
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T4 vs. T3
T4 is the most commonly secreted
| T3 is the most biologically active
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Thyroid hormone functions
Regulation of Metabolism
| Sympathomimetic (increases responses to catecholamines)
82
Adrenal cortex produces
Steroids (Mineralocorticoids, glucocorticoids, sex hormones)
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Main mineralocorticoid
Aldosterone - Na retention
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Main Glucocoricoid
Cortisol - Increases blood glucose; anti inflammatory and immunosuppresive
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Adrenal medulla produces
Catecholamines
| *Primarily epinephrine
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Catecholamine receptors
alpha and beta ONE: excitation
| alpha and beta TWO: inhibition
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Hypercalcemia -->
Decreased excitability
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Hypocalcemia -->
Increased excitability
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Parathyroid hormone
Increases plasma Ca (from bone)
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Calcitonin
Movement of Ca from bone into blood
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Vitamin D
Facilitates absorption of Ca in intestine
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Insulin
Beta cells of pancreas
Promotes uptake and storage of glucose by cells
Stimulated by increased BG
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Glucagon
Alpha cells of pancreas
Promotes release of stored glucose and gluconeogenesis
Stimulated by decreased BG
94
Catecholamines
Promote glycolysis and lypolysis
| Shunt blood away from non-working tissue
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Cortisol function re: glucoregulation
Stimulates breakdown of protein and works with catecholamines to shunt blood
GH is a cortisol antagonist
96
Goal vs. diabetes Fasting Plasma glucose values
Goal: 110
Diabetes: 126+
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Normal vs. Diabetes HbA1c values
Normal: 3-6%
Diabetes: >6%
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DM Type I treatment
Exogenous insulin, diet
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DM Type II treatment
Exercise, diet, medications (not necessarily insulin)
100
Greatest risk for exercise induced hypoglycemia (time):
6-14 hrs p exercise.
| Large risk for Type I, some risk for Type II
101
Hyperpituitarism
Gigantism, Acromegaly
102
Hypopituitarism
Dwarfism
103
Hyperthyroidism conditions
Graves disease (most common hyper condition - increased T4), thyrotoxicosis (increased TH), thyroid storm (Acute episode)
104
Hyperthyroidism symptoms
Increased basal metabolism, increased sympathetic action, lipid depletion, nutritional deficiency, goiter, exopthalmus
Thyroid storm: fever, dehydration, delusion
105
How is hyperthyroidism diagnosed?
Decreased TSH levels
106
Hyperthyroidism treatment
Antithyroid meds
Radioactive iodine to induce hypothyroidism
Thyroidectomy
107
Hypothyroidism
*most common thyroid disorder
| Decreased basal metabolism --> fatigue, myxedema, bradycardia, decreased mental function
108
Hypothyroidism causes
Autoimmune, iatrogenic
109
Hypothyroidism diagnosis
T4 levels gradually decrease
| TSH levels increased
110
Hypothyroidism treatment
Exogenous thyroid hormone replacement
111
Hyperparathyroidism
Hypercalcemia, bone demineralization, kidney stones
| Increased fracture risk
112
Hyperparathyroidism diagnosis
Increased PTH levels and Ca serum levels.
| Skeletal damage per X-ray
113
Hyperparathyroidism treatment
Parathyroidectomy
| Meds to inhibit Ca release from bone
114
Hypoparathyroidism
Decreased serum calcium levels
Increased neuromuscular irritability (can --> tetany)
Increased serum phosphate levels
Calcifications
115
Hypoparathyroidism treatment
Acute tetany: Ca IV
Chronic: Medications
Calcifications irreversible
116
Adrenal Insufficiency AKA:
Addison's Disease
117
Gender tendencies for diseases:
Addisons: = men and women
Thyroid, parathyroid: more common in women
Non-iatrogenic Cushings: more common in women
118
Addison's symptoms
Decreased cortisol --> weakness, hypotension, fatigue, weight loss, N/V, tan appearance, hypoglycemia b/c of decreased gluconeogenesis
Decreased aldosterone --> Dehydration, hypotension, decreased cardiac output
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Addison's diagnosis
Decreased ACTH, positive response to ACTH treatment
120
Adrenal Hyperfunction AKA:
Cushing's disease
121
Cushing's
Excess cortisol--> weakening of protein structures, hyperglycemia, abnormal fat distribution, proximal muscle weakness (steroid induced myopathy),
