Brainscape's Knowledge GenomeTM

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


See full index

Patho 1 > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Antiport

A

Na - K Movement of two different ions in opposite directions

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

Symport

A

sodium and glucose Carries two different ions in the same direction

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

Uniport

A

Lone glucose Carries one ion

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

Hyperpolarization

A

Movement further away from zero during after an action potential (overcorrection to a negative state). Protects the cell from stimulation during repolarization.

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

Gap Junctions

A

Form direct cytoplasmic junctions between cells

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

Contact Dependent Signals

A

e.g neurotransmitters and synapses

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

Contact Dependent Signals

A

e.g neurotransmitters and synapses

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

Autocrine Signals

A

Act on the cell that secreted them

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

Paracrine Signals

A

Secreted by one cells and diffuse to adjacent cells

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

Mendelson’s First Law

A

The Law of Segregation: Each gamete carries only one allele for each gene (egg has one, sperm has one)

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

Mendelson’s Second Law

A

Law of Independent Assortment: Genes for different alleles can segregate independently when gametes come together

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

Epistasis

A

A gene at one locus alters the expression of another gene at a second locus

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

Penetrance

A

The degree of display of a gene

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

Carcinoma

A

Ca arising from epithelial tissues

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

Adenocarcinomas

A

Arise from ductal or glandular tissues

(breast duct CA = mammary adenocarcinoma)

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

Sarcomas

A

Ca arisinf rom mesenchymal tissues (connective tissues, skeletal mm, bone)

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

Lymphomas

A

Ca arising from lymph cells

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

Leukemias

A

Blood Cancers

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

Carcinoma In Situ

A

preinvasive tumors (“In place”)

glandular or squamous cell origin

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

Neoplasm

A

Abnormal growth following uncontrolled cellular proliferation but NOT necessarily cancer

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

Cancer

A

disease in whcih abnormal cells dicide without control and are able to invade other tissues

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

Anaplasia

A

Hallmark of Ca

Loos of differenctiation

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

Pleomorphic

A

Hallmark of CA

cell with marked variability of size and shape

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

The hallmarks of Cancer

A

Sustaining proliferative signaling

Avoiding immune destruction

evading growth suppressors

enabling replicative immortality

tumor promoting inflammation

activating invasion and metastasis

genomic instability

inducing agiongenesis

resisting cell death

deregulating cellular energetics

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

driver mutations

A

drive the progression of cancer. A critical number of these drivers are required in order for a cell to become cancerous

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

passenger mutations

A

random events that do not contribute to malignancy

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

Stroma

A

The tumor microenvironment that surrounds and infiltrates the tumor

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

What are Receptor Tyrosine Kinases?

A

cell membrane receptors that initiate proliferation

mutations causing lung cancer are associated with activation of RTKs

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

Autocrine Stimulation

A

Ability of a cancer to create its own growth hormone

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

RAS

A

Protein on the membrane which is normally inactivated, but once activated in turns activates multiple signalling pathways that guide the cell into proliferation.

A point mutation in RAS converts it from an unregulated proto-oncogen to an unregulated oncogene

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

What kind of mutation is Burkitt Lymphoma an example of?

A

Example of a translocation which causes inappropriate production of a proliferative factor (in this case it produces a factor that leads to proliferation of B lymphocytes)

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

What mutation causes Chronic Myeloid Leukemia?

A

Example of a translocation leading to novel protein production with growth promoting properties

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

What is Translocation?

A

when a piece of one chromosome is swapped with a piece from another chromosome.

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

What are Tumor supressor genes

A

Anti-oncogenes

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

Retinoblastoma gene is an example of what kind of mutation?

A

Example of tumor supressor gene mutation

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

What is TP 53?

A

p53 Tumor supressor

“Guardian of the genome”

monitors cell stress and activates caretaker genes

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

What is unique about Tumor Suppressor Gene Inactivations?

A

REQUIRES TWO INACTIVATIONS BECAUSE A COPY IS RECEIVED FROM EACH PARENT

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

What is Genomic Instability?

A

When caretaker genes are mutated or silenced, more mutations occur and accumulate

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

Oncomirs

A

miRNA that stimulate cancer development by regulating pathways controlling stability

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

What are BRCA 1 and 2?

A

TSGs and caretaker genes that repair double stranded DNA breaks

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

Angiogenesis

A

Production of vasculature to support a tumor

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

What is HIF-1a?

A

regulator of angiogenesis in normal tissue

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

What is TSP-1?

A

Angiogenesis inhibitor

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

What are MMPs?

What do they do?

A

Matrix Metaloproteinases

Break down ECM to release/activate stored angiogenesis factors

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

What does OXPHOS stand for?

A

mitochondrial oxidative phosphorulation AKA normal cellular aerobic respiration

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

Warburg Effect

A

When cancer cells reprogram to glycolysis instead of OXPHOS

AKA “Aerobic glycolysis”

Beneficial shift that creates more products of glycolysis which are then used for more efficient production of proteins etc

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

reverse Walburg Effect

A

when cancer cells use OXPHOS but manipulate the cancer associated fibroblasts to undergo aerobic glycolysis, increasing byproduct availability for production

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

How is GLUT1 used by cancers?

A

upregulated by oncogenes etc to increase tranpsort of glucose into the cytoplasm

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

What is the Mitochondrial Pathway for Apoptosis

A

In normal cells, when DNA damage is irreparable T53 is activated and induces transcriprtion of pro-apoptotic factors which lead to cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the “Death Receptor”

A

Fas, Fas associated death domain (FADD)

When activated on the cell membrane, triggers internal apoptosis via caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the role of TAM in protecting cancer?

A

Tumor Associated Macrophage

Tumor cells secrete factors (CCL2, CSF1, MCP1) that draw immature monocytes into the tumor, and alter their development into TAMs that mimic M2 versions of macrophages (which produce anti-inflammatory mediators)

This protects the tumor from the immune systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a CAF? What does it do?

A

Cancer associated fibroblasts

synthesize the extracellular matrix surounding and permeating the tumor

Growth factors, MMPs etc secreted by them to aid the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Tumor Associated Antigens

A

Products of oncogenes, antigens from oncogenic viruses oncofetal antigens etc

Should attract T lymphocyte and NK cells to attack

Most malignancies are suppressed by efficient immune response against these tumor antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are TILS?

A

Tumor infiltrating lymphocytes

Treg cells that ordinarily promote wound healing by limiting autoimmune reastions

Tumors actively recruit these and alter them to precent destructive antitumore immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Epithelial-mesenchymal Transition (EMT)

A

Transition to metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Anoikis

A

When normal cells are separated from their extracellular matrix, they undero anoikis (a form of apoptosis)

In order to metastasize, CA cells have to overcome this via changes in their membrane similar to hypoxic states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are Paraneoplastic Syndromes?

Examples?

A

Caused by cancer, but not directly linked

E.g. hormones released from a tumor or an immune response triggered by the tumor that attacks the nervous system

May be the earliest symptoms of an unknown cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Cancer Cachexia

A

Caused by muscle wasting 2/2 ca deregulation

white adipose tissue (WAT) loss 2/2 thermogenesis

Appetite pathways (orexigenic and anexorgenic) pathways altered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the hallmarks that guide Cancer Staging

I-IV?

A

1: confined to orginal organ
2: locally invasive
3: spread to regional structures (lymph nodes)
4: spread to distant sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Multigenerational Phenotype

A

Direct exposure of multiple generations to the same environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Transgenerational Phenotype

A

Transmitted to future generations through germline inheritance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Myokines

A

proteins release from skeletal mm during exercise that increase insulin sensitivity and can induce apoptosis in breast and colon CA cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the Non-targeted Effects (NTEs) of Ionizing Radiation?

A

cells not directly exposed to radiation but descended from cells that are

Bystander effects

Genomic Instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Most common cancers in early childhood

A

Brain Tumors

Leukemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Most common cancers in adolescents

A

lymphomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Most childhood cancers originate from the _____

A

mesodermal germ layer

gives rise to connective tissue, bone, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Embryonal Tumors

A

Originate during intrauterine development

These cancers often include blast cell in their name

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Most common childhood cancer

A

ALL

Acute lymphoblastic leukemia (75% of children, 67% of adolescents)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is MYCN? What type of cancer is it associated with?

A

An oncogen identified in pediatric cancer

Neuroblastoma and glioblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is Genomic Imprinting? Is it common?

A

Only occurs in 1% of autosomal cells

Only one allele (either the sperm of egg version) is active. The other is inactivated in ALL OF THE BODY’S SOMATIC CELLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Biallelic

A

The vast majority of autosomal genes have both a maternal and paternal allele expressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Diseases Related to Genomic Imprinting

A

Prader-Willi and Angelman

Beckwith - Wiedmann

Russel-Silver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Prader - Willi Syndrome

A

GENOMIC IMPRINTING

Inherited from Father

Short stature, truncal obesity, mental retardation, small hands and feet, small upper lip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Angelman

A

GENOMIC IMPRINTING

Same chromosome (15) as Prader Willi

Mother’s gene is effected

Severe ID, bouts of laughter, ataxic gait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Beckwith-Wiedmann Syndrome

A

GENOMIC IMPRINTING

Associated with Wilms Tumors

Caused by IGF2 Overgrowth

Identifiable at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Russel Silver Syndrom

A

GENOMIC IMPRINTING

IGF2 Undergrowth (opposite of Beckwith)

Growth retardation, small face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the Basic Model of Multifactorial Inheritance

A

Degrees of Expression

E.g. Height

Multifactorial, and tend to follow a bell curve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Threshold Model of Multifactorial Inheritance

A

Diseases that are BINARY but do not follow the inheritance pattern of single-gene diseases

People either have the disease or don’t, but there’s a threshold of liability, meaning the more risk factors the person has the more likely the are to express the disease

Pyloric Stenosis: Girls require more risk factors in order for the disease to be displayed than boys, so their Liability threshold is higher than for boys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Liability Threshold

A

Applies to Threshold model of inheritance

female babies have carry genetic markers for pyloric stenosis have a higher threshold of liability for developing the stenosis. This means they have to be exposed to more disease-causing factors to actually develop the disease. That’s why if you have a baby girl born with pyloric stenosis, there’s higher concern that future children will have it than if you had a boy and they displayed the disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Recurrence Risk

A

If my mom has it, how likely am I to get it?

E.g. heart disease: recurrence risk higher if affected relative was female and less than 55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What inherited defects play a role in colorectal CA

A

APC gene mutations play a role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

DM1 Inheritance

A

Incidence higher in offspring if Father is diabetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

BMI Calculation

A

Weight/Height-sq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Genetic Mutations associated with early onset Alzheimer’s

A

Mutations that affect amyloid-beta precursor deposits

Most common is amyloid precursor protein (APP) abnormality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Mutations associated with late onset Alzheimer’s

A

APOE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Fragile X Syndrome

A

Both genetic and epigenetic

More severe in Males

ID, delyed talking, anxiety, hyperactivity, seizures

large ears, long face, prominent jaw, flat peak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Glutathione - S- Transferase

A

Enzyme housekeepers

Reactive to ROS to prevent damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the resting potentional of nerve fibers?

A

-70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the resting potential of skeletal muscle cells?

A

-90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What occurs during depolarization of a nerve cell?

A

The cell membrane suddenly becomes permeable to sodium ions and sodium pours into the cell, reducing its negative charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What occurs during repolarization of a cell?

A

Sodium channels close

Potassium channels open wide, spewing potassium out of the cell and re-establishing a negative potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What causes activation and inactivation of the voltage gated Na channel?

A

When the membrane potential climbs above -55, it actually both activates AND inactivates the NA channel. The inactivation process just takes slightly longer so the gate only stays open for 1/10,000th of a second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What activates the voltage gated K channel?

A

K channel are actually activated when the cell membrane potential dips above -55 (just like the Na channels) but it takes slightly longer in opening, so that the K channel is opening around the same time that the Na channel is closing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the role of Ca ions in action potentials?

A

Ca serves along with (or instead of) Na in creating the membrane potential

Ca ion concentration is 10,000x greater in the ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the “fast” and “slow” channels of membrane depolarization?

A

Na voltage gates are “fast channels”

Ca voltage gates are “slow channels”

Sodium channels initiate action potentials

Ca channels sustain them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

In what types of cells are calcium channels numerous?

A

Cardiac and smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How does a decrease of extracellular calcium concentration effect nerve fibers?

A

Sodium channels have calcium ions attached to them. The ca’s positive charge makes the channel slightly less receptive. When calcium levels are low, the sodium channels become activated at lower thresholds, and the nerve fiber becomes “irritable”.

Only a 50% reduction in ECF Ca causes tetany!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the threshold of stimulation in action potentials?

A

-55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is a nerve or muscle impulse?

A

The propagation of the action potential along a nerve (moves in both directions from the original impulse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the all-or-nothing principle?

A

If conditions are right, once initiated an action potential will span the entire fiber. But if conditions aren’t right, it won’t be propagated at all.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is responsible for the plateau during depolarization seen in cardiac cells?

A

Slow ca voltage channels maintain a longer depolarization (like the purkinje fibers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the three examples of spontaneous rhythmicity in the body?

A
  1. Heart Beat
  2. Rhythmic Breathing
  3. Peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Why doesn’t re-excitation occur immediately in cardiac cells?

A

Hyperpolarization from potassium conductance creates a period of 1 second in which repolarization is not possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Node of Ranvier

A

In myelinated axon sheaths almost no ions can diffuse through, except at the node of ranvier. The nodes are where action potentials occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is saltatory conduction?

A

In myelinated sheaths, action potentials take place at the Node of Ranvier and are conducted through the ECF and the axoplasm from node to node along the fiber

Jumping from node to node. Faster.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are the benefits of saltatory conduction?

A
  1. MASSIVELY Increases velocity of transmission
  2. Conserves energy for the axon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is an example of mechanical excitation of an action potential?

A

mechanical pressure exciting sensory nerves in the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is an example of chemical excitation of nerves?

A

Neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are some examples of electrical excitation in nerves?

A

Electrical signals between the cells of the heart and small intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What mechanism creates the absolute refractory period?

A

Once sodium channels are inactivated, nothing except a return to the resting negative potential can reactivate them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What happens to excitability when serum calcium levels are high?

A

membrane permeability to sodium is decreased, and excitability is reduced

Calcium is a stabilizer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Sarcolemma

A

Thin membrane enclosing enclosing a skeletal muscle fiber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Myofibrils

A

Building blocks of muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are miofibrils made of?

A

Actin filaments (about 3000)

Myosin Filaments (about 1500)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are actin and Myosin

A

large proteins responsible for muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the cross-bridge cycle?

A

Driving force behind contraction

Interaction of thick (myosin) and thin (actin/troponin) filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Titin

A

Maintains the side by side relationship of actin and myosin

One of the largest proteins in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Sarcoplasm

A

The Intracellular fluid between myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is in the sarcoplasm?

A

Potassium, Magnesium, Phosphate

Protein enzymes

mitochondria

Sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Sarcoplasmic Reticulum

A

Regulates calcium storage, reuptake, release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is the resting length of a sarcomere?

A

2 micrometers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the three sources to reconstitute ATP during muscle contraction?

A
  1. Phosphocreatine
  2. Glycolysis
  3. Oxidative Metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Phosphocreatine

A

Has a phosphate bond with higher energy than ATP, so it gets cleaved and the excess phosphate replenishes ADP to ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What is the most efficient velocity of contraction in muscle cells?

A

About 30% of maximum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Motor Unit

A

All the muscle fibers innervated by a single nerve fiber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are the two ways of increasing muscle contraction intensity (summation)?

A
  1. Increasing the number of motor units contracting simultaneously (multiple fiber summation)
  2. Increasing the frequency of contraction (frequency summation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the size principle?

A

When a weak signal is sent from the CNS, a smaller motor unit is stimulated. As the strength of the signal grows, so does the size of the motor unit stimulated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Tetanization

A

The point at which muscle contraction is smooth and continuous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What causes contractures?

A

In the final stages of denervation atrophy, the muscle fibers are broken down and replaced with fibrous and fatty tissue. The fibrous tissue has a tendency to continue shrinking for several months. If it isn’t actively stretched, it will contort the joint into abnormal positions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Macromotor Units

A

When some but not all nerve fibers to a muscle are destroyed, the remaining fibers will form new axons to the paralyzed fibers

Won’t regain the same level of control, but will be able to use the muscle

polio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Why does Rigor Mortis occur?

A

ATP is required to separate the cross bridge from the actin filament. After death the muscles contract without action potentials until the proteins deteriorate at 15-20 hours later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Mesenchymal Stem Cells

A

nonhematopoietic

bone, cartilage and fat cell production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Which bone marrow produces blood cells?

A

skull

vertebrae

ribs

sternum

shoulders

pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Osteo -

Chondro -

Myo -

Stromal -

A

Bone

Cartilage

Muscle

Marrow

136
Q

What three types of cells are found in bone?

A
  1. Osteoblasts
  2. Osteocytes
  3. Osteoclasts
137
Q

Osteoblasts

A

Mesenchymal Origin

Initiate bone formation

deposit calcium and collagen to form a matrix called osteoid

138
Q

Osteocytes

A

Differentiated osteoblasts

most abundant

mechanoreceptors that sense bone loading, stress etc

Communicate with other bone cells to guide formation and resorbtion of bone

139
Q

Osteoclasts

A

Hematopoeitic

migrate over bone surfaces, breaking down areas that have been stripped of osteoid

140
Q

How does calcitonin suppress bone resorption?

A

It binds with osteoclasts’ receptors, knocking them off the bone’s surface

141
Q

OPG/RANKL/RANK System

A

RANKL increases bone loss by proliferating osteoclasts

OPG is secreted by osteoblasts and B lymph, binds to RANK so RANKL can’t

If the two get out of sync, you get problems

142
Q

What are the two types of Bone?

A

Compact bone tissue (85%)

Spongy bone tissue (15%)

143
Q

What is the axial skeleton?

A

80 bones

skull, vertebral column, thorax

144
Q

What is the appendicular skeleton?

A

126 bones

Upper and Lower Extremities

Shoulder (pectoral) girdle

Pelvic girdle (os coxae)

145
Q

Ground Substance

A

Gelatinous material found in bone

146
Q

Harversian System

A

Structural Unit of Compact Bone

147
Q

Components of Long Bone

A

Epiphysis (broad end)

Diaphysis (long narrow portion)

Metaphysis (neck)

148
Q

Remodeling

A

Osteoclasts take bone apart

Obsteoblasts deposit new bone

149
Q

What are the 5 stages of bone repair?

A
  1. Hematoma formation (hours)
  2. Procallus formation (days)
  3. Callus formation (weeks)
  4. Replacement
  5. Remodeling (years)
150
Q

Synarthrosis

A

Immovable Joint

151
Q

Amphiarthrosis

A

Slightly moveable joint

152
Q

Diarthrosis

A

Freely movable joint

153
Q

Syndesmosis

A

Fibrous Joint

two bony surfaces connected by a ligament or membrane

Radial-Ulnar

Tibial-Fibial

154
Q

Gomphosis

A

Fibrous Joint

Conical projection fits into a socket

Teeth

155
Q

Symphysis

A

Cartilagenous Joint

Bones united by pad or disc of cartilage

Symphysis pubis

intervertebral discs

156
Q

Synchondrosis

A

Connected by hyaline cartilage

Ribs

157
Q

Three terms that describe skeletal muscle

A

Voluntary (controlled directly by the CNS)

Striated (striped under the microscope)

Extrafusal

158
Q

Where do the axons of motor nerves originate?

A

Anterior horn cell of the spinal cord

159
Q

Motor Unit

A

Consists of a single motor neuron and ll the skeletal muscle fibers it innervates

160
Q

Neuromuscular Junction

A

Junction between the axon of the motor neuron and the plasma membrane of the muscle cell it’s acting on

161
Q

Ryanodine Receptors

A

Primary ion channel controlling calcium release in the sarcoplasmic reticulum

162
Q

What are the four steps of muscle contraction?

A
  1. Excitation
  2. Coupling
  3. Contraction
  4. Relaxation
163
Q

What happens during the coupling phase of muscular contraction?

A

Calcium ions released by ryanodine receptors couple with troponin

164
Q

When does muscular relaxation begin?

A

When calcium ions move back into the sarcoplasmic reticulum

165
Q

Sarcopenia

A

Age related loss in skeletal muscle

166
Q

Which declines faster after age 50: muscle strength or muscle mass?

A

muscle strength

167
Q

Synaptic Cleft

A

The space between the axon (nerve cell) and the muscle cells, where acetylcholine is transferred

20-30 nm wide

This is where acetylcholinesterase resides

168
Q

Where is acetylcholine synthesized?

A

In the cytoplasm of the axon terminal, then rapidly formed into synaptic vessicles

169
Q

What stimulates acetylcholine release from the axon active site?

A

Calcium!

170
Q

Subneural cleft

A

clefts in the muscle cell membrane where acetylcholine interacts with the muscle cell

Lined with acetylcholine gated channels

and Na voltage gated channels

171
Q

End plate potential

A

When acetylcholine interacts with the acetylcholine gated ion channels, sodium pours into the cell creating a positive charge that lowers the threshold below -55 and triggers voltage gated sodium channels

172
Q

What does the high safety factor of the neuromuscular junction refer to?

A

each impulse that arrives at the neuromuscular junction causes about three times as much end plate potential as that required to stimulate the muscle fiber

173
Q

What organic insecticide is particularly lethal to humans because it inhibits acetylcholine for WEEKS?

A

diisopropyl fluorophosphate

174
Q

How do nerve impulses penetrate deep into muscle fibers?

A

T Tubules - they are essentially extensions of the cell membrane

The T tubule action potentials cause release of calcium ions inside the muscle fiber in the immediate vicinity of the myofibrils, and these calcium ions then cause contraction

175
Q

Fusiform Muscles

A

Long and slender

176
Q

Pennate Muscles

A

Fan Shaped

177
Q

“KUSSMAL”

A

Ketones

Uremia

Salyciates

Sepsis

Methanol

Aldehyde

Lactic Acid

178
Q

What diseases would cause an elevated anion gap metabolic acidosis

A

Lactic Acidosis

Ketoacidosis

Uremia

Methanol/Ethylene Glycol

Salycilates

Paraldehyde

179
Q

What disease could cause a normal anion gap metabolic acidosis?

A

Anything where Bicarb is being lost and Cl is being reabsorbed

Renal Tubular Acidosis

GI Losses

Carbonic Anhydrase Inhibitors

180
Q

What’s the difference between eukaryotes and prokaryotes?

A

Prokaryotes have no organelles and thus no nucleus

181
Q

The outer membrane of the nucleus is continuous with the _________

A

endoplasmic reticulum

182
Q

What causes DNA to fold into chromosomes?

A

Histones

183
Q

Where is protein primarily synthesized and broken down?

A

cytoplasm

184
Q

Where are ribosomes synthesized?

A

the nucleus, then float out through NPCs to cytoplasm or rough ER

185
Q

What is the function of the rough endoplasmic reticulum?

A

membrane factory

synthesizes the proteins and lipids needed for membranes both of the cell and organelles

186
Q

What is the function of the smooth ER?

A
  1. synthesis of steroid hormones
  2. removing toxic substances from the cell by communicating with the golgie complex, lysosomes and peroxisomes
187
Q

What is the role of the golgi complex?

A

Stores secretory vesicles, stacked like pancakes

a refinery of substances that will ultimately be released from the cell or form lysosomes

188
Q

What type of disease are lysosomes often associated with?

A

disease leading to cellular injury and death

189
Q

What are the four pathways of degradation in lysosomes?

A

endocytosis

phagocytosis

macropinocytosis

autophagy

190
Q

What is endocytosis?

A

Uptake of macromolecules from the ECF

191
Q

What is phagocytosis?

A

Uptake of large particles or microorganisms by phagocytic cells (macrophages and neutrophils)

192
Q

What is Macropinocytosis

A

nonspecific uptake of fluids, membrane and particles attached to the membrane

193
Q

What is autophagy?

A

Cellular self destruction

begins in the cytosol and is used to digest cytosol and ineffectual organelles

194
Q

When does a primary lysosome become a secondary lysosome?

A

lysosomes maintain a relatively neutral pH until they are activated by binding with a vacuole or organelle, with converts it into a highly acidic internal environment (secondary status)

195
Q

What are peroxisomes?

A

Similar to lysosomes, but they use oxygen

Oxidative reaction produces peroxide

Catalase uses the hydrogen peroxide to oxidize alcohols

important in detoxifying cells

196
Q

Where in mitochondria does the respiratory chain take place

A

Inner membrane

197
Q

What takes place in the mitochondrial matrix?

A

Metabolism of carbs, lipids, amino acids

198
Q

Where does most cellular metabolism take place?

A

Cytosol

199
Q

Where is extra glucose stored?

A

converted into glycogen in the cytosol

forms a temporary mass called an inclusion

200
Q

What is mechanotransduction?

A

Performed by cytoskeleton

Translates mechanical stimuli into biochemical signals

Allows cell to adapt to their surroundings

201
Q

What is the function of microtubules?

A

add strength

moves organelles

moves pretty much anything in the cell that needs to move

202
Q

What’s the difference between flagella and cilia

A

Flagella move the cell

cilia moves things around the cell, cell stays stationary

both involve microtubules

203
Q

What are glycolipids and glycoproteins?

A

Both found on membranes

carbs and lipids: glycolipids

carbs and proteins: glycoproteins

204
Q

Why are lipids said to be amphipathic?

A

Fancy word for polar

hydrophobic: uncharged
hydrophilic: charged

205
Q

What are transmembrane proteins?

A

Proteins that sit in the membrane and create an aqueous pathway between ECF and ICF

206
Q

What are the three ways proteins move through the cytosol?

A

Gated transport (NPCs)

Protein translocation

Vesicular Transport

207
Q

Proteostasis

A

protein regulation

208
Q

What are four examples of proteolytic cascades?

A

Caspase mediated apoptosis

coagulation cascade

degrading membrane enzymes

complement cascade

209
Q

What are proteases?

A

Enzymes that break down proteins

210
Q

What is the glycocalyx?

A

The cell coat

Formed by carbohydrates

211
Q

What does the glycocalyx do?

A

Protects cell from mechanical damage

creates a slimy surface that helps with motility

cell-to-cell recognition and adhesion

212
Q

What is a ligand?

A

small molecule that bind to the cellular receptor proteins

hormones are ligands

213
Q

What are three ways cells are held together to form tissues?

A
  1. extracellular matrix
  2. cell adhesion molecules
  3. specialized cell junctions
214
Q

What is the basal lamina, and what kind of cells have it?

A

type of extracellular matrix

thin, tough, flexible

lies beneath epithelial cells, over muscle cells, fat cells, schwann cells

215
Q

What are the four major roles of the ECM?

A

mechanical support

control of cell proliferation

formation of scaffold for regeneration

tissue microenvironment

216
Q

What are cell adhesion molectules (CAM)

A

cell surface PROTEINS that bind cells both to eachother and to the ECM

217
Q

TIght junctions

A

barriers to diffusion

prevent movement through membranes and leakage out

218
Q

Gap junctions

A

communicating tunnels from one cell to another

219
Q

Why does increased cytoplasmic calcium cause decreased permeability of the junctional complex?

A

Because dying cells release calcium, so when there’s increased calcium the cells shut down to protect themselves

220
Q

What happens when a ligand binds to a receptor protein?

A

Signal transduction!

The message from the extracellular messenger (first messenger) is transferred to the internal messenger (second messenger)

The second messenger triggers a cascade

221
Q

What is the difference between electrolytes and nonelectrolytes

A

Electrolytes dissociate into ions when placed in a solution

nonelectrolytes do not (glucose, urea, creatinine)

222
Q

What are the three types of passive transport?

A

Diffusion

Filtration

Osmosis

223
Q

What is the difference between diffusion and osmosis?

A

Diffusion is the movement of a SOLUTE MOLECULE down its concentration gradient

Osmosis is the movement of WATER down a concentration gradient

224
Q

What is filtration?

A

Movement of water and solutes due to pressure/force

Glomerular filtration is driven by blood pressure

225
Q

Which substances diffuse rapidly across the cell membrane?

A

Nonpolar, lipophilic substances:

CO2, O2, steroid hormones, fatty acids

226
Q

What substances diffuse very slowly across the cell membrane?

A

Water soluble substances:

sugars, inorganic ions

IONS ARE POLAR. THAT’S WHY IT’S SO HARD FOR THEM TO DIFFUSE

227
Q

If water soluble substances find it difficult to get through the membrane, why can water readily diffuse through the cell membrane?

A

the dipolar structure of water allow it to cross the lipid bilayer easily

228
Q

What is osmotic pressure?

A

The amount of hydrostatic pressure required to oppose the osmotic movement of water

229
Q

What is the osmolality of an isotonic solution?

A

285 mOsm/kg

230
Q

What percentage of cellular ATP produced is used for Na-K ATPase?

A

60-70%

231
Q

How do sugars and amino acids get across the cell membrane?

A

Sodium dependent symport

232
Q

What’s the difference between pinocytosis and phagocytosis?

A

Pinocytosis is the taking up of specific macromelecules for use or metabolism (like antigen presenting cells)

Phagocytosis is bring something in specifically to eat it

Both require energy

233
Q

What are somatic cells

A

Anything that isn’t sperm or eggs

234
Q

What two factors determine a cell’s progress through the cell cycle

A

Cyclin-dependent kinases

Cyclins

235
Q

What is a mitogen?

A

extracellular signal molecule that stimulates mitosis

236
Q

What are cytokines?

A

Growth factors

237
Q

Hypertrophy

A

Increase size of cells due to increased work demands

238
Q

Hyperplasia

A

Increased NUMBER of cells caused by increased cellular division

Regeneration, pregnancy

239
Q

Dysplasia

A

Abnormal change in size, shape or organization of mature tissue cells

Differ from cancer in that they don’t involve entire thickness of epithelium

240
Q

Metaplasia

A

reversible replacement of one mature cell type with another less differentiated cell type

241
Q

What are the components of R-A-A

A

Renin: enzyme released from kidney

Angiotensin 1: Inactive polypeptide

Angtiotensin 2: ACE in lungs converts, causes vasoconstriction

Aldosterone: Retains sodium, excretes K

242
Q

Hypovolemic Hyponatremia

A

loss of body sodium AND greater loss of water

loop diuretics

osmotic diuresis (DKA, mannitol)

GI losses

non-concentrated urine in kidneys

243
Q

Euvolemic Hypernatremia

A

MOST COMMON

244
Q

Why does hypokalemia cause membranes to become hyperpolarized?

A

Potassium diffused freely out of the membrane, so if ECF levels drop suddenly, potassium leaves and the cell develops a more negative charge and is more difficult to excite

245
Q

What happens to cell polarity with hyperkalemia?

A

Hypopolarized (becomes more positive), easier to excite

246
Q

What is Chvostek’s Sign

A

Hypocalcemia

Facial Nerve

247
Q

Trousseau Sign

A
248
Q

Does hypocalcemia increase or decrease excitability?

A

Increases

BECAUSE it decreases the threshold potential

249
Q

Why does giving calcium protect the heart from loss of function during hyperkalemia?

A

An increase in serum potassium will increase (make less negative) the resting potential of the cell membrane. This means the cell needs less positive stimulation to reach the threshold potential and depolarize.

Giving calcium increases the threshold potential, so that even though the resting potential is altered, it will still take a large amount of positive ions to cause a depolarization

250
Q

Why would respiratory aklalosis from hyperventilation cause hypophosphatemia?

A

It increases ATP use, decreasing phosphate

251
Q

How does hydrogen transport through the cell membrane occur?

A

Primary active transport in gastric glands and distal tubule

Secondary active transport via Sodium-hydrogen countertransport in the proximal tubules

252
Q

How is calcium transported across the cell membrane?

A

Active transport through calcium pump

Secondary active transport through na-ca countertransport

253
Q

How do glucoses and amino acids cross the cell membrane?

A

Secondary active transport via co-transport with Na

254
Q

What are codons?

A

All amino acids are specified by triplets of bases called codons

255
Q

How is the end of a gene identified?

A

By stop or nonsense codons.

3 of the 64 possible codons are stop codons

256
Q

Why is the genetic code said to be redundant?

A

There are 61 codons that code for AAs in the body, but only 20 different types of amino acids

257
Q

In DNA Adenine pairs with _______

Guanine paires with ______

A

Thymine

cytosine

258
Q

DNA polymerase

A

travels alongside the single DNA strand, adding nucleotides and proofreading

259
Q

What is a missense mutation?

A

Base pair substitution that alters a single amino acid

260
Q

What is a nonsense mutation?

A

base pair substitution that results in any of the three stop or nonsense codons

261
Q

What is the difference between a frameshift mutation and a base pair substitution

A

In a base pair substitution, the number of base pair isn’t altered, one of them is just different, so the rest of the strand isn’t affected

with frameshift mutations, it alters the way the entire strand is read by inserting or deleting an entire base pair

262
Q

What are the purines and pyrimidines?

A

Purines: Adenine and Guanine

Pyrimidines: Thymine/Uracil and Cytosine

263
Q

When does transcription begin?

A

When RNA polymerase binds to the promoter site of a DNA sequence (gene)

264
Q

What does transcription stop?

A

When a termination sequence codon is reached

265
Q

What are introns and exons?

A

Introns are the excised bits that are not translated

Exons are translated

266
Q

What are miRNA

A

noncoding RNA (introns) that bidn to specific mRNA sequences and down regulate their expression

267
Q

What is a polypeptide?

A

A chain of amino acids

The building block of a protein

268
Q

Mutations in only one kind of cell can be transmitted to offspring. Which kind?

A

Germine cells aka gametes

somatic cells DO NOT pass on mutations

269
Q

What are haploid and diploiod cells?

A

Gametes are haploid cells: they only have one member of each chromosome pair

Somatic cells are diploid: they have complete chromosome pairs

270
Q

What are autosomes?

A

The chromosomes that are not sex linked

271
Q

Which chromosomes are homologous?

A

Means each side of the chromosome is identical. All autosomes are homologous. The x chromosome is homologous.

THE X AND Y CHROMOSOME ARE NOT HOMOLOGOUS IN MALES

272
Q

What is the euploid form of a gamete and a somatic cell?

A

“Normal”

a haploid gamete and a dipload somatic cell

273
Q

What’s the difference between aneuploidy and polyploidy?

A

Aneuploidy is the presence of an extra chromosome

Polylploidy is the presence of an extra chromosome piece (three copies of a chromosome instead of two). There are still the same number of chromosomes.

274
Q

Is trisomy 21 an aneuploidy or a polyploidy?

A

Aneuploidy. There is an entire extra chromosome.

275
Q

Why aren’t there disease associated with monosomy?

A

It’s lethal

276
Q

What’s more serious: an aneuploidy in an autosome or a sex chromosome?

A

Autosome

277
Q

What are the three trisomies seen in live children?

A

13, 18, 21

278
Q

What usually causes a trisomy?

A

nondisjunction: failure of the chromatids to separate during meosis or mitosis

279
Q

Turner Syndrome

A

Sex chromosome aneuploidy

No y or second x chromosome

They are ALWAYS female

Sterile, webbed neck, coarctation of aorta

280
Q

Klinefleter

A

Sex chromosome aneuploidy

At least two x chromosomes and a Y

Degree of pentrance increases with number of extra x’s

small testes, gynecomastia, sterile, male appearance

281
Q

Cri du chat

A

chromosomal deletion on chromosome 5

ID, LBW, hear defects

282
Q

What is unique about chromosomal abnormalities leading to inversions?

A

Usually don’t affect the individual, but their offspring will often have duplications or deletions that ARE harmful

283
Q

Which is more harmful: a deficiency of genetic material or an excess?

A

A deficiency. This is why deletions are more harmful that duplications

284
Q

What is a translocation?

A

Interchanging of genetic material between non-homologous chromosomes

285
Q

What is fragile X?

A

a fragile site on the x chromosome associated with ID

286
Q

Describe the alleles of heterozygous and homozygous individuals?

A

At a given locus on each chromosome, one is from mother and one is from father. If mom and dad’s are identical, they’re homozygous. If not, heterozygous.

287
Q

Penetrance

A

percentage of individuals with the gene who also express disease (phenotype)

288
Q

What is the most common and severe x-linked recessive disorder?

A

DMD!

289
Q

Recurrence risk becomes higher if:

A
  1. More than one family member is affected
  2. The expression of disease in the proband is more severe
  3. The proband is of a less commonly effected sex
290
Q

Aberrant DNA methylation is responsible for misregulation of ______ and ______

A

Tumor suppressor genes

oncogenes

291
Q

What epigenetic mechanism is responsible for x inactivation?

A

DNA methylation

292
Q

What is a nucleosome?

A

A set of histones and the segment of DNA wound around them

293
Q

What does heterochromatic mean?

A

Epigenetically blocked and inaccessible by transcription factors

294
Q

DNA methylation and histones impact _______

miRNA impact _______

A

transcription

translation

295
Q

Imprinted genes are likely to control what?

A

Organismal growth

If maternal version expressed, offspring generally smaller

If paternal version expressed, offspring generally larger

296
Q

Which gene (maternal or paternal) codes for brain development in chromosome 15?

A

maternal. That’s why angelman (where maternal deletion is inherited) results in severe ID

297
Q

Which two disease are the result of aberrant imprinting on chromosome 11?

A

Beckwith-Weidman (overexpression of IGF2 = fat)

Russel-Silverman (underexpression of IGF2 = tiny)

Paternal gene contains IGF2 gene, so in BW it’s doubled (no maternal present)

In RS no paternal present, so IGF2 low

298
Q

What happens to methylation as tumors progress?

A

Methylation density steadily declines in as tumors progress

299
Q

In cancer, the promoter regions of tumor-suppressor genes are _______

A

hypermethylated (inhibited)

300
Q

What are two examples of growth/tumor suppressor genes?

A

Tp53

RB (retinoblastoma) gene

301
Q

What do Burkitt’s Lymphoma and CML have in common?

A

Both due to translocations

302
Q

_____ is the intrinsic trigger for apoptosis

______ is the extrinsic trigger

A

TP53

Fas/FADD

303
Q

When is surgery used in cancer treatment?

A

Non-metastatic

palliative

304
Q

Cancer development due to chronic inflammations is due to what factors?

A

ROS

COX-2

5-LOX

MMPs

transcription factors

305
Q

Developmental Plasticity

A

Degree to which an organism’s development is contingent on its environment

306
Q

how does botulism effect acetylcholine?

A

Blocks release of acetylcholine

307
Q

How does nerve gas alter acetylcholinesterase

A

Blocks its function

308
Q

What are spindles?

A

mechanoreceptors on mm cells that respond to muscle stretching

309
Q

Golgi Tendon Organs

A

dendrites that terminate and branch to tendons near the neuromuscular junction

Sense stretching?

310
Q

Neuregulin

A

increase the number of Ach receptors

helps in formation of spindles

311
Q

RyR1

A

skeletal muscle

312
Q

RyR2

A

cardiac muscles

313
Q

RyR3

A

diaphragm, smooth muscle, brain

314
Q

Articular cartilage is made up of what two things?

A

Collagen (anchors cartilage to bone)

Proteoglycans (control the loss of fluid from the cartilage)

315
Q

What age groups have the highest incidence of fractures?

A

Males 15-24

Adults > 65

316
Q

What kind of fractures are more prevalent in women?

A

Hip and wrist

317
Q

complete fracture

A

integrity of bone is broken into two pieces

318
Q

comminuted fracture

A

breaks into more than two pieces

319
Q

Three types of incomplete fractures

A

greenstick

buckle (torus)

bowing (common in kids)

320
Q

Fragility Fracture

A

often due to osteoparosis

results from trauma that wouldn’t normally cause a fracture

321
Q

pathologic fracture

A

break at the site of a pre-existing abnormality (like a cancer)

322
Q

Simple vs complex dislocation

A

Simple: doesn’t involve a bone break

complex: associated fracture

323
Q

Difference between a sprain and a strain

A
324
Q

Chondrosarcoma

A

2nd most common malignant bone tumor

ill defined tumore that infiltrates trabeculae in spongy bone, usually metaphysis or diaphysis

325
Q

Fibrosarcoma

A

Collagenic tumor

Solitary tumor in metaphyseal region of femur or tibia

326
Q

Osteosarcoma

A

Osteogenic (bone forming)

38% of bone tumors

Usually persons less than 20yo

327
Q

Giant Cell Tumor

A

Myelogenic tumor (bone marrow cells)

benign, solitary, circumscribed

cause extensive bone resorption

overexpression of OPG

328
Q

How do glucocorticoids effect bone density?

A

Decrease density

increase RANKL expression by inhibiting OPG production

329
Q

Osteoarthritis is characterized by ____ (3)

A

loss of articular cartilage

sclerosis of underlying bone

formation of bone spurs (osteophytes)

330
Q

What organs does RA affect?

A

heart/lungs,

kidneys

skin

joints

331
Q

What is ankylosing spondilitis?

A

stiffening and fusing of spine and sacroiliac joints

332
Q

Is ankylosing spondilitis caused by inflammation of the connective tissue?

A

No. Caused by synovitis and bone marrow inflammation

333
Q

The greater the innervation ratio, the greater its:

A

endurance

334
Q

higher innervation ratios

vs

lower innervation ratios

A

higher: prevent fatigue
lower: provide precision of movement

335
Q

Dynamic contraction

A

muscle maintains a constant tension

length changes

336
Q

Isometric

A

maintains a constant length while tension increases

Patho 1 (17 decks)

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