Brainscape's Knowledge GenomeTM

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


See full index

Unit 2 MTP > Unit 2 LGS > Flashcards

Unit 2 LGS Flashcards

1
Q

Identify the type of lesion and give an example

A

Atrophy - stretch marks, aged skin

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

Identify the type of lesion and give an example

A

Bulla - blisters

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

Identify the type of lesion and give an example

A

Cyst - cystic acne

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

Identify the type of lesion and give an example

A

Erosion - blister after rupture

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

Identify the type of lesion and give an example

A

Excoriation - scratch

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

Identify the type of lesion and give an example

A

Fissure - Cracks in dry skin, corners of mouth

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

Identify the type of lesion and give an example

A

Keloid - scarring

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

Identify the type of lesion and give an example

A

Lichenification - Chronic atopic dermatitis

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

Identify the type of lesion and give an example

A

Macule - freckle, flat nevi, petechiae

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

Identify the type of lesion and give an example

A

Nodule - dermatofibroma

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

Identify the type of lesion and give an example

A

Papule - Wart, elevated nevi

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

Identify the type of lesion and give an example

A

Patch - vitiligo, cafe au lait spots

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

Identify the type of lesion and give an example

A

Plaque - psoriasis, atopic dermatitis

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

Identify the type of lesion and give an example

A

Pustule - acne

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

Identify the type of lesion and give an example

A

Scale - dry skin, psoriasis, seborrheic dermatitis

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

Identify the type of lesion and give an example

A

Ulcer - stasis ulcer

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

Identify the type of lesion and give an example

A

Vesicle - Varicella, herpes zoster

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

Identify the type of lesion and give an example

A

Wheal - insect bite, allergic reaction

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

What is the cause of vitiligo?

A

Having a decreased amount or lack of melanocytes in an area of the epidermis

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

What is the classis presentation of herpes zoster?

Predict the histological findings.

A

Erythematous vesicles in a dermatomal pattern, typically unilaterally on one side of the trunk.

Acantholysis - separation of the skin in the stratum spinosum

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

A 4 year old presents with a quickly spreading rash all over. It’s pruritic and she has a fever. The rash shows papules, vesicles and crusts. What is the likley diagnosis?

A

Varicella

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

A patient presents with a velvety appearance in the fold of the neck. The pt’s hx is significant for diabetes. Predict the histological findings.

A

Acanthoses nigricans

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

Explain the pathophysiology of alopecia areota

A

Lymphocytes around the hair follicles lead to alopecia in one spot

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

A punch biopsy is used to

A

give full thickness sample to the subQ area

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

What are the functions of the skin?

A

Thermoregulation - sweat glands, fat
Containment of internal contents
Sensation - Merkel cells, free nerve endings, corpuscles
Vitamin D synthesis
Protective covering

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

What are two ways to confirm or rule out fungal involvement in a lesion?

A

Wood’s Lamp - fungi release bioctorins which fluoresce under UV light - doesn’t detect endothrix or non-fluorescent fungi

KOH test - KOH dissolves non-fungal cells, leaving fungi behind

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

Describe the type of glial cells and their function

A

Oligodendrocytes - “Schwann cells of the CNS” - form myelin sheaths around axons to provide insulation for AP

Astrocytes - form BBB - separates blood from extracellular fluid, allows nutrients to reach the brain while preventing pathogens from entering

Microglial cells - phagocytic cells - reactive to injury and mediate immune reactions

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

Define the structural components of a typical neuron

A

Dendrites - receive signals through synaptic cleft
Soma - cell body, houses nucleus and organelles
Axon hillock - absence of nissl bodies
Axon - contains dense bundles of microtubules and neurofilaments
Axon terminal - site of synapse
Oligodendrocytes/Schwann cells - myelinate axons

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

What’s the difference between a nerve and a nerve fiber?

A

A nerve fiber is a single neuron with a single axon and it’s myelin sheath

A nerve is a bundle of nerve fibers

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

Cell bodies are housed in the ____ matter while axons are housed in the _____ matter.

A

grey

white

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

What is the structural and functional unit of the nervous system, and it’s general function?

A

Neurons - electrochemical signaling to communicate sensory and motor information to and from the CNS, respectively

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

What is the function of epineurium, perineurium, and endoneurium?

A

Endoneurium covers individual nerve fibers
Perineurium covers fascicle of nerve fibers
Epineurium covers a nerve

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

Compare and contrast myelinated vs unmyelinated nerve fibers

A

Myelinated nerve fibers have abundant Schwann cells
Unmyelinated nerve fibers still have Schwann cells, but one SC engulf several nerve fibers

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

Which ions have a higher concentration inside the neuron than outside?

A

K+ ~145
(4-5 outside)

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

Which ions have a higher concentration outside the neuron than inside?

A

Na ~140 (~10 inside)

Cl ~100 (~3 inside)

Ca2+ ~8-10 (<1 inside)

HCO3 ~25-30 (7-10 inside)

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

Explain the ionic basis of a resting membrane potential

A

Difference in charge between the intracellular and extracellular space created by a chemical and electrical gradient, mostly dependent on K+

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

What would happen if a neuron was permeable to K+ only?

A

K+ would leave the cell quickly due to the concentration gradient pulling them outside of the cell –> sending RMP more negative.
As K+ leaves and the inside of the cell gets more negative, the electrical gradient reattracts positively charged K+ –> sending RMP more positive.
This would continue until an equilibrium is reached closer to the K+ resting potential

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

Explain why the rising phase of the action potential peaks at the value that it does, including critical factors that determine the actual value.

A

The peak of the rising phase is dependent on the concentration of Na+ ions inside and outside of the cell. When the sodium channels open, allowing Na+ ions to move down the concentration gradient into the cell, the resting membrane potential rises closer to the Na+ equilibrium potential. Once the RMP increases to approximately +30, potassium channels sodium channels begin closing and potassium channels open. With the opening of K+ channels, K+ leaves the cell decreasing the RMP once again toward the K+ equilibrium.

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

Describe the structure, function and significance of myelin in the process of AP conduction

A

Myelin sheaths prevent leakage of ions down the body of the axons which force AP forward
Nodes of Ranvier are necessary for depolarizing current to flow

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

How does hyper/hypokalemia effect APs

A

HyperK –> too much K+ outside of cell –> more positive RMP –> less stimuli needed to meet threshold

HypoK –> too little K+ outside of cells –> more negative RMP –> more work needed to meet threshold

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

How does hyper/hyponatremia affect APs?

A

HyperN –> too much Na+ in blood –> more positive RMP –> less stimuli needed to meet threshold

HypoN –> too little Na+ in blood –> more negative RMP –> not enough to create AP/ too much work –> reduced/no activity

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

If cells were made permeable to only one ion (K+ or Na+), when will the RMP voltage stop changing?

A

When the chemical force is equal to the electrical force.

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

Norepinephrine and Epinephrine bind to what class of receptors?

A

Adrenergic receptors

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

Acetylcholine binds to what class of receptors?

A

Cholinergic receptors

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

Describe the two Adrenergic receptors, where they are typically found, and what part of the nervous system uses them.

A

Alpha receptors - GPCR - generally found in smooth muscle - sympathetic nervous system

Beta receptors - GPCR - found in heart and lungs - sympathetic nervous system

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

Describe the two Cholinergic receptors, where they are typically found, and what part of the nervous system uses them.

A

Nicotinic receptors - Ligand gated channel - found in nerves and skeletal muscle - sympathetic and parasympathetic nervous system

Muscarinic receptors - GPCR - found in glands and smooth muscle - mostly parasympathetic nervous system (exception: sweat glands - sympathetic nervous system)

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

Describe the parasympathetic pathway to their effector organ

A

Presynaptic (long) neuron releases ACh –> Nicotinic receptor of postsynaptic (short) neuron which releases ACh –> Muscarinic receptor of effector organ

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

Describe the sympathetic pathway to sweat glands

A

Presynaptic (short) neuron releases ACh –> Nicotinic receptor of postsynaptic (long) neuron which releases ACh –> Muscarinic receptor of sweat gland

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

Describe the sympathetic pathway to the lungs or cardiac muscle

A

Presynaptic (short) neuron releases ACh –> Nicotinic receptor of postsynaptic (long) neuron which releases NE –> Beta receptors of the lungs or the heart

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

Describe the sympathetic pathway to effector organs via the Adrenal medulla

A

Presynaptic (short) neuron releases ACh –> Nicotinic receptor on chromaffin cells of the adrenal medulla which releases Epi, NE, or DA –> alpha or beta receptor of effector organs

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

Describe the pathway of a somatic neuron to skeletal muscle

A

Neuron releases ACh onto Nicotinic receptor of effector organ

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

How do alpha receptors regulate smooth muscle contractions?

A

SNS releases NE or Epi to alpha receptors –> Gaq activates PLC –> IP3 –> increase of SR Ca2+ –> increases cell Ca2+ –> increase of Ca2+-CM complex –> increase myosin light chain kinase activity –> Phosphorylates MLC –> contraction

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

How do beta receptors regulate smooth muscle contractions?

A

SNS releases NE or Epi to beta receptors –> Gas activates adenylyl cyclase –> cAMP –> inhibits myosin light chain kinase activity –> no phosphorylation of MLC –> relaxation

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

How does Nitric Oxide regulate smooth muscle contractions?

A

NO activates cGMP –> activates myosin light chain phosphatase –> breaks phosphorylation bond of MLC –> relaxation

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

Ascending paralysis is a hallmark clinical presentation for what disease?

Explain how it leads to neuropathy

A

Guillan Barre Syndrome - an immunologically mediated demyelinating peripheral neuropathy

T-cell mediated immune response leads to macrophage destruction of myelin sheaths

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

Explain how diabetes can lead to neuropathy

A

Hyperglycemia –> nonenzymatic glycosylation of proteins, lipids, nucleic acids –> formation of AGEs –> activates inflammatory signaling

Excess glucose -> depletes NADPH –> increase injury via ROS

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

Progressive symmetrical proximal to distal weakness which develops over months, along with reduced tendon reflexes are indicative of which disease

Explain how it leads to neuropathy

A

Chronic inflammatory demyelinating polyneuropathy

T cells and antibodies target molecules at Schwann cell-axon junction –> IgG and IgM found on myelin sheaths lead to recruitment of macrophages that strip myelin from axons –> over proliferation of SC –> onion bulb

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

What is Froment’s sign and what does it indicate?

A

Froment sign shows if a patient is able to hold a piece of paper between their fingers without flexing them.

Positive sign can be indicative of Cubital Tunnel syndrome which impinges the ulnar nerve

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

If someone says a patient has “Saturday night palsy”, what does that mean?

A

The patient had a compressed radial nerve for a prolonged period, causing weakness and inability to extend the thumb, along with sensory deficits

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

Location and function of Pacinian corpuscles

A

Deep dermis (subQ)

Deep transient pressure, high frequency vibration

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

Location and function of Ruffini corpuscles

A

Reticular layer of the dermis

Stretch, joint angle change, finger positioning

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

Location and function of Merkel cells

A

Papillary layer of dermis - base of epidermis

Light touch, texture, fine discrimination

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

Location and function of Meissner corpuscles

A

Papillary layer of dermis, projects into epidermis

Fine touch and pressure, low frequency vibration

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

Location and function of zonula occludens

A

(tight junction)

Located between epithelial cells circumferentially, close to apical side

Prevents paracellular movement, creates impermeable barrier

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

Location and function of zonula adherins

A

(adherins junction)

Located between epithelial cells circumferentially, basal to the zonula occludens

Create “belt-like” support between cells through E-cadherin connecting proteins

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

Location and function of desmosomes

A

(macula adherin)

Scattered on sides of epithelial cells

Connects keratinocytes to stratum spinosum with desmoglian, provides structure

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

Location and function of hemidesomsomes

A

Basal side of epithelial cell

Connects cell to basement membrane

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

Location and function of gap junctions

A

Sides of epithelial cells

facilitate electrochemical communication b/t cells

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

Which sensory receptors have large receptive fields?

A

Pacinian corpuscles
Ruffini corpcuscles

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

Which sensory receptors have slow adaptation?

A

Ruffini corpuscles
Merkel disks

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

Describe warm thermoreceptors

A

Small, unmyelinated

Increase AP frequency with increase skin temp (30C-45C)

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

Describe cold thermoreceptors

A

Two types: myelinated (Aδ) and unmyelinated (C) fibers

increase AP frequency with decrease skin temp (43C-25C)

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

Outline the four types of nociceptors and their sensitivities to tissue damage

A

Chemical: secretions associated with inflammation, substances released from ruptured cells, caustic agents (acid)

Thermal: extremes of temperature >45C, <20C (hot stove, dry ice)

Mechanical: extreme pressure (blunt trauma, crush injuries)

Polymodal: responds to at least 2 of the 3

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

What determines core temperature?

A

Heat gain + Body heat content - heat loss to environment

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

When core temp __________, the body responds with vasodilation.

A

increases

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

When core temp _________, the body responds with vasoconstriction

A

decreases

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

What is the role of PGE2 in inflammation/infection?

A

Infection causes release of inflammatory response (IL1, TNFa, IL6) and endogenous pyrogens to produce PGE2 –> stimulates hypothalamus to increase body temp to new “Tset”

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

What are the thermoregulatory responses during the onset of fever?

During the return to normothermia?

How do cytokines play a part in this?

A

When cytokines are released, the Tset increases which causes the body to conserve heat to raise it’s temp (shivering, vasoconstriction). Once concentration of pyrogens has decreased, the Tset decreases and body begins releasing heat to get back to Tcore (evaporation, vasodilation)

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

How does the core temp and set temp change with exercise? What is the body’s response to this?

A

The set temp does not change.

As muscles contract, the body generates heat which raises core temp. The body begins releasing heat through evaporation to get back to normothermia

Exercising in heat adds to heat gain. Exercising in humidity decreases ability to sweat which can be dangerous as the body cannot get back to core temp.

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

How do sympathetic responses of blood flow differ in apical skin vs nonapical skin?

A

The apical skin has glomus bodies connecting venules and arterioles to bypass capillaries which aid in reduction of heat loss when constricted in response to sympathetic NS signals

The nonapical skin lacks these AV anastomoses, and responds to both sympathetic and parasympathetic signals to vasoconstrict and vasodilate

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

What are the four key components included in an assessment of a pt’s capacity?

A

Communicating a choice
understanding
Appreciation
Rationalization/Reasoning

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

Describe the composition and neural control of sweat secretion by sweat glands

A

Eccrine (not apocrine) SG contribute to temp regulation

Sympathetic n releases ACh onto muscarinic receptor of secretory coiled cells –> activated phospholipase C –> stimulates PKC, increases Ca2+ –> triggers primary secretion –> absorption of Cl- in the duct –> attraction/absorption of Na+ in the duct –> osmotic gradient drives secretion of water into duct –> secretion flows along duct to skin –> reabsorption of NaCl out of duct –> limited reabsorption of water –> loss of solute-free water

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

What are the four proponents of ethical decision making?

A

Medical indications - hx, goals of treatment, probability of success
Patient preferences - pt’s decision being respected, living will
Quality of life - chances to return to normal life, comfort, deficits
Contextual features - religious, economic, financial factors

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

What are the five models of osteopathic care?

A

Biomechanical model - relationships within MSK
Respiratory-circulatory model - respiratory mechanics and vascular and lymphatic drainage
Neurological model - normalization of somatic and autonomic nervous tone
Metabolic energy model - minimizing energetic demands on the body and optimizing metabolic and physiologic processes
Behavioral model - improving health through effect of the mind and spirit

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

Differentiate between linear and non-linear systems

A

Linear is when events happen consecutively (multiple causes for multiple effects)

Non-linear is when one intervention can cause multiple effects in the body in multiple systems

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

Describe the structure and function of fascia

A

Network of irregular connective tissue (collagen, glycoproteins, proteoglycans, hyaluronic acid, water)

Interpenetrates and surrounds all muscles bones and organs creating a unique environment for the body to function

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

Explain the physics behind viscoelasticity

A

Viscosity changes when put under stress due to electric charge accumulation in tissue
Hydrated proteins go from fluid to gel-like substance

Why blunt force trauma hurts the body so much –> feels like hitting concrete

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

Differentiate between interoception and proprioception

A

Interoception - sense of what’s going on inside the body
- pain, weakness, instability, mental status, etc

Proprioception - sense of where the body is in space

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

Define pandiculation

A

Stretch after period of rest or inactivity

yawning and stretching –> myofascial reset process - “gearing up” enzymes in muscles, warming up body for activity

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

Outline the phases of wound healing

A

Hemostasis - vasoconstriction, platelet aggregation, leukocyte migration

Inflammatory phase - neutrophil influx, chemoattractant release, macrophages, phagocytosis

Proliferative phase - fibroblast proliferation, collagen synthesis, ECM reorganization, angiogenesis, granulation tissue formation

Remodeling/maturation phase - epithelialization, ECM remodeling, increase of tensile strength of wound

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

What products are released from dense and alpha granules?

A

alpha - vWF, IGF-1, PDGF, TGF-B, VEGF, chemokines

dense - ADP, ATP, Ca2+, serotonin

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

What growth factors are chondroinductive and what is their function?

A

BMP-2 signaling pathways are major source to design and develop chondroinductive peptides for cartilage tissue engineering

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

How does a whole muscle fiber contract synchronously when the signal occurs only at a small area of the muscle membrane?

A

The depolarization at the NMJ propagates an action potential down the muscle fiber

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

Explain the generation and roles of the end-plate potential and muscle action potential

A

AP of the nerve releases ACh into synaptic cleft –> attached to nicotinic, ligand-gated Na/K channels –> depolarization of end plate on sarcolemma –> generation of AP

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

The epiblast and hypoblast become…

A

Epiblast - endoderm, mesoderm, ectoderm

Hypoblast - endoderm

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

Explain the steps of neurulation

A

Neural plate forms as ectoderm thickens and flattens on posterior side
Edges of neural plate move towards each other to form neural tube
Edges of plate fuse together to form tube
Neural tube detaches from rest of ectoderm
Neurulation is complete when last neuropores close

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

Explain the process of gastrulation

A

A migration of blastocyst cells inward to establish the three germ layers via invagination. The inner cell mass folds in on itself forming an indentation. The cells continue to push inward, forming the endoderm. Cells that remain on the outer surface are the ectoderm. Additional cells migrate between the endo and ectoderm forming the mesoderm

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

Define molar pregnancy

A

Enucleated egg fertilized by two sperm - basically tumor of a trophoblast

Obv signs are significantly high hCG levels

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

Outline the different pathways of epiblast formation

A

Ectoderm –> epidermis, brain, spinal cord, neural crest

Mesoderm –> notochord
Mesoderm –> somite –> sclerotome, dermatome, myotome
Mesoderm –> internal organs, connective tissue

Endoderm –> epithelial lining, glands, digestive and resp tracts

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

What part of the blastocyst becomes the placenta?

A

Trophoblast

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

These embryonic tissues become what adult tissues:
Neural tube –>
Neural crest –>
Somites –>
Lateral mesoderm –>
Trunk vessels –>

A

Motor neurons
Sensory neurons
Myoblasts and endothelial cells
Bone, cartilage
Circulatory structures

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

How does thalidomide affect limb growth?

A

It reduces the amount of FGF8 produced –> decreases or causes abnormal limb growth

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

Explain the characteristics and gene defect involved in Hand-foot-genital syndrome

A

HOXA13

Fusion of carpal bone and small, short digits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Explain the characteristics and gene defect involved in Synpolydactyly

A

HOXD13

Webbing of digits 3/4 fingers, 4/5 toes
Partial or complete duplication

105
Q

Explain the characteristics and gene defect involved in Holt-Oram syndrome

A

TBX5

Lack of left thumb, little growth of right thumb
Incomplete clavicle

106
Q

Explain the characteristics and gene defect involved in Scott-Taor syndrome

A

TBX4

Small patellae, abnormal morphology
hypoplastic medial femoral condyles in knees

107
Q

Explain the characteristics and gene defect involved in Club foot

A

PITX1-TBX4

Fore foot adducted, short foot, heel varus in plantarflexion, thin calves

108
Q

Explain how the excitation-contraction coupling works

A

Depolarization of the motor end plate –> sends AP down T-tubule –> depolarization of T-tubule –> conformational change of DHP receptors –> binds to Ry receptors on nearby SR –> opening of pore in SR –> release of Ca2+ from SR into ICF –> Ca2+ binds to troponin C –> pulls tropomyosin away –> unbinds from actin to expose binding site –> myosin head binds to actin

109
Q

Relate myotonia congenita to ECC

A

Myotonia congenita disorder doesn’t have the Cl- receptors in the T-tubles –> cannot repolarize –> delayed relaxation of muscles –> temporary rigor mortis after exertion

110
Q

Relate malignant hyperthermia to ECC

A

AD inherited disorder with abnormal RyR

Depolarizing muscle relaxants or anesthetics –> RyR stays open –> uncontrolled release of Ca2+ –> sustained muscle contractions –> continuous ATP use (hypermetabolism) –> continuous generation of heat

111
Q

Outline the cycle of cross-bridging

A

Actin and Myosin unbound, ADP and P : relaxed muscle
Binding A-M releases ADP and P
A-M : muscle contracts
ATP binding releases A-M
ATP hydrolysis
A+M, ADP and P : relaxed muscle

112
Q

What is the benefit of using Pancuronium as a nondepolarizing medication?

A

Pancuronium is a lipophilic steroid - less soluble = stays near site of action longer = longer duration of action

113
Q

Contrast the mechanisms of action of depolarizing and nondepolarizing neuromuscular blockers

A

In normal physiology, ACh binds to receptor to open channel and Na+ enters and remaining ACh is broken down by AChE

With depolarizing NM blockers, competitive inhibitors bind to receptor to prevent ACh from binding –> keeps channels open for continuous Na+ influx –> no repolarization preventing further AP –> muscle fatigues –> spastic paralysis ?

With nondepolarizing NM blockers, competitive inhibitor binds to open channel but blocks Na+ from influxing ?

114
Q

What is the mechanism of the malignant hyperthermia rescue therapy drug?

A

Dantrolene - binds to RyR to inhibit further Ca2+ release

115
Q

What is the reversal agent for nondepolarizing NM blockers?

A

AChE inhibitors (Edrophonium -shortest half life, Physostigimine - crosses BBB, Pyridostigmine - used to treat MG)
Sugammadex

116
Q

Outline the pathogenesis of Duchenne MD

A

Loss of function mutation in dystrophin gene on X-chromosome

Dystrophin critical in contraction of muscle fibers

117
Q

Outline pathogenesis of Myotonic dystrophy

A

Autosomal dominant multisystem disorder caused by CTG repeats in 3` noncoding region of DMPK gene

118
Q

Outline pathogenesis of malignant hyperthermia

A

Autosomal dominant trait with variable penetrance coupled

Mutation in Ry receptors, sometimes DHP receptors

119
Q

Define motor unit recruitment, and compare slow vs fast twitch motor units

A

Process in which number of active motor units increase
Weakest motor units always recruited first (Type I) –> progressively stronger units added as more force is added

Slow twitch motor units - small, innervated by easily excitable aMN
Fast twitch motor units - large, innervated by aMN that are more difficult to excite

120
Q

Compare and contrast Type I, Type IIa and Type IIb muscle fibers

A

Type I: Slow oxidative (fatigue-resistant)
Type IIa: Fast oxidative (fatigueable)
Type IIb: Fast glycolytic (fatigueable)

Type I: high oxidative capacity, moderate glycolytic capacity
Type IIa: moderate oxidative capacity, high glycolytic capacity
Type IIb: low oxidative capacity, high glycolytic capacity

Type I and IIa: moderate diameter
Type IIb: large diameter

Type I: moderate SR Ca2+ pumping
Type IIa and IIb: high SR Ca2+ pumping

121
Q

Explain the physiologic mechanism of a tetanic response

A

First stimulus causes a twitch
Another stimulus during the relative refractory period –> more Ca2+ –> further contraction
Force of contraction builds with each stimulus
Continuous, high frequency stimulus –> continuous muscle contraction

122
Q

Describe how the forceful and repetitive muscular activity causes muscle hypertrophy

A

Repeated muscle contraction –> increased production IGF-1 –> activation PI3K –> increased AKT/mTOR pathway –> increased protein synthesis –> increased fiber size

Increased AKT/mTOR pathway –> inhibits FoxO-atrogene pathway –> decreased protein degradation –> increased fiber size

Repeated muscle contraction –> increased intracellular Ca2+, decreased [ATP] –> activation PGC-1a signaling –> increased slow fiber oxidative capacity

123
Q

Explain how individuals infected by polio develop muscle weakness and atrophy

A

Viral replication in anterior horn cells (efferent cell bodies) and brainstem motor neuron cells –> destruction of somatic motor neurons to skeletal m fibers –> loss of stimulation –> disuse atrophy

Disuse atrophy –> decrease in size –> replaced by fibrous connective tissue –> denervation atrophy

Lack of stimulation to diaphragm –> respiratory paralysis

124
Q

Compare the signs of UMN to LMN lesions

A

Upper motor neuron lesions
- Hyperreflexia (reflexes up)
- Hypertonicity (muscle tone up)
- Spasticity (contraction up)
- Disuse atrophy
- Babinski + (toes point up)

Lower motor neuron lesions
- Hyporeflexia (reflexes down)
- Hypotonicity (muscle tone down)
- Flaccid paralysis (muscle contraction down)
- Denervation atrophy
- Babinski - (toes point down)

125
Q

Explain the difference between concentric, eccentric, and isometric contractions

A

Concentric and eccentric are isotonic - muscle tone is the same but length differs
- Concentric: contraction with muscle shortening
- Eccentric: contraction with muscle lengthening

Isometric contraction - Length is same but muscle tone differs - contraction without shortening or lengthening

126
Q

During muscle contraction, which bands change and which stay the same?

A

I bands shrink as thick and thin filaments come together
A band does not change - area of thick filament and M line - where thin filaments overlap with thick

127
Q

Explain Force-Velocity relationships of skeletal muscle

A

The more load increase, the less velocity of shortening
Once max load is reached, muscle begins to stretch

Max load is proportional to max rate of energy turnover

128
Q

Contrast the basic mechanisms of C. Botulinum and C. Tetani

A

Botulinum blocks the release of ACh in the NMJ by cleaving SNARE proteins and binding to receptors –> no ACh –> no muscle activity

Tetani blocks the release of GABA and glycine which inhibit release of ACh –> nothing to inhibit release of ACh –> continuous ACh activity –> muscle spasms

129
Q

Define fatigue in terms of biochemical mechanisms and its purpose

A

The inability of ATP turnover to keep paces with ATP usage –> reduction in ATP turnover, reduction in ability to produce force

Helps prevent ATP levels from dropping too low –> avoid rigor or irreversible muscle damage

130
Q

Outline the two Phosphagen system reactions for skeletal muscle energy

A

Creatine Phosphate is a storage forms of ATP - holding Pi ready to easily phosphorylate ADP

Creatine Kinase
ADP + H + CrP –(CK)–> ATP + Cr

Adenylate Kinase
ADP + ADP –(AK)–> ATP + AMP

131
Q

List the benefits of AMP as a biproduct of the phosphagen system

A

AMP stimulates Glycolysis
- increases PFK-1
- increases F2,6P
- stimulates AMPK –> inhibits glycogen synthesis, blocks FA metabolism, activates GLUT4, stimulates glycogenolysis

132
Q

With what type of activity does the Phosphagen system dominate?

A

Short-term singular muscle contraction
Limited amount of repeated intense muscle contraction
Maximal muscular effort for 5-6s
-Weightlifting, start-stop events, sprinting, jumping events

133
Q

What factors control the rate of Phosphagen system energy being regenerated/used?

A

[CrP] reduction
Severity of metabolic acidosis
Motor unit and fiber type used

134
Q

What are the key enzymes and regulators of the Glycolytic energy system?

A

Enzymes: HK, PFK1, PK

Glucose + 2 NAD + 2 ATP –(HK)–> G6P –(PFK1)–> FBP –> 3-C Metabolites ——(PK)–> Pyruvate + 2 NADH + 4 ATP (2 net total)

HK regulator: G6P inhibits
PFK1 regulators: ATP, Citrate inhibit; AMP/ADP, F26B activate

135
Q

Outline the five sources of Skeletal muscle Glycolysis

A
  1. Dietary glucose: GI –> liver –> blood –> tissue –> glycolysis
  2. Liver glycogenolysis: Glycogen –> liver glucose –> blood –> tissue –> glycolysis
  3. Cori Cycle (Lactic Gylcolysis): Tissue pyruvate –> tissue lactate –> blood lactate –> liver lactate –> liver glycogenolysis –> liver glucose –> blood glucose –> tissue –> glycolysis
  4. Cahill Cycle: Tissue AA oxidations –> convert a-KG to Glutamate –> convert Pyruvate to Alanine –> blood alanine –> liver alanine –> convert alanine back to Pyruvate –> liver gluconeogenesis –> blood glucose –> tissue –> glycolysis
  5. Muscle glycogenolysis: Glycolysis –> G6P –> muscle glycogenesis –> Glycogen stored in muscle –> muscle glycogenolysis –> finish glycolysis
136
Q

At what point does Glycolysis take over as the dominant energy system?

A

10-15s after exercise begins

137
Q

Outline the Lactic Glycolysis (Anaerobic respiration) system reaction

A

Pyruvate + NADH + H —(Lactate Dehydrogenase) —> Lactate + NAD

138
Q

Why is Lactic Glycolysis important during intense exercise?

A

Lactate - substrate of Cori Cycle –> replenishes muscle glucose
Pyruvate production exceeds mt uptake capacity
Prevents inhibition of Glycolysis
Regenerates NAD+
Slows metabolic acidosis by buffering H+

139
Q

What are the possibilities and limitations of mitochondrial respiration?

A

Possibilities
Can power muscle contraction for as long as fuel is available to the muscle as long as exercise intensity is at a level the system can meet the demand

Limitations
Cannot meet energy demands of muscle at the beginning of (any) exercise
Cannot meet energy demands of muscle in very-high intensity

140
Q

What are the fuels used by mitochondrial respiration?

A

Carbohydrates
Fatty acids
Ketone bodies
Amino acids

141
Q

When does mitochondrial respiration take over as the dominant energy system?

A

~2-3 minutes after beginning of exercise in low, moderate, or high(ish) intensity exercise

142
Q

Explain “hitting a wall” and “getting a second wind”

A

“Hitting a wall” is when there is a near total depletion of liver and muscle glycogen stores, meaning no fuel for glycolysis to make ATP

“Second wind” comes after this when the body switches to FA oxidation as the predominant ATP production system

143
Q

What fuel source is used during higher-intensity, shorter duration activity?

A

Glucose - muscle glycogenolysis

144
Q

What fuel source is used during lower-intensity, longer duration activity?

A

Fatty acids

145
Q

How does insulin stimulate the body to use glucose/glycolysis as it’s primary fuel source?

A
  1. Increases [GLUT4] (↑ glucose uptake)
  2. Stimulates PFK-1 (↑ glycolysis)
  3. Promotes glycogen synthase (↑ glycogenesis)
  4. Promotes inhibition glycogen phosphorylase (↓ glycogenolysis)
  5. Stimulates protein synthesis (↓ AA oxidation)
  6. Inhibits FA uptake (↓ FA oxidation)
146
Q

How does epinephrine control muscle energetics and the body’s fuel source?

A

↑ glycolysis - stimulates production of F26P –> stimulates PFK-1
↓ glycogenesis - inhibits glycogen synthase
↑ glycogenolysis - stimulates glycogen phosphorylase
↑ FA oxidation - stimulates FA uptake

147
Q

How does Pompe Disease (GSD Type II) affect muscle energetics

A

Loss of a-1,4-glucosidase –> lysosomal enzyme responsible for glycogen degradation –> glycogen accumulation in lysosomes and cytosol

148
Q

How does Cori Disease (GSD Type III) affect muscle energetics

A

Loss of glycogen debranching enzyme –> enzyme required for full removal of glycogen branches during glycogenolysis –> storage of structurally-abnormal glycogen

149
Q

How does Andersen Disease (GSD Type IV) affect muscle energetics

A

Loss of glycogen branching enzyme –> enzyme required for synthesis of glycogen branches during glycogenolysis –> storage of structurally-abnormal, insoluble glycogen

150
Q

How does McArdle Disease (GSD Type V) affect muscle energetics

A

Loss of myophosphorylase –> muscle isoform of glycogen phosphorylase - plays major role in breakdown of glycogen during glycogenolysis

151
Q

How does Tarui Disease (GSD Type VII) affect muscle energetics

A

Loss of PFK-1 activity –> backflow of glycolysis from F6P to G6P –> shuttled to glycogenesis –> excess glycogen

152
Q

How does Diabetes Mellitus affect muscle energetics

A

Insulin loss/sensitivity –> muscle unable to engage in insulin-dependent glucose uptake –> glycolysis and glycogenesis impaired –> excessive FA and KB delivered to muscle for primary fuel source

153
Q

How does exercise help relieve hyperglycemia of diabetes?

A

Exercise-stimulated AMPK –> ↑ GLUT4 –> ↑ insulin-independent uptake of glucose into muscle

154
Q

How does Primary Carnitine Deficiency affect muscle energetics?

A

AR inheritance - mutation of SLC22A5 gene

Loss of plasma membrane transporter for carnitine –> accumulation of fatty acyl-CoA in cytosol –> inability to do B-oxidation (FA oxidation) –> ↑ FA in blood –> hyperlipidemia

155
Q

What are the major adaptive responses of Learning, Endurance Training, and Strength Training?

A

Learning: ↑ rate and accuracy of motor units (CNS)
Endurance: ↑ oxidative capacity in all involved motor units
Strength: Hypertrophy and enhanced glycolytic capacity of motor units

156
Q

A lesion in nerve roots L2-L4 would result in the dysfunction of what nerve and DTR?

A

Femoral n, patellar DTR (dominant L4)
Obturator n, adductor DTR (dominant L3)

157
Q

A lesion in nerve roots C5-C6 would result in the dysfunction of what nerve and DTR?

A

Musculocutaneous n, biceps DTR

158
Q

A lesion in nerve roots C6-C7 would result in the dysfunction of what nerve and DTR?

A

Radial n, triceps DTR (dominant C7)
Radial n, Brachioradialis (dominant C6)

159
Q

A lesion in nerve roots S1 would result in the dysfunction of what nerve and DTR?

A

Sciatic n, Achilles DTR

160
Q

What dermatome and myotome contribute to the medial hamstring DTR?

A

L5, Tibial n

161
Q

What dermatome and myotome contribute to the finger flexor DTR?

A

C8-T1, Ulnar n

162
Q

Outline the normal pathway of a reflex arc

A

Lengthening of tendon (tap) –> stretch of muscle –> muscle spindle activation –> AP in Ia fiber –> aMN or interneuron –> activating aMN to affected muscle, inhibitory aMN to antagonist muscle –> contraction –> shortening of muscle –> unload of muscle spindle –> signal ends

163
Q

How does the Golgi tendon pathway differ from the muscle spindle reflex pathway?

A

Golgi tendon pathway senses tension and sends inhibitory signals to agonist muscle, excitatory signals to antagonist muscle –> causing relaxation

Reflex pathway senses lengthening and sense excitatory signals to agonist muscle, inhibitory signals to antagonist muscle –> causing contraction

164
Q

Describe the process of kinetic firing

A

The kinetic chain is a sequence of individual body segments and joints working together to accomplish a task

165
Q

Compare closed vs open kinetic chains

A

Closed kinetic chains occur against resistance
–> when walking, the feet/legs are in closed kinetic chain because it’s in contact with a structure.
–> Closed has distal extremity stabilized, body moving around it

Open kinetic chains occur without resistance, not in contact with other structures
–> arms swinging freely when walking
–> open has proximal extremity stabilized, distal moving

166
Q

Briefly describe BioTensegrity

A

Dysfunction of one joint affects the entire system

167
Q

Which muscle is most likely to be inhibited by arthrogenic
muscle inhibition (AMI) of the knee? Why?

A

Vastus medialis (obliquus)

VMO is critical for stabilizing the knee joint

168
Q

Explain how the principles of muscle energy technique takes
advantage of agonist and antagonist muscle groupings

A

Reciprocal inhibition - agonist muscle group (dysfunctional muscle) is relaxed and stretched further when antagonist muscle group is contracted

MET retrains neuromuscular firing patterns associated with SD

169
Q

Increased __________ –> more prone to patellar dislocation and tracking issues

A

Q angle

170
Q

What groupings give rise to neurokinetic chains?

A

Somites to myotomes, dermatomes and sclerotomes

171
Q

Polymerized form of collagen type I and where is it mostly found?

A

Fibril

Bone, dermis, tendon, ligaments

172
Q

Polymerized form of collagen type II and where is it mostly found?

A

Fibril

Cartilage, IV discs

173
Q

Polymerized form of collagen type III and where is it mostly found?

A

Fibril

Dermis, blood vessels, lymphatic tissue, liver, lung
Important for repair of tendons

174
Q

Polymerized form of collagen type V?

A

Associated fibril with collagen Type I

175
Q

Polymerized form of collagen type XII?

A

FACIT to collagen type I

176
Q

Polymerized form of collagen type XI?

A

Associated fibril with collagen Type II

177
Q

Polymerized form of collagen type IX?

A

FACIT to collagen type II

178
Q

What is the function of FACITs?

A

Crosslink cartilages

179
Q

What are the functions of proteoglycans in the ECM?

A
  1. Binds and releases water
  2. Lubricant for articular cartilages
  3. Allows for diffusion of nutrients in and waste out of the connective tissue
  4. Acts as barrier to bacteria
180
Q

What is the principal collagen in tendon and ligaments?

A

Type I (two a1 chains and one a2 chain)

181
Q

What collagens regulate the structure of a tendon?

A

Type V, XII, and XIV (the associated fibrils and FACITs)

182
Q

What is a tenocyte?

A

Secretes and builds ECM found between collagen fibers

183
Q

What type of collagen is produced in the proliferation phase of wound healing?

A

Collagen Type III

184
Q

What is the primary proteoglycan associated with cartilage?

A

Aggrecan

185
Q

Hyaline cartilage:
–>ECM
–>Type of cells
–>Organization of cells
–>Presence of perichondrium
–>Locations/functions
–Histology

A

ECM: Type II collagen, abundant aggrecan, proteoglycans, GAGs
Cells: chondroblasts, chondrocytes, fibroblasts
Organization: Isolated in lanucae or in small isogenous groups
Perichondrium: Yes - contains fibroblasts, stem cells, blood vessels, small nerves
Location/Function: Aids in sliding within joints; model for bone growth; provides structural support in airway
Histology: homogenous and glossy, very pink

186
Q

Elastin cartilage:
–>ECM
–>Type of cells
–>Organization of cells
–>Presence of perichondrium
–>Locations/functions
–>Histology

A

ECM: Type II collagen, elastin fibers, aggrecan, proteoglycans, GAGs
Cells: chondroblasts, chondrocytes, fibroblasts
Organization: small isogenous groups in lanucae
Perichondrium: Yes - contains fibroblasts, stem cells, blood vessels, small nerves
Location/Function: Provides flexible shape and support to soft tissues (external ear, auditory tube, epiglottis)
Histology: similar to Hyaline but abundant in elastin fibers

187
Q

Fibrocartilage:
–>ECM
–>Type of cells
–>Organization of cells
–>Presence of perichondrium
–>Locations/functions
–>Histology

A

ECM: Type I collagen, Type II collagen, aggrecan
Cells: chondrocytes, fibroblasts
Organization: Isolated in lanucae; sometimes in small groups in rows
Perichondrium: No
Location/Function: Provides cushioning, strength, resistance to tearing and compression within IC discs, meniscus, pubic symphysis
Histology: Varying combinations of hyaline cartilage in dense connective tissue

188
Q

What type of cartilage is this?

A

Hyaline cartilage

189
Q

What type of cartilage is this?

A

Elastic cartilage

Can see elastin fibers

190
Q

What type of cartilage is this?

A

Fibrocartilage

191
Q

Where are stem cells housed in articular cartilage?

A

Superficial zone

192
Q

Characteristics of Articular Cartilage

A
  1. Avascular
  2. Four layers
  3. No perichondrium
193
Q

Collagen types in articular cartilage

A

Type II, VI, IX, X, XI

194
Q

Collagen function in articular cartilage

A

Type II - Major component of fibrils, tensile strength
Type VI - forms microfibrils, pericellular
Type IX - FACIT, proteoglycan and collagen, interactions between II and proteoglycans
Type X - Hypertrophic and calcified cartilage
Type XI - Nucleation control within collagen fibril

195
Q

Proteoglycans in articular cartilage and their functions

A

Decorin - Controls size/shape of fibrils; binds collagen II and TGF-B; interterritorial
Biglycan - Pericellular; binds collagen VI and TGF-B
Aggrecan - Compressive stability
Versican - Low level throughout articular cartilage life
Perlecan - Pericellular

196
Q

Differentiate between Regeneration and Scar Formation

A

Regeneration is the complete restoration to normal state by differentiated cells and stem cells

Scar formation is when there is severe damage and it is replaced with connective tissue (fibrosis)

197
Q

What determines a tissues ability to repair itself?

A

Type of tissue (labile, stable, permanent)
ECM integrity
GF produced at injured site (macrophages, stromal cells, epithelial cells, etc)
Integrins

198
Q

Continuously dividing tissue with a short life span and can regenerate readily

A

Labile Tissue

Hematopoietic stem cells in bone marroe

199
Q

Quiescent cells that proliferate in response to injury with limited capacity to regenerate

A

Stable Tissue

Most solid organs (liver, kidney, pancreas) and endothelial cells, smooth muscle cells, fibroblasts

200
Q

Terminally differentiated cells with very long life that heal by scar formation

A

Permanent tissue

Cardiac cells, Neurons, skeletal muscles (kind of)

201
Q

How is liver regenerated?

A

Kupffer cells (liver macrophages) autocrine release TNF to act on itself –> secretes IL6 paracrine to hepatocytes to initiate G0 to G1 –> GF released from injured area bind to EGFR and MET of hepatocyte –> cell proliferation –> TGF-B initiates termination once sufficient number of cells and hepatocytes return to G0

202
Q

Explain the timeline of first intention wound healing

A

First 24 hrs: neutrophil accumulation
24-48 hrs: epithelial cells close wound
Day 3: neutrophils replaced with macrophages to clear debri; granulation tissue invades
Day 5: Neovascularization peaks; fibroblasts migrate/proliferate into granulation tissue
Week 2: Decrease in leukocyte infiltrate, edema, vascularity of GT
Week 4: essentially normal epidermis by end of month 1

203
Q

Healing by first intention leads to ______% wound strength by 3 months

A

70-80

204
Q

Outline healing by second intention

A

Severe wound –> necrotic debri and fibrin deposits –> increased inflammation and injury –> increased granulation tissue; loss of dermal appendages –> scar by end of 1 month (acelluar connective tissue) –> wound contractions to 5-10% original size by myofibroblasts

205
Q

Fibrosis in tissue space occupied by an inflammatory exudate is called

A

Organization

206
Q

Outline the synthesis of collagen

A

Inside rER: Collagen mRNA translation –> SRP –> pre-procollagen synthesized –> hydroxylation w/ Vit C (adds OH to lysine/proline) –> glycosylation (adds sugar to mark for exocytosis) –> linkage of three chains via disulfide bonds –> procollagen triple helix

In extracellular space: Procollagen peptidase cleavage of N- and C-terminals –> tropocollagen –> spontaneous fibril assembly –> lysine-hydroxylysine cross linkages by Lysyl oxidase and copper –> collagen

207
Q

What is the significance of Glycosylation in collagen formation?

A

It marks the procollagen for exocytosis from the cell to continue synthesis

208
Q

What is the significance of Vitamin C in collagen formation?

A

Required for hydroxylation

Lack of Vitamin C –> poor wound healing –> scurvy

209
Q

Osteogenesis Imperfecta pathogenesis and clinical features

A

AD mutation COL1A1/COL1A2 mutation –> decreased bonding between a-chains –> failed triple helix –> “brittle bone disease”

Growth delay, skeletal abnormalities, recurrent fractures, opalescent teeth

210
Q

Ehlers-Danlos pathogenesis and clinical features

A

AD mutation COL5A1/COL5A2 –> ↓ procollagen peptidase –> ↓ tropocollagen synthesis –> ↓ fibril assembly
Defect in lysine-hydroxylysine crosslinking –> unstable collagen fibrils

Hypermobility
Tissue fragility, atrophic scars, poor wound healing
MV prolapse, easy cruising, varicosis, prominent eyes

211
Q

Marfan Syndrome pathogenesis and clinical features

A

AD mutation of FNB-1 –> defective fibrillin (glycoprotein that forms protective sheath around elastin) –> defective elastin fibers

Tall stature, long extremities, hypermobility, arachnodactyly, hyperextensive skin, visual impairments, aortic disease, MV prolapse

212
Q

Differentiate between interstitial growth and appositional growth in cartilage

A

Interstitial growth - mitosis of existing chondroblasts in lacunae

Appositional growth - formation of new chondroblasts peripherally from progenitor cells in perichondrium

213
Q

Describe the structure of a typical proteoglycan

A

Core protein - made of serine residues - attachment points for GAGs
GAGs - negatively charged sugars that attract positive ions and water
Tetrasaccharide linkage - carbon chain binding GAG to core protein

214
Q

Describe the embryological origin of tendons and ligaments

A

Progenitor cells (tenocytes) originate from ventral and lateral ectoderms
Syndetome - embryonic structural origin of tendons from somite

215
Q

What is the key regulator in formation of tendons and ligaments?

A

Transcription factor SCX (scleraxis)

216
Q

Describe the cell line of origin, morphological features and primary function of osteoblasts

A

Cell line of origin: Mesenchymal cells –> osteoprogenitors

Morphological features: cuboidal cells

Primary function: secretes organic extracellular matrix components and attracts inorganic ECM to build bone; lines the bone

217
Q

Describe the cell line of origin, morphological features and primary function of osteocytes

A

Cell line of origin: Mesenchyme –> osteoprogenitors –> osteoblasts

Morphological features: cytoplasmic projections

Primary function: communication and mechanosensory

218
Q

Describe the cell line of origin, morphological features and primary function of osteoclasts

A

Cell line of origin: monocytes

Morphological features: large, multinucleated, “macrophage-like”; integrins protein surround “feet” and suction to seal resorption hollow

Primary function: secrete hydrolytic enzymes and acid to digest matrix and resorb bone through phagocytosis and release into blood

219
Q

Describe the cell line of origin, morphological features and primary function of bone-lining cells

A

Cell line of origin: osteoblasts ?

Morphological features: thin cells along periosteum and endosteum

Primary function: facilitate movement of calcium into and out of bone

220
Q

Explain the function of alkaline phosphatase in bone remodeling

A

Osteoblasts secrete AP to attract inorganic ECM components from the diet such as calcium and phosphatase

Elevated levels of AP –> elevated osteoblastic activity

221
Q

Explain the relationship between the Haversian canal, Volkmann’s canal, and the osteon

A

The Osteon is defined as a Haversian canal and it’s surrounding lamellae layers running lengthwise in the cortex of bone

The Haversian canal houses the capillaries and nerves

The Volkmann’s canal connects adjacent osteons to each other via the Haversian canals, and the osteons to the periosteum

222
Q

Site of primary ossification

A

Diaphysis

223
Q

Site of secondary ossification

A

Epiphysis

224
Q

Contrast woven bone from lamellar bone

A

Woven bone is immature bone with poorly arranged collagen fibers and is generally very weak. It is the beginnings of all bone and gets remodeled into lamellar bone.

Lamellar bone has collagen fibers arranged in parallel sheets. It’s very strong and differentiates into two different types: Trabecular and Cortical

225
Q

Differentiate Trabecular bone from Cortical bone

A

Trabecular - spongy bone - branching irregular network
–> occupies the center volume of long bones and houses bone marrow in trabeculae spaces

Cortical bone - compact bone - forms the edges of long bones

226
Q

Explain the difference between the nutrient foramen and canaliculi

A

The nutrient foramen houses the nutrient artery that supplies the bone - typically entering through the diaphysis

The canaliculi house the osteocyte cytoplasmic projections which allow for intracellular communication and mechanosensory

227
Q

Dysfunction of what transcription factor would disrupt intramembranous ossification?

A

RUNX2

MSC cell condensation –> RUNX2 –> osteoblasts

228
Q

Dysfunction of what transcription factor would disrupt endochondral ossification?

A

SOX9

MSC cell condensation –> SOX9 –> chondrocytes –> osteoblasts

229
Q

PTH has a (direct/ indirect) affect on osteoblasts, and a (direct/indirect) effect on osteoclasts

A

Direct on osteoblasts
Indirect on osteoclasts

Binds osteoblast –> increase RANKL –> stimulates osteoclasts

230
Q

Calcitonin has a (direct/ indirect) affect on osteoblasts, and a (direct/indirect) effect on osteoclasts

A

Indirect on osteoblasts
Direct on osteoclasts

231
Q

Biggest players of height in fetal, infantile, childhood, and puberty

A

Fetal: mother’s health
Infantile: nutrition, genetics
Childhood: growth hormone, thyroid development
Puberty: Estrogen

232
Q

How do you measure bone age?

A

Xray of the left hand/wrist - measuring growth plate

233
Q

What two factors stop the proliferation of chondrocytes in endochondral ossification?

A

Estrogen and Fibroblast growth factor receptor 3

234
Q

What transcription factors regulate the hypertrophy of chondrocytes in EO?

A

SOX9 inhibits hypertrophy –> keeps cell alive
RUNX2 promotes hypertrophy –> apoptosis

235
Q

Describe the relationship between PTHrP, IHH, and SOX9 in EO?

A

Parathyroid hormone-related peptide is secreted onto proliferating chondrocytes. PTHrP stimulates proliferation by secreting SOX9 which delays hypertrophy –> chondrocytes replicate and are pushed further from PTHrP and SOX9 –> begin to hypertrophy until meeting IHH which then stimulates more proliferation

236
Q

Differentiate the characteristics of cortical and trabecular bone remodeling

A

Spongy bone - osteoclasts break down trabeculae –> osteoprogenitors differentiate into osteoblasts –> osteoblasts secrete osteoid

Compact bone - osteoclasts tunnel through bone –> blood vessels and nerves occupy tunnel –> blood provides osteoprogenitors –> osteoblasts line tunnel –> secrete osteoid from periphery inward –> osteocytes trapped in layers of lamellae

237
Q

Explain steps of intramembranous ossification

A
  1. Mesenchymal cells aggregate in area where bone will form
  2. Differentiate into osteoprogenitors and osteoblasts
  3. Osteoblasts secrete osteoid –> osteoblasts become separated but remain attached through cytoplasmic processes
  4. Osteoid mineralizes; osteoblasts completely surrounded by matrix –> osteocytes
  5. Tissue vascularization brings in osteoclasts for remodeling bone
238
Q

Explain steps of endochondral ossification

A

Hyaline cartilage template surrounded by perichondrium except at articulating surfaces –> perichondrium becomes periosteum –> bone collar forms impeding nutrient diffusion to cartilage –> chondrocytes undergo hypoxia, become hypertrophic, calcify, and undergo apoptosis –> apoptosis releases angiogenic factors –> recruits blood vessels –> blood delivers osteoclasts –> osteoclasts removed calcified cartilage matrix –> osteoprogenitors come and become osteoblasts –> osteoblasts secrete osteoid –> forms primary center of ossification in diaphysis –> bone collar extends –> osteoclasts and osteoblasts continue –> woven bone formed –> remodeling –> bone follows cartilage

239
Q

List and describe the 5 growth plate zones

A

Zone of Reserve Cartilage - “clueless cartilage” - most distant from primary ossification - rich in Type II collagen

Zone of Proliferation - Site of chondrocyte mitosis - regulated by GH, IGFs, IHH, BMPS

Zone of Hypertrophy - Chondrocyte swelling - inhibited by IHH and PTHrP - cells release ECM Type X collagen

Zone of Calcification - Chondrocytes begin apoptotic pathway –> release AP and ATPase –> cleave calcium, phosphate from environment –> form calcium-P aggregates –> calcification

Zone of Ossification - Removal of calcified cartilage and remodeling of woven bone - closure accelerated by estrogen

240
Q

Explain how each GF plays a part in bone growth: SOX9, GH, IHH, PTHrP, IGF-1, FBFR3, RUNX2

A

SOX9 - inhibits hypertrophy
RUNX2 - stimulates hypertrophy
GH - pro-proliferative (regulates longitudinal growth)
IHH - inhibits hypertrophy, stimulates proliferation
PTHrP - inhibits hypertrophy; maintains chondrocytes in proliferative state (Gs activation –> cAMP –> PKA –> P of SOX9)
IGF-1 - mediator of GH, stimulates hypertrophy
FBFR3 - expressed by proliferating/early hypertrophic chondrocytes to inhibit further proliferation by inhibiting IHH

241
Q

Describe the regulation of parathyroid secretion and its role in calcium homeostasis including the role of Vitamin D, Phosphate and Magnesium

A

Release of PTH is controlled by a feedback system.

High calcium –> ↓ PTH secretion; low calcium –> ↑ PTH secretion

Vitamin D [1,25(OH)2D] - ↑ Vitamin D –> reduces PTH gene expression and transcription
Phosphate - ↑ serum phosphate –> ↑ PTH release
Magnesium - ↑ or ↓↓ magnesium –> ↓ PTH –> possible hypocalcemia

242
Q

Explain the pathway of Parathyroid Ca2+ Sensing Receptor

A

GCPR receptor –> activates PI-PLC –> Ca2+ mobilization –> PKC activation –> Phospholipase A2 –> Arachidonic acid –> Leukotrienes –> Degradation of preformed PTH, decreased release of PTH

243
Q

Explain how PTH promotes bone resorption

A

PTH is released –> binds to osteoblast PTHR1 –> increases RANKL expression –> osteoclast precursor RANK binds to RANKL –> activates osteoclast gene transcription –> differentiation into osteoclast –> increase of osteoclast activity

244
Q

Label the regulators of the hematopoietic monocyte/osteoclast lineage

A
  1. MCSF (Macrophage colony stimulating factor) - contributes to differentiation, migration, survival; does not differentiate from macrophage
  2. RANKL - expressed by osteoblasts and osteocytes to commit cells to osteoclasts
  3. Osteoclast attaches to bone via integrins; cell reorganization begins
  4. OPG (Osteoprogesterin) - soluble decoy receptor - prevents RANKL from binding to RANK receptor
245
Q

Describe the role of osteoprogesterin

A

Secreted by osteoblasts and osteocytes –> Competitively binds to RANK to stop formation of osteoclasts

246
Q

Label the regulators and secretions of the mesenchymal/osteoblast lineage

A
  1. RUNX2 - transcription factor that helps commit to osteoblast
  2. Osterix - cellular production of Type I cartilage
    -No osterix –> cells driven to cartilage
  3. WTN pathway (LRP5) - paracrine or autocrine signaling
  4. Sclerostin - inhibits WNT LRP5 pathway - inhibits further differentiation/proliferation - induces osteoblast apoptosis - only secreted by osteocytes
  5. ECM production
  6. RANKL expression (OB life starts with release of RANKL to stimulate osteoclasts and break down bone)
  7. OPG secretion (as OB matures, it secretes OPG to stop osteoclastic activity and begin building)
247
Q

Characterize the effect of estrogen on osteoblasts

A
  1. Increased OPG production - greater survival of OB
  2. Decreased Sclerostin production - more bone production
  3. Decreased RANKL production - greater survival of OB
  4. Increased osteoclast apoptosis
248
Q

How do estrogen and glucocorticoids effect OPG?

A

Estrogen increases OPG production

Glucocorticoids decreases OPG production –> Increased apoptosis in osteocytes and osteoblasts, decreased in osteoclasts –> decreased bone formation, increased resorption
Short term –> GCC initially cause a rapid decrease in apoptosis and induce survival of osteoclasts. This leads to a small burst in resorption.
Long term –> GCC cause decreases in Ob proliferation. Cells that survive begin to produce increased levels of RANKL and less OPG. Bone formation goes down due to fewer cells, resorption goes up for the same reason plus increased RANKL production –> Osteoporosis

249
Q

Explain how bisphosphonates effect bone growth

A

BP interrupt the production of signaling proteins and the maintenance of the ruffled border of osteoclasts –> inhibited bone resorption

BP attach to hydroxyapatite binding sites on bony surfaces (semi-permanent) –> osteoclast resorbs BP impregnated bone and cannot form ruffled border to adhere to bony surface, or produce protons necessary for continued resorption

BP also reduce osteoclasts activity by decreasing osteoclast progenitor development, promoting osteoclast apoptosis

BP also prevents osteocyte and osteoblast apoptosis

250
Q

Describe how a RANKL antagonist (Denosumab) inhibits osteoclast proliferation, differentiation, and resorption.

A

Denosumab binds to RANKL to preventing binding to RANK –> prevents osteoclast differentiation/proliferations –> prevents bone resorption

251
Q

Explain how Intermittent Teriparatide affects bone remodeling

A

Increased OB proliferation/survival - lay down ~30% more bone
Increased osteocyte survival
Increased bone formation
Delayed, increased RANKL expression –> increased resorption

Pulsative waves allow mature OB to live longer forming bone while pumping out OPG before any great amount of RANKL expression by new OB –> ~ 3 month bone formation head start –> PTH eventually kickstarts resorption –> OC begin to resorb

252
Q

What is the purpose of the salvage pathway and why is it easily used?

A

Saves bases for reuse when not needed for nucleotides
Major source of lymphocytes
Energetically favorable

253
Q

What are the four stages of bone healing in a fracture?

A

Stage 1 - Inflammation
- hematoma formation
- platelets signal fibroblast & inflammatory cells

Stage 2 - Soft callus
- MSC recruited Fibrin-rich granular tissue form
- VEGF creates new vessels

Stage 3 - Hard Callus
- External hard callus formed
- Low O2 –> chondrocyte differentiation
- Woven bone formed

Stage 4 - Remodeling
- Bone remodels
- Lamellar bone is formed

254
Q

Differentiate between a segmental fracture, avulsion fracture, and comminuted fracture

A

Segmental - Bone broken in two places creating free-floating segment

Avulsion - fragment of bone pulled away from by attachment of ligament of tendon

Comminuted - bone shattered into multiple fragments
- complicated treatment, slower healing

255
Q

Differentiate between an impacted fracture and compression fracture

A

Impacted - one fragment driven into another causing compression
- usually from one great force

Compression - Bone crushed or collapsed from loss of integrity
- vertebra, common in osteoporosis

256
Q

Define greenstick fracture

A

Not completely fractured through with one side of the bone fractures and other side bending

257
Q

Outline the Salter-Harris classification of fractures

A

Type 1 - Straight across the growth plate
Type 2 - Above the growth plate
Type 3 - beLow the growth plate Type 4 - Through the growth plate (above and below)
Type 5 - ERasure of growth plate (crushed)

SALTER

258
Q

Define fascial creep

A

deformation of fascia at sufficient tensile prolonged stretch

Describes how it deforms over pressure and stress, and feeling under our hands when we manipulate it

259
Q
A

Unit 2 MTP (5 decks)

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