Brainscape's Knowledge GenomeTM

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


See full index

Clin Med I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Components of cytoskeleton

A

Microtubules, Microfilaments, Intermediate filaments

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

Microtubules

A 
Largest cytoskeletal component
--> Cell shape
Transport of secretory vesicles
Rigidity of cilia and flagella
Mitotic spindle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Kinesin

A

Proximal –> Distal

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

Dynein

A

Distal –> Proximal

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

Microfilaments

A

Smallest cytoskeletal element
Actin and myosin (contractile)
Enhance cell structure and stability

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

Myofibroblasts

A

Contain actin, important in wound closure

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

Intermediate Filaments

A

Cytoskeletal component that provides resistance to externally applied cell stress (e.g. shear)
e.g. Neurofilaments, keratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cytoplasm

A

Everything inside cell except nucleus

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

Cytosol

A

Liquid portion filling cell (mostly H2O)

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

Endoplasmic Reticulum function

A

Protein and lipid production

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

Rough ER

A

Synthesizes proteins for secretion and internal membrane support
Synthesizes lipids for new membranes

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

Free ribosomes of ER (within cytosol)

A

Produce proteins for internal cell use only

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

Smooth ER

A

“Packaging and discharge” - forms buds that are sent to Golgi
Transports proteins
Synthesizes lipid hormones
Detoxification

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

Golgi

A

Receives and sends out vesicles
Raw materials processed into finished product
Sorts finished product to final destination

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

Lysosomes

A

Sacs of hydrolytic enzymes

Paired with phagocytosis

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

Peroxisomes

A

Contain oxidative enzymes –> H202

Also contain catalase to break down H202

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

Vaults

A

Transporters from nucleus –> cytoplasm?

Possibly sequester CA drugs, rendering them ineffective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Components of Plasma Membrane

A

Lipids (phospholipids and cholesterol), proteins, CHO

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

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

Components of Extracellular Matrix

A

Collagen, elastin, fibronectin

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

ECM disorders

A

Emphysema: Elastin destruction

Ehlers-Danlos: Collagen dz

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

Desmosomes

A

Hold cells together, found in tissues subject to stress

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

Tight junctions

A

Block passage between cells

e.g. blood brain barrier

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

Gap Junctions

A

Facilitate passage between cells

e.g. cardiac cells

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

Osmotic pressure

A

Pulls H2O into cell

AKA oncotic, colloid pressure

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

Hydrostatic pressure

A

Pushes H2O out of cell

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

3 properties of receptors

A

Specificity
Competition
Saturation

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

Cholesterol function in membrane

A

Provides stability of membrane while allowing pliability

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

Extracellular Matrix function

A

Structural connection from cell to cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Immediate energy sources

A

ATP–>ADP + Pi
ADP +Creatine phosphate
Adenylate kinase system
^Small quantities readily available in cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Intermediate energy source

A

Glycolysis

glucose –> 2 ATP + 2 pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Long term energy source

A

Oxidative Metabolism

Uses byproducts from glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What drives source of ATP?

A

Intensity of activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Glycolysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

NADH

A

“energy escort” - escorts H to MT for oxidative metabolism

Anaerobic: NADH degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Oxidative Metabolism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Steps of Oxidative Metabolism

A

3C pyruvate –> 2C acetic acid
Acetic acid + CoA –> Acetyl CoA
Acetyl CoA–> MT –> 15 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Lipid (Fat) Metabolism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Review Steps of Lipid Metabolism

A

There are 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

“Mobilization” Step of Lipid metabolism

A

Breakdown of lipid to FFA
Inhibited by increased insulin, blood glucose levels
Stimulated by degreased blood glucose, increased sympathetic stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Carnitine

A

Transports energized fatty acid into MT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Beta oxidation

A

Breaking off 2C units from fatty acid to enter Krebs cycle

Each cleavage of 2C unit –> 5 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

CHO vs. lipid metabolism

A

CHO produces ATP more quickly and can produce ATP anaerobically. Lipids produce more ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Lipid vs. CHO metabolism at low intensity

A

60% lipid, 40% CHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Lipid vs. CHO metabolism at moderate intensity

A

50/50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lipid vs. CHO metabolism at around 65%

A

CHO becomes primary source of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

“Off Label” Prescriptions

A

Prescriptions for drug for use other than it’s approved purpose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Threshold dose

A

Smallest dose that will elicit a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Plateau/ Ceiling effect/ Maximal efficacy

A

Further increase in dose will not increase response

50
Q

Potency

A

A more potent drug requires a lower dose to produce the same effect

51
Q

Median effective dose (ED50)

A

Dose at which 50% of population responds to drug in specified manner

52
Q

Median toxic dose (TD50)

A

Dose at which 50% of population exhibits adverse effects

53
Q

Therapeutic Index

A

Assesses relative safety of drug
TI = TD50/ED50
Larger TI = Safer drug

54
Q

Pharmacokinetics

A

What the body does to the drug

55
Q

Pharmacodynamics

A

What the drug does to the body

56
Q

Enteral Administration

A

Oral, Sublingual, Buccal, Rectal
Oral: First pass effect
Rectal: Poor absorption

57
Q

Parenteral

A

Inhalation, Injection, Topical, Transdermal
Topical: Poor absorption - local treatment
Transdermal: High absorption

58
Q

Bioavailability

A

% of administered amount of drug that reaches blood stream

59
Q

Storage of drugs

A

Fat (primary source b/c many drugs are lipid soluble)
Muscle
Bone
Organs (liver, kidney)

60
Q

Biotransformation

A

Drug changed to inactive or less active metabolite while still in body

61
Q

Excretion of drugs

A

Primarily lungs, also GI tract

62
Q

1 factor affecting response and metabolism of drug

63
Q

3 Types of extracellular receptors for drugs

A

Channels, enzyme linked, G-protein linked

64
Q

Agonist vs. Antagonist

A

Agonist binds and –> Change (Has affinity and efficacy)

Antagonist binds and –> NO change (Has affinity and no efficacy)

65
Q

Competitive Antagonist

A

Has equal affinity to receptor as agonist, binding is reversible
–> Whichever compound is in higher concentration will rule

66
Q

Noncompetitive antagonist

A

Forms a strong permanent bond to receptor (for life of receptor protein)
Increasing levels of agonist does not displace antagonist

67
Q

Receptor desensitization

A

Temporary period of decreased receptor responsiveness

Temporary decrease in functional receptors

68
Q

Receptor downregulation

A

Prolonged, permanent decrease in number of receptors, decrease in responsiveness
Only reversed when receptor is replaced

69
Q

Receptor Supersensitivity

A

Increased receptor sensitivity following decreased stimulation

70
Q

Lipophilic hormones

A

Bind directly to target cell nucleus to influence production of new proteins
Circulate in blood bound to proteins

71
Q

Lipophobic hormones

A

Bind to surface membrane to activate 2nd messenger systems and affect activity of existing proteins
Circulate freely in plasma

72
Q

Tropic glands

A

Glands that regulate other endocrine glands

73
Q

Anterior Pituitary

A

Glandular tissue
Linked to hypothalamus via vascular pathway
Produces and secretes 6 hormones

74
Q

Posterior Pituitary

A

Neural tissue
Linked to hypothalamus via neural pathway
Stores and releases 2 hormones (vasopressin and oxytocin) - these are produced in hypothalamus

75
Q

Vasopressin

A

AKA ADH

Increases H2O retention; BP regulation

76
Q

Oxytocin

A

Uterine contractions, milk ejections

77
Q

Hypothalamus

A

Endocrine and ANS control center

78
Q

Follicular cells form follicle enclosing:

A

Colloid - mostly thyroglobulin (Tg)

79
Q

Parafollicular cells produce

A

Calcitonin

80
Q

T4 vs. T3

A

T4 is the most commonly secreted

T3 is the most biologically active

81
Q

Thyroid hormone functions

A

Regulation of Metabolism

Sympathomimetic (increases responses to catecholamines)

82
Q

Adrenal cortex produces

A

Steroids (Mineralocorticoids, glucocorticoids, sex hormones)

83
Q

Main mineralocorticoid

A

Aldosterone - Na retention

84
Q

Main Glucocoricoid

A

Cortisol - Increases blood glucose; anti inflammatory and immunosuppresive

85
Q

Adrenal medulla produces

A

Catecholamines

*Primarily epinephrine

86
Q

Catecholamine receptors

A

alpha and beta ONE: excitation

alpha and beta TWO: inhibition

87
Q

Hypercalcemia –>

A

Decreased excitability

88
Q

Hypocalcemia –>

A

Increased excitability

89
Q

Parathyroid hormone

A

Increases plasma Ca (from bone)

90
Q

Calcitonin

A

Movement of Ca from bone into blood

91
Q

Vitamin D

A

Facilitates absorption of Ca in intestine

92
Q

Insulin

A

Beta cells of pancreas
Promotes uptake and storage of glucose by cells
Stimulated by increased BG

93
Q

Glucagon

A

Alpha cells of pancreas
Promotes release of stored glucose and gluconeogenesis
Stimulated by decreased BG

94
Q

Catecholamines

A

Promote glycolysis and lypolysis

Shunt blood away from non-working tissue

95
Q

Cortisol function re: glucoregulation

A

Stimulates breakdown of protein and works with catecholamines to shunt blood
GH is a cortisol antagonist

96
Q

Goal vs. diabetes Fasting Plasma glucose values

A

Goal: 110
Diabetes: 126+

97
Q

Normal vs. Diabetes HbA1c values

A

Normal: 3-6%
Diabetes: >6%

98
Q

DM Type I treatment

A

Exogenous insulin, diet

99
Q

DM Type II treatment

A

Exercise, diet, medications (not necessarily insulin)

100
Q

Greatest risk for exercise induced hypoglycemia (time):

A

6-14 hrs p exercise.

Large risk for Type I, some risk for Type II

101
Q

Hyperpituitarism

A

Gigantism, Acromegaly

102
Q

Hypopituitarism

103
Q

Hyperthyroidism conditions

A

Graves disease (most common hyper condition - increased T4), thyrotoxicosis (increased TH), thyroid storm (Acute episode)

104
Q

Hyperthyroidism symptoms

A

Increased basal metabolism, increased sympathetic action, lipid depletion, nutritional deficiency, goiter, exopthalmus
Thyroid storm: fever, dehydration, delusion

105
Q

How is hyperthyroidism diagnosed?

A

Decreased TSH levels

106
Q

Hyperthyroidism treatment

A

Antithyroid meds
Radioactive iodine to induce hypothyroidism
Thyroidectomy

107
Q

Hypothyroidism

A

*most common thyroid disorder

Decreased basal metabolism –> fatigue, myxedema, bradycardia, decreased mental function

108
Q

Hypothyroidism causes

A

Autoimmune, iatrogenic

109
Q

Hypothyroidism diagnosis

A

T4 levels gradually decrease

TSH levels increased

110
Q

Hypothyroidism treatment

A

Exogenous thyroid hormone replacement

111
Q

Hyperparathyroidism

A

Hypercalcemia, bone demineralization, kidney stones

Increased fracture risk

112
Q

Hyperparathyroidism diagnosis

A

Increased PTH levels and Ca serum levels.

Skeletal damage per X-ray

113
Q

Hyperparathyroidism treatment

A

Parathyroidectomy

Meds to inhibit Ca release from bone

114
Q

Hypoparathyroidism

A

Decreased serum calcium levels
Increased neuromuscular irritability (can –> tetany)
Increased serum phosphate levels
Calcifications

115
Q

Hypoparathyroidism treatment

A

Acute tetany: Ca IV
Chronic: Medications
Calcifications irreversible

116
Q

Adrenal Insufficiency AKA:

A

Addison’s Disease

117
Q

Gender tendencies for diseases:

A

Addisons: = men and women
Thyroid, parathyroid: more common in women
Non-iatrogenic Cushings: more common in women

118
Q

Addison’s symptoms

A

Decreased cortisol –> weakness, hypotension, fatigue, weight loss, N/V, tan appearance, hypoglycemia b/c of decreased gluconeogenesis
Decreased aldosterone –> Dehydration, hypotension, decreased cardiac output

119
Q

Addison’s diagnosis

A

Decreased ACTH, positive response to ACTH treatment

120
Q

Adrenal Hyperfunction AKA:

A

Cushing’s disease

121
Q

Cushing’s

A

Excess cortisol–> weakening of protein structures, hyperglycemia, abnormal fat distribution, proximal muscle weakness (steroid induced myopathy),

Clin Med I (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions