Skeletal vs. Smooth vs. Cardiac Muscle

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Cliff Huxtable

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What are the differences between these types?
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Cliff Huxtable said:
What are the differences between these types?
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Skeletal muscle is made of bone (ie. skeletal system). Smooth muscle feels like silk (they will provide a sample if asked on usmle) and cardiac muscle is what you use to drive a car when you are manic.

:sleep:
 
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One major thing is skeletal muscle is innervated by the somatic nervous system(SNS), while smooth muscle is innervated by the ANS and is seen in organs, blood vessels, glands, etc (internal orgrans). Skeletal muscle control is conscious (you can contract and dilate via voluntary conscious control) and smooth muscle contraction is unconscious (can't vasodilate just by think you want to LOL). SNS synapses are fast and myelinated vs ANS synapses which are slow and unmyelinated. Skeletal muscle injuries present with somatic pain vs smooth muscle pain which is visceral and is either painless or referred pain (internal hemorrhoids --> painless/visceral innervation vs external hemorrhoids --> painful/somatic innervation). Skeletal m is striated, smooth m is not striated (exception is cardiac smooth m which is striated); clinical significance seen in the esophagus where the upper 1/3 is striated(skeletal), middle is both, and lower 1/3 is smooth.

Skeletal muscle fibres contract with different velocities, depending on their ability to split ATP. Faster contracting fibres have greater ability to split ATP. Based on various structural and functional characteristics, skeletal muscle fibres are classified into three types: Type I fibres, Type II B fibres and type II A fibres.

In terms of drugs, skeletal m only has N receptors and ACh neurotransmitters, while smooth muscle have multiple receptors (M, N, a1, a2, b1, b2, d, etc) and neurotransmitters (ACh, NE, Epi, Dopamine). Think about this when getting questions about certain drug effects, and whether that drug innervates skeletal m, smooth m or both.
 
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Cliff Huxtable said:
Do both skeletal and cardiac muscles have calcium-induced calcium release?
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No.
Skeletal m has the ryanodine receptor which causes opening of the SR releasing Ca, the opening being d/t the depolarisation signal going down the T-tubule.
Cardiac m contraction involves outside Ca coming in & causing the SR to open releasing Ca.

Also if you don't have BRS physio.....buy it... Nice charts for all these types of "compare & contrast" scenarios.
 
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Cliff Huxtable said:
How about smooth muscle?
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Mr. Madison, what you've just said is one of the most insanely idiotic things I have ever heard. At no point in your rambling, incoherent response were you even close to anything that could be considered a rational thought. Everyone in this room is now dumber for having listened to it. I award you no points, and may God have mercy on your soul.
 
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A 4-year-old girl presents with chorea, diaphoresis, and nausea after ingesting a Chinese popsicle that was later found to be contaminated with arsenic and carbon tetrachloride. It was 105 degrees outside and she has not had anything to drink today, but she did ingest 20 of her mother's oxycodone thinking they were mints. What is the likely mechanism of the child's metabolic disorder?
 
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ZagDoc said:
A 4-year-old girl presents with chorea, diaphoresis, and nausea after ingesting a Chinese popsicle that was later found to be contaminated with arsenic and carbon tetrachloride. It was 105 degrees outside and she has not had anything to drink today, but she did ingest 20 of her mother's oxycodone thinking they were mints. What is the likely mechanism of the child's metabolic disorder?
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Lupus :laugh:
 
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In Klinefelter's syndrome (47 XXY), there's primary gonadal failure, leading to decreased testosterone and increased levels of FSH and LH. Patients often have increased estradiol because LH continues to act on Leydig cells which will make androstenedione which gets aromatized by adipose tissue. My question is: why are these patients stereotypically tall? Estrogen is needed to fuse the epiphyseal plates, and these patients have increased circulating estrogen, so how come they're tall and not short? Does it have to do with delayed puberty? Do the bones have to be primed by androgen before estrogen can fuse the plates?
 
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Do ACE Inhibitors normall vasodilate the efferent renal arteriole but in the case of bilateral renal artery stenosis they vasoconstrict the efferent renal arteriole?

Or do they ALWAYS constrict the efferent renal arteriole?
 
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Cliff Huxtable said:
Do ACE Inhibitors normall vasodilate the efferent renal arteriole but in the case of bilateral renal artery stenosis they vasoconstrict the efferent renal arteriole?

Or do they ALWAYS constrict the efferent renal arteriole?
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Wrong post!
 
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Cliff Huxtable said:
Do ACE Inhibitors normall vasodilate the efferent renal arteriole but in the case of bilateral renal artery stenosis they vasoconstrict the efferent renal arteriole?

Or do they ALWAYS constrict the efferent renal arteriole?
Click to expand...


Ace Inhibitors always dilate the efferent. people w/ renal artery stenosis rely on an AT-II mediated constriction of the efferent arteriole to protect their GFR.
 
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Why is the medial circumflex artery more often damaged in a pelvic fracture as opposed to the lateral circumflex artery?
 
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A 7 year-old boy with Kearns-Sayre syndrome was fishing in S. America when he was bitten by an Amazon River Dolphin. According to local custom he was fed 12L of kerosene to treat the bite. He presents to the ER with diplopia and a diffuse non-pruritic truncal rash. His mother states he used to always do well in school but lately his grades have been slipping. What will most likely be seen on MRI of this child's head?
 
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ZagDoc said:
A 7 year-old boy with Kearns-Sayre syndrome was fishing in S. America when he was bitten by an Amazon River Dolphin. According to local custom he was fed 12L of kerosene to treat the bite. He presents to the ER with diplopia and a diffuse non-pruritic truncal rash. His mother states he used to always do well in school but lately his grades have been slipping. What will most likely be seen on MRI of this child's head?
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Dolphin eggs?:confused:
 
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Cliff Huxtable said:
How do you think about TIBC when you figure out anemias?
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Id look at it only when you look at anemia of chronic dz vs iron deficiency. Total iron binding capacity is low in aocd but high in iron deficiency because, well ferritin levels are low and transferrin tends to be the opposite of ferritin

hope that made sense
 
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ENThopeful said:
Id look at it only when you look at anemia of chronic dz vs iron deficiency. Total iron binding capacity is low in aocd but high in iron deficiency because, well ferritin levels are low and transferrin tends to be the opposite of ferritin

hope that made sense
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It's easy to reason out when you consider what the body is hoping to accomplish in each situation.

In iron def anemia, TIBC is high because the body is desperately trying to hold onto all iron it can to contribute to erythropoiesis.

In AoCD, the body is in a chronic inflammatory state and the immune system assumes it is under the attack. As a result, it wants to sequester iron away, because iron is more important to growing bacteria than it is to us (said facetiously). As a result, TIBC is down.
 
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