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MSS 1 > Exam 2 Drugs and Diseases > Flashcards

Exam 2 Drugs and Diseases Flashcards

1
Q

muscarinic (M) receptor agonists

A

acetylcholine, bethanechol

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2
Q

Muscarinic antagonists:

A

atropine, ipratropium

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3
Q

α adrenergic receptor agonists

A
  • norepinephrine, epinephrine, phenylephrine (α1), clonidine (α2)
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4
Q

α adrenergic antagonists

A

phentolamine (non-selective)

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5
Q

β adrenergic agonists

A
  • norepinephrine, epinephrine, levabuterol, albuterol (β2)
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6
Q

β adrenergic antagonists

A

propanolol (non-selective)

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7
Q

Effects of SNS vs PSNS

A
  • smooth muscles in eye
    • 2 sets of smooth muscles in the eye: dilator papillae (radial) and constrictor papillae (circular or iris sphincter)
    • Dilator papillae innervated by sympathetic fibers causes constriction via α1 adrenergic receptor (mydriasis- increased pupil size)
    • Constrictor papillae innervated by PSNS causes constriction by M3 receptor (mitosis- decreased pupil size)
    • PSNS is dominant in the eye

Typical changes in SNS activation

* Increased HR and BP and increased blood Glc
* Decreased GI mobility (relaxation) and increased urinary and bowel retention
* Bronchodilation and mydriasis
* Blood flow shifts from visceral organs to skeletal muscle

Typical changes in PSNS activation

* Decreased HR, BP, and blood Glc
* Increased GI motility (contraction) and urinary and bowel movement
* Bronchoconstriction and miosis
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8
Q

Sympathomimetics

A

drugs that mimic NE or E: targets are post sympathetic and parasympathetic adrenergic receptors, NT release, storage, and re-uptake

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9
Q

Parasympathetomimetics

A

drugs that mimic ACh: targets are postsynaptic and presynaptic nicotinic and muscarinic AChRs NT release

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10
Q

efficacy vs potency

A
  • Efficacy: maximal response from a drug: drug with a larger response has a higher efficacy
  • Potency: how much of a drug is needed to achieve the result: drug that only needs 100 μg/mL is more potent than a drug that needs 500 μg/mL
  • Epinephrine has a higher efficacy in α receptors but a higher potency in β receptors
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11
Q

Epinephrine metabolism

A
  • Degradation: through MAO (monoamine oxidase) and COMT (catechol-O-methyltransferase)
  • E and NE are degraded to metanephrine and nometanephrine by COMT or to dihydroxymandelic acid by MAO
  • dihydroxymandelic acid is then degraded to 3-methoxy-4-hydroxy-mandelic acid (aka vanilylmandelic acid VMA) by COMT and metanephrine and nometanephrine are degraded to VMA by MAO
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12
Q

Phenylephrine

A
  • α1 agonist: causes vasoconstriction (not methylated by COMT)
  • Used to support blood pressure in septic shock and to prevent cerebral ischemia, treatment of hypotension, nasal decongestion, mydriasis, and helps treat open-angle glaucoma (helps unblock trabecular meshwork)
  • Adverse reaction: hypertension and angina (myocardial ischemia)
  • Absolute contraindications: hypertension and/or ventricular tachycardia, closed-angle glaucoma, and neonates/infants (more susceptible to cardiac effects)
  • Black box warning- needs experienced clinician
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13
Q

Clonidine

A
  • α2 agonist: causes decreased release of NE because α2 is expressed in both the presynaptic and postsynaptic cells; so NE release is inhibited
  • Causes decreased HR and BP by decreasing sympathetic output through decreased NE output by inhibiting Ca influx in the presynaptic cell and activates K channels to cause hyperpolarization
  • α2 receptors are also present on the postsynaptic cell, so causes contraction mildly, but this effect is overwhelmed by the PSNS input from the CNS (SNS output is inhibited by this drug), so leads to vasodilation because the peripheral signal for vasoconstriction is much less than the central signal for vasodilation
  • Note: drugs that don’t cross blood brain barrier do not cause decrease in BP
  • Used for hypertension and severe and neuropathic pain (inhibits α2 receptors on pain neurons)
  • Major adverse reactions:
    • Hypotension, heart failure, abdominal pain, severe hypertension (rebound) during withdrawal (need to come off slowly), fatigue/drowsiness, xerostomia (dry mouth), nausea/constipation
    • No absolute contraindications an
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14
Q
  • Phentolamine
A
  • Non-selective short-acting α agonist
  • α1 block causes vasodilation (inhibits resistance to vasodilation), leading to decreased peripheral resistance and decreased BP
  • α2 block leads to increased NE release, leading to increased cardiac stimulation which increases HR and oxygen demand (can lead to ischemia)
  • Uses:
    • pheochromocytoma- hypertensive crisis cased by adrenal gland tumor that secretes large amounts of catecholamines. α blockers reduce BP until tumor is surgically removed (also use β blockers to inhibit tachycardia) (will be tested on later)
    • Prevention of tissue necrosis: α blockers can reverse excessive vasoconstriction by NE extravasation, E effects in local anesthesia, frostbite, and Reynaud syndrome
  • Major adverse reactions: hypotension, tachycardia/arrhythmias, nasal congestion, weakness/dizziness
  • Absolute contraindications: angina (because it increases oxygen demand) and myocardial infarction
  • Black box warning-none
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15
Q
  • Levabuterol and albuterol
A
  • Relatively selective short acting β2 agonists in smooth muscle of lungs, uterus, and peripheral vasculature that cause bronchodilation and vasodilation, gluconeogenesis in liver to increase blood Glc, and increased K uptake which decreases blood K
  • Albuterol is a racemic texture of R/S isomers, the R isomer is levabuterol which is a bronchodilator (the S isomer lacks bronchodilator effects and may be bronchoconstrictor)
  • Major uses:
    • Bronchospasm in asthema
    • Hyperkalemia
  • Black box warning- none
  • Major adverse reactions: rhinitis, muscle tremors, hyperglycemia, hypokalemia, restlessness, tachycardia/arrhythmias
  • Absolute contraindications: hypersensitivity to levabuterol/albuterol
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16
Q

Propanolol

A
  • Non-selective β antagonist
  • Β 1 block leads to decreased HR and BP
  • Β 2 block leads to increased peripheral vasoconstriction and bronchoconstriciton
  • Β 1 has a higher efficacy than β2 so overall effect is decrease in BP
  • Propanolol is racemic mixture of L and D isomers; only L isomer blocks β adrenergic receptors
  • Uses:
    • Hypertension (not first line therapy)
    • Angina (decreases oxygen demand
  • Black box warning- against rapid discontinuation (similar to clonidine)
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17
Q

Adrenergic receptors

A
  • α1: linked to Gq/11 receptors which use PLC-IP3 cascade
  • α2: linked to Gi receptor that uses cAMP-PKA cascade leads to inhibition
  • β: linked to Gs receptor that also acts by cAMP-PKA cascade leads to stimulation
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18
Q

Cholinergic receptors

A
  • Either muscarinic (metabotropic; M1-5 GPCRs) or nicotinic (ionotropic; muscle type: α1, β1, δ, or γ (embryonic)/ ε (adult)/ neuronal type: α 2-10, β 2-4)
  • ACh is synthesized in nerve from choline and acetyl coA through choline acyltransferase (CAT)
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19
Q

Major problems with muscarinic receptors

A
  • defecation
  • Nausea
  • Urination
  • Motility and Pain (GI)
  • Miosis
  • Hypotension
  • Bradycardia
  • Bronchoconstriction
  • Bronchorrhea (hypersecretion of sputum)
  • Emesis (vomiting)
  • Lacrimation
  • Salivations
  • Secretions
  • Sweating (sympathetic)
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20
Q

Bethanechol

A
  • Nonselective mAChR agonist (not hydrolyzed by ChEs)
  • Uses: treatment of urinary retention and stimulation of GI motility
  • Black box warning-none
  • Adverse reactions: typical muscarinic adverse reactions
  • Absolue contraindications (incomplete list): asthma, bradycardia, peptic ulcer, GI/urinary obstruction, hypotension, etc
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21
Q

Atropine

A
  • Nonselective competitive antagonist of mAChRs
  • Crosses blood brain barrier (tertiary amine)
  • Inhibits “typical muscarinic adverse reactions” above
  • Uses: treating bradycardia, adjunct anesthetic agent (reduce secretions prior to surgery), causes mydriasis (ophthalmic procedures), and treatment of nerve agent and insecticide poisoning
  • Black box warning- none
  • Adverse reactions (typical anti-muscarinic effects): Xerostomia (dry mouth), Blurred vision, Cycloplegia (loss of accommodation), Mydriasis, Constipation Ileus(decreased GI motility), Tachychardia Urinary retention, Central effects e.g., hallucinations, confusion.
  • Absolute contraindications (incomplete list): closed angle glaucoma (because of mydriasis leading to increased intraocular pressure), prostatic hyperplasia (because of urinary retention), pyloric stenosis (because of decreased GI motility
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22
Q

Ipratropium

A
  • Nonselective competitive antagonist of mAChRs (like atropine)
  • Twice as potent a bronchodilator and does not cross blood brain barrier (quaternary amine) so no CNS effects
  • Allied topically via an inhaler
  • Major uses: first line therapy for COPD
  • Black box warning- none
  • Adverse reactions: xerostomia, dizziness, cough, nausea, bad taste
  • Absolute contraindications: bromide hypersensitivity
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23
Q

Edrophonium

A
  • Rapid acting short duration ChE inhibitor, so good for diagnosing MG
  • Onset of action: <2 min IV and <10 min IM (intramuscular)
  • Duration: dose dependent- <60 min IV and < 30 min IM
  • Main uses: assessing whether ChEI therapy can be effective, diagnosing MG, reversing effects of non-polarizing NMJ blockers, and differentiating cholinergic and myasthenia crises
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24
Q
  • Neostagmine
A
  • Oral (bromide) and parenteral (methyl sulfate; IV and IM) ChE inhibitor approved for treatment of MG
  • Onset of action: 2-4 hrs PO, <20 min IV, <30 min IM
  • Duration of action: dose dependent- <4 hrs
  • Main uses: treatment of MG and reversing effects of non polarizing NMJ blockers
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25
Q

Pralidoxime

A
  • AChE reactivator
    • Pralidoxime (aka 2-PAM)- disconnects organophosphates from AChE and makes AChE work again- used as antidote for organophosphates. Should be used with mAChR antagonists (e.g. atropine) and respiratory support if possible. Atropine neutralizes effects of excessive ACh while AChE is recovering. Pralidoxime + atropine is 35x more effective than atropine alone
      • Onset: <15 min
      • Does not penetrate blood brain barrier
      • Side effects are minimal at therapeutic doses, but acid IV administration will cause hypertension, tachycardia, and muscle rigidity and transient paralysis
      • No absolute contraindications
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26
Q

Nicotinic Cholinergic receptors

A
  • Formed as 5 subunit complexes that include subunits α 1, β 1, δ, and γ (embryonic)/ ε (adult) for muscles and α 2-10 and β 2-4 on neurons that can make different combinations with different functions or levels of functionality. Need at least 2 alpha subunits to have a working channel because need 2 ACh binding sites and only α subunits have these binding sites
  • nAChRs are ion channels (ionotropic)
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27
Q
  • nAChRs vs mAChRs:
A
  • mAChRs respond slower
  • Activation of mAChRs cause excitation or inhibition
  • mAChRs are not on skeletal muscle, only smooth and cardiac muscle
  • nAChRs are always excitatory because they are nonselective channels that allow Na, K, and Ca to cross, so leads to depolarization
  • mAChRs can be both excitatory or inhibitory. Mainly K channels, so mostly inhibitory
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28
Q

Nondepolarizing blockers

A

nAChR competitive antagonists- no depolarization, only paralysis; binds to active site, but prevents channel from opening: tubocurarine (non selective, no longer used), pancuronium, rocuronium, α-bungarotoxin (research tool)

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29
Q

Depolarizing blockers

A

nAChR agonists- depolarization, then paralysis: succinylcholine aka suxamethonium

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30
Q

components of depolarizing NMJ block

A
  • depolarization (no muscle response) and desensitization (no AChR response)- e.g. succinylcholine is not hydrolyzed by AChE; only by PChE
    • Depolarization (phase I)- results in muscle contraction/fasciculation
    • Followed by phase II (flaccid) muscle paralysis resulting from nAChR desensitization and continuing membrane depolarization because of the continuous presence of succinylcholine (note: ligand gated channels undergo desensitization similar to inactivation of Na voltage gated channels where they have a pseudo refractory period; the cells will therefore not be sensitive to new ACh during phase II)
    • AChE inhibitors are used to augment nAChR/muscle responses during the early stage of phase I but not early stage of phase II (because nAChRs are desensitized)
    • AChE inhibitors augment nAChR/ muscle responses during late stage of phase II because succinylcholine is partially cleared from cleft by diffusion
    • Mechanisms:
      • Non depolarizing blockers bind to active site, but prevent channel from opening
      • Depolarizing causes channel to open, but can go into the channel to block it up
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31
Q
  • Tubocurarine
A
  • Quaternary ammonium, long acting, non depolarizing NMJ blocker
  • Used for skeletal muscle during surgery and facilitation of artificial/mechanical ventilation (not used anymore)
  • Adverse reactions: apnea/dyspnea, respiratory depression, high potential for histamine release (which could lead to hyper salivation, vasodilation, and hypotension), and ganglionic block (which could inhibit GI tract motility and tone)
  • Absolute contraindications: none
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32
Q
  • Procuronium
A
  • Quaternary ammonium long lasting, non depolarizing NMJ blocker: ~5x more potent than tubocurarine
  • Clinical uses: skeletal muscle relaxation during surgery and facilitation of artificial/mechanical ventialtion
  • Major adverse reactions: apnea/dyspnea and respiratory depression. Causes minimal histamine release and minimal ganglionic block and vagolytic activity (i.e. more potent with fewer side effects than tubocurarine)
  • Absolute contraindications: bromide hypersensitivity or in neonates (for benzyl alcohol-containing formulations
  • Black box warning: none
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33
Q

Rocuronium

A

Short acting, rapid onset NMJ blocker similar to pancuronium

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34
Q

Succinylcholine

A
  • Highly ionized, does not cross BBB
  • Competes with ACh for nAChRs in NMJ and activates nAChRs
  • Resists AChE which prolongs muscle depolarization and desensitization
  • Susceptible to pChE
  • Adverse effects: prolonged respiratory depression, may cease malignant hyperthermia (treated with dantrolene), may induce vagal stimulation (bradycardia and hypotension), some histamine release, and hyperkalemia (due to excessive K release from neurons). 10% is excreted in urine, rest is hydrolyzed slowly by PChE; due to slow hydrolysis, can accumulate and cause prolonged apnea and patients with lower PChE levels may experience longer durations of action
  • Black box warning: pediatric patients: only in emergency intubation because of ventricular dysrhythmias and cardiac arrest have been reported
35
Q

Adrenergic receptor agonists effects

A
  • Adrenergic receptor agonists are non-selective
    • Epinephrine is non selective for α and β receptors
    • Causes vasoconstriction (α1) and cardiac stimulation (β1) and causes dilation of vessels in skeletal muscle (β2): leads to increased blood flow to skeletal muscle through increased cardiac output and rerouting bloodflow (exception- pulmonary hypoxia causes hypoxic vasoconstriction)
    • Norepinephrine is non selective, but works on α and β1»> β2
    • NE acts as vasoconstrictor (α1) and cardiac stimulant (β1)
36
Q

ChEI effects at NMJ

A

reversible ChEIs can prolong activation of ACh and reverse non-depolarizing NMJ block, but does not work on depolarizing NMJ blockers because they work by the same mechanism as ACh, so increased ACh will just exacerbate the problem of desensitization

37
Q
  • Myasthenia gravis (MG)
A
  • Autoimmune disorder where Abs are released that target the muscle nAChRs and cause their destruction
  • Symptoms: extremem muscle weakness, dysphagia (difficulty swallowing), diplopia (double vision), ptosis (eyelid drooping), and respiratory depression (myasthenia crisis)
  • Cases can be both congenital or acquired. MG patients are highly sensitive to NMJ blockers
  • Diagnosis: edroponium test: temporary increase in muscle strength, blood analysis, repetitive nerve stimulation: decreased decline in muscle actin potential (accumulation of weakness; progressive decrease of AP amplitude), single fiber electromyography (SFEMG): detects impaired nerve to muscle transmission (non specific- e.g. lamber-eaton, amyotrophic lateral sclerosis-ALS), or imaging like CT or MRI to detect thymoma
  • Treatments: immunosuppression, plasmapheresis, IV IgG, thymectomy, or AChEI that does not cross BBB) e.g. neostigmine)
38
Q
  • Myastheniac crisis vs cholinergic crisis
A

Cholinergic crisis is overstimulation of cholinergic receptors

  • Both involve muscle weakness and respiratory depression
  • MC is improved by edrophonium, but CC is aggravated by edrophonium
  • CC treatments is removal of AChEI, addition of mAChR antagonists (e.g. atropine) and artificial ventilation if necessary
39
Q
  • Muscle relaxants
A
  • NMJ blockers- produce paralysis for surgery- do not cross BBB so have no CNS activity
  • Spasmolytics- used to treat muscle hyperactivity; include antispacticity drugs (baclofen, dantrolene) or motor nerve blocking drugs (botulinum toxin)
    • Spasticity is increased muscle tone due to hyper excitability of α (lower) motor neurons and resistance to passive movements from damage to upper motor neurons
    • Caused by cycle from OMM that leads to muscle spasticity
    • Drugs that block this are baclofen or tizanidine
40
Q

Dandrolene

A
  • Blocks Ca release from SR by blocking RyRs
  • Uses: malignant hyperthermia crisis (halothane and succinylcholine) and chronic spasticity (from MS, cerebral palsy, stroke, or injury)
  • Absolute contraindications: hepatic diseases
  • Precautions: pregnancy/breast feeding, none for malignant hyperthermia
  • Major adverse reactions: hepatotoxicity, diarrhea, weakness, dizziness, fatigue, general malaise
  • Black box warning: hepatic disease; hepatotoxicity is greater in females >35 yrs old
  • Why dantrolene is not cardiotoxic:
    • Skeletal muscles express type I RyR which is liked to and can be opened by SERCA, but are insensitive to Ca release to be activated
    • In cardiac and smooth muscles, RyR type II is expressed and are sensitive to Ca ions, so can be opened that way
41
Q
  • Malignant hyperthermia
A
  • Rare heritable disorder
  • Can be initiated by some general anesthetics and succinulcholine
  • Signs: muscle stiffness/contracion, increased temp, dark brown urine, hyper metabolism (increased oxygen consumption and increased CO2 production)
  • Causes- accumulation of intracellular CA
  • Dantrolene inhibits RyR and reduces Ca release
42
Q

baclofen

A

Muscle relaxer; antispastic drug

43
Q

tizanidine

A

muscle relaxer; antispastic drug

44
Q

Xerosis

A
  • Dryness of the skin
  • Caused by reduced water content and barrier function of aging epidermis exacerbated by decreased humidity from cold or central heat, irritated by hot water, or harsh soaps
  • Skin findings more often on the legs
  • Rough itchy skin or scales; if severe, may manifest as eczema craquele (dry cracked appearance)- can lead to infection
  • Treatment- decreased temperature of water, reduced bathing frequency, moisturizer after bathing (sedafil is good option), increased water intake, moisturizing agents with lactic acid or α-hydroxyacid, and maybe mild topical corticosteroid; avoid bath oils (bad place to slip) and systemic anti-proritics
45
Q

Onychomycosis

A
  • Caused by dermatophytes, yeasts, and nondermatophytic molds
  • Often preceded by or concomitant with tinea pedis
  • On exam; brownish-yellow nail discoloration and sublingual hyperkeratosis (yellow-brown debris under nail bed
  • Diagnose by KOH preparation or fungal culture
  • Can be treated by Vick’s vapor rub on nail
46
Q
  • Actinic Keratoses
A
  • Also solar keratoses; from UV damage
  • Poorly circumscribed, occasionally scaly
  • Considered premalignant, but mostly resolves without therapy
  • Usually treated by cryotherapy, topical acids, topical 5-fluorouracil, or excision
47
Q

Blepharochalasis/dermatochalasis

A

as opposed to ptosis-drooping of the eye lid which may be neurological; this condition must be treated surgically if affecting vision

48
Q

ectropion and entropion

A

ectropion (eversion) or entropion (inversion) of the lower lid- may cause discomfort or conjunctivitis

49
Q

Agin musculoskeletal system

A
  • Stooped posture, knees and hips flexed, neck tilted, narrowed shoulders, wider pelvis, slower movements, unsteady gait, and less arm swinging may occur
  • Due to decreased water content, increased fibrosis, narrowed joint spaces leading to more viscous synovial fluid
  • Bone mass may also decrease
  • Muscle fiber size decreases, replaced by fat/necrosis and macrophages, decreased mitochondria and ATP activity, decreased Ca release and contractile force, decreased muscle mass, decreased muscle strength, decreased tendon size (sclerosis), and decreased elasticity
  • Changes are more pronounced in the lower limb
  • Increased type I collagen fibers and decreased type II fibers (type I is broader, but not as elastic)
  • This leads to stiffer tendons and leads to increased risk of rupture of tendons and ligaments
50
Q
  • Get up and go test
A
  • Timed from rise from hard-back chair with arms, walk 10 feet, turn, return to chair, and sit down
  • Abnormal if greater than 14 seconds- correlates with increased fall risk
  • Greater than 20 seconds needs comprehensive evaluation
51
Q

Deep tendon reflex changes

A

Deep tendon reflects may also be decreased due to aging IF SYMMETRICAL- asymmetrical reflex changes may indicate neurological problems

52
Q

AHA recommends 4 parts of exercise program

A

aerobic exercise, weigh training, flexibility, and balance training

53
Q

Myosin Cross bridge cycle

A
  • Pi-ADP-myosin binds to the thin filament
  • The “power stroke” caused by the release of Pi causes the myosin to pull itself along the thin filament
  • Myosin then releases ADP
  • Myosin then binds ATP and is allowed to release the thin filament
  • ATP hydrolysis causes the myosin to change conformation into the pre-power stroke shape (primed for another stroke)
54
Q
  • Sequence of an action potential in skeletal muscle
A
  • The upper motor neuron transmits a signal down the spinal cord and synapses with a lower motor neuron that takes the signal out to a muscle
  • The release of NT from the presynaptic neuron in the NMJ activates ion channels in the myofibril membrane. The ligand gated Na channels cause a graded potential not enough for AP generation but does cause depolarization enough to activate voltage gated Na channels that are permeable enough to cause an action potential
  • The wave of depolarization in the action potential travels across the sarcolemma and down the T-tubules
  • The T tubules contain a voltage sensitive protein called DHPR that plugs up the SR RyR proteins with a foot protein domain
  • When the AP reaches the DHPR molecules, the foot protein is removed from the RyR channels and it releases Ca ions from the SR
  • The Ca ions interact with the subunits of the troponin-tropomyosin complex and inhibit it, allowing myosin access to the thin filaments
  • Studies have shown that there SR contains all the Ca needed for an action potential. The SR expresses 3 key proteins:
    • Ryanodine receptor (RyR)- releases Ca ions from the SR
    • SERCA- takes the Ca ions back up into the ER; inhibiting SERCA increases muscle contraction force and stimulating it causes the opposite
    • Calsequesterin- Ca binding protein that increases SR capacity for Ca ions
55
Q

Varicose veins

A

vein that becomes so dilated that valves no longer can close and lead to backup because of loss of unidirectional flow

56
Q

Deep vein thrombosis (DVT)

A

clotting caused by veinous stasis; failure of musculovenous pump (from fascial incompetence or muscular inactivity) or external compression of the vein. Can lead to swelling of the leg distal to the blockage and the proximal part throwing off smaller clots. Thrombophlebitis = DVT + inflamation

57
Q

Lymphedema

A
  • obstruction of lymph drainage leading to edema
    • Primary forms are autoimmune, congenital, or rare forms
    • Secondary forms are surgical destruction of lymph nodes/vessels, radiation related scarring, cancer, infection of the nodes, or parasites. These are more common than primary forms
58
Q
  • Patellar reflex
A
  • Myotactic reflex- initiated with a muscle is stretched; tapping patellar ligament causes stretching of quads and leads to loop that causes knee extension
  • Mainly mediated by L4; reflex tests this nerve
59
Q

Calcaneal tendon reflex aka ankle jerk reflex

A

myotactic reflex that is done by tapping on the calcanea ligament (achilles tendon); leads to plantarflexion reflex; tests S1

60
Q

“drop foot”

A

Common fibular nerve is very superficial around the head and neck of fibula so is prone to injury; can be done along with injuries of LCL, fibular head, peroneus and biceps femoris tendons, and proximal tibiofibular ligaments; causes lack of dorsiflexion- “drop foot”

61
Q
  • Shuffling gaits
A

These prioritize static stability- decreased step length, arm swing, and speed and increases step width. Seen in elderly or Parkinson’s patients

62
Q

Steppage gait- dropfoot

A
  • Caused by paralysis/paresis of dorsiflexors
  • Inability to dorsiflex
  • Tibialis anterior performs both concentric and eccentric contractions, so loss leads to toe drag and slapping foot down; may lead to compensation through high stepping or swinging leg outward to avoid foot slap and toe drag
  • May be due to injury to deep fibular nerve
63
Q
  • Trendelenburg gait
A
  • Isometric contractions of hip abductors stabilize and level hip during single leg stance; prevents COG from pulling you laterally toward unsupported leg
  • People with Trendelenburg gait tip towards their unsupported leg during swing phase if the contralateral gluteal region has problems with innervation (if there is a problem with the left gluteal region, there will be leaning to the right side during swing phase)
  • Trendelenburg’s sign
    • Hip drops toward the contralateral side
    • Head and torso deviates towards the ipsilateral (affected) side
64
Q
  • Fracture types
A
  • Simple- bowing (no actual break), greenstick (incomplete break), transverse (strait across), oblique, spiral, longitudinal (along the bone axis), avulsion (where the bone gives way under the stress of the tendon and the tendon pulls off part of the bone)
  • Comminuted- multiple pieces; includes butterfly fractures (union of 3 break lines) and segmental (breaks in 2 places)
  • Fractures are also either simple (not violating the skin) or compound (violating the skin)
  • Fractures are classified by compound or simple and the actual type of fracture
  • Fracture alignment
    • Classified by displacement, angulation, length (shortening or distraction), and rotation of the bone fragments
65
Q
  • Fracture immobilization
A
  • Closed reduction
    • Non-surgical
    • Includes sling, split, casting, percutaneous pinning (pins through the bones), closed reduction and external fixation (plate outside the body)
  • Open reduction (ORIF)- involves surgery; usually a plate is placed in the body to fixate the joint
66
Q
  • DEXA scan for osteoporosis diagnosis
A
  • Dual energy Xray absorptiometry
  • Shoot x rays at 2 different voltages to give different energy X-ray photons that may or may not make it through
  • The denser the bone, the more the lower energy X-rays will be stopped
  • used as a diagnostic test for osteoporosis
67
Q
  • Avascular necrosis
A
  • Occurs when the blood flow to a bone is disrupted and the bone dies
  • If it occurs at the epiphysis, it is avascular necrosis, if in the diaphysis, it is a bone infarct
  • Can occur if the femoral neck is broken, disrupting blood flow from the femur to the femoral head
  • Necrosis looks like more sclerotic areas of the bone where it has died on the distal areas
  • Infarcts look like sclerotic, irregular areas; mostly in the distal femur or proximal tibia
68
Q

Osteoarthritis

A

leads to joint space narrowing, sclerosis on imaging of the joints, and spurring

69
Q

Gout

A
  • leads to cloudy appearance around the joint- tophus; no joint space narrowing
70
Q

Psoriatic arthritis

A

leads to pencil in cup deformity, soft tissue swelling (sausage digits), and joint ankylosis

71
Q

Rheumatoid arthritis

A

leads to loss of joint spaces (almost always bilateral* unlike others), and joints may burrow like femoral head burrowing into the acetabular joint

72
Q
  • Hyalin cartilage
A
  • Cells are single or in groups of 2 or 4
  • Fibers are collagen type II
  • Found at the ends of long bones
  • Supports and reinforces ends, provides cushion, and resists stress
  • Fond in most of the embryonic skeleton, ends of long bones, costal cartilage, nose, trachea, and larynx
  • Chondroblasts become chondrocytes when they are completely encased in cartilage
  • Territorial matrix; where the cartilage stains very dark surrounding an isogenous group of chondrocytes
73
Q
  • Elastic cartilage
A
  • Cells are larger, more numerous, and packed more closely
  • Contains colagen (collagen II) and elastic fibers
  • Has a perichondrium and undergoes appositional growth
  • Functions to maintain shape and structure and allows flexibility
  • Found in the ear, epiglottis, and Eustachian tube
  • Fewer isogenous groups
74
Q

Fibrocartilage

A
  • Cells are fewer, smaller, an in scattered single rows
  • Contains collagen I fibers
  • There is no perichondrium- gets nutrition from surrounding vessels
  • Undergo interstitial growth
  • Function: gives tensile strength and ability to absorb compress shock
  • Found in the intervertebral disks, pubic symphysis, and disks of knee joint
  • Rows of adjoining chondrocytes are called isogenous groups
75
Q

epiphyseal plate divisions

A
  • epiphyseal plate is divided into the resting, proliferating, hypertrophic calcification, and ossification zones from the end toward the diaphysis
    • In the zone of rising, the cells are quiescent and no growth occurs; farthest from the medullary cavity and closest to the epiphysis
    • In the zone of proliferation- larger chondrocytes alleged in stacks that undergo rapid mitotic division
    • In zone of hypertrophy, the cells are enlarged
    • In the zone of falcification, chondrocytes die and the zone is occupied by osteoblasts and osteocytes that lay down minerals that make the matrix opaque
    • In the zone of ossification, the walls between lacunae break and forma channels that become invaded by capillaries and osteoprogenitor cells
76
Q
  • Calcium regulation
A
  • Calcitonin- removes osteoclasts boarder which prevents reabsorption (stimulates calcium storage)
  • Parathyroid hormone (PTH) stimulates osteoclast production (stimulates calcium release from bone)
77
Q
  • Psoas syndrome
A
  • Lower back pain
  • Lumbar lordosis
  • Excessive anterior curvature of lumbar spine may be related to muscular imbalances
  • Anterior pelvic till can also be related to weak abdominal or hamstring muscles
78
Q

Psoas sign: aka Cope’s test or Obraztsova’s sign

A

two methods:

* Passive stretch of right poses in patient laying on side
* Patient asked to fix right thigh at hip agains resistance
* If abdominal pain results (positive) indicated inflammation of appendix
79
Q
  • Vertebrobasilar insufficiency (VBI)
A
  • Impingement of vertebral arteries that leads to insufficient blood flow to the brain
  • Leads to lightheadedness, dizziness, nausea, and vomiting (brainstem centers)
  • Caused by atherosclerosis, mechanical compression during head rotation (trauma, bow hunter’s syndrome), clot formed from prolonged hyperextension of the neck (Beauty parlor stroke), or subclavian seal syndrome (if there is a blockage in the subclavian artery, the blood flow from the contralateral vertebral artery will redirect from the basilar artery and flow the wrong way down the other vertebral artery, leading to VBI)
80
Q
  • Vertebral artery dissection (VAD)
A
  • Micro tear in the tunica media that causes clot formation and stenosis of the artery
    * Caused by physical trauma to the neck or can be spontaneous
    * Symptoms include head pain, vertigo, difficult speaking, impaired coordination, and vision loss
81
Q

botulinum toxin

A
  • Vesicle fusion involves 4 major proteins: synaptotagmin, synaptobrevin, SNAP-25 and syntaxin
  • Synaptotagmin and synaptobrevin are on the vesicular membrane while the other proteins are on the plasma membrane
  • Synaptobrevin, syntaxin, and SNAP25 molecules (2) make a 4 protein complex to dock to vesicles
  • Synaptotagmin senses Ca ions; when Ca is present, synaptotagmin makes contact with the membrane and facilitates fusion, allowing NT to be released
  • This vesicular fusion is prevented by botulinum toxin which blocks vesicular docking and fusion by degrading SNARE proteins
    • Uses for BoTox- opthamology, spasticity, overactive bladder, cosmetic adjustments, chronic migraine prophylaxis, and axillary hyperhidrosis (excessive underarm sweating)
    • Black box warning- risk of adverse effects of BT spread beyond site of injection
82
Q
  • AChE inhibitors:
A
  • Short term: edrophonium (rapid onset <2min and short acting <10-60 min)
  • Intermediate (aka carbamates) neostigmine and physostigmine (long acting 3-4 hrs)
  • Irreversible (by phosphorylation of AChEs): organophosphates (nerve gases like serine, pesticides like malathion, and opthamologic agents like echothiophate)
  • Mechanisms of action: competes with ACh for binding site on AChE
83
Q
  • AChEI toxicity
A
  • Mixture of muscarinic and nicotinic symptoms
  • In children, nicotinic symptoms dominate (unknown reason)
  • Cause of death is respiratory arrest due to bronchoconstriction, bronchorrhea, central respiratory depression, and paralysis of respiratory muscles
  • Muscarinic adverse reactions are in lecture 18
  • Nicotinic adverse reactions: weakness, fasciculations, and respiratory failure
84
Q

O’Donoghue’s Triad

A 
Frequently caused by a blow to the
lateral side of the extended knee or
excessive lateral twisting
• Classic definition (1950s): ACL, MCL,
medial meniscus
• Anatomical reasoning: MCL is attached to
medial meniscus
• Current definition (1990s): ACL, MCL,
lateral meniscus
• Statistical reasoning: athletes are more
likely to tear lateral meniscus

MSS 1 (8 decks)

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