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Medical Physiology > Exam #5: Review Material > Flashcards

Exam #5: Review Material Flashcards

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USMLE® Step 1 flashcards
1
Q

How does smooth muscle differ from skeletal muscle?

A
  • Smooth muscle is non-striated vs. striated skeletal muscle
  • Different types of smooth muscle exist (multi-unit vs. unitary) in different organs
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2
Q

What contractile component is missing from smooth muscle that is present in skeletal muscle?

A

Troponin Complex
- Indicative of a different role of Ca++ in smooth muscle

Smooth muscle does contain actin, myosin, and tropomyosin

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3
Q

How are myosin heads arranged in smooth muscle? How is this different from skeletal muscle?

A

Mysoin heads in smooth muscle are NOT all arranged in the same direction

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4
Q

What takes the place of z-discs in smooth muscle?

A

Dense bodies

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5
Q

What is the function of dense bodies?

A
  • Transmission of force from once cell to another

- Anchor for thin filaments

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6
Q

How does the point of regulation differ from skeletal muscle to smooth muscle?

A

Remember, smooth muscle DOES NOT contain TnC; thus:

Skeletal=

1) Ca++ from SR binds TnC
2) Ca++/TnC= tropomyosin moves to expose myosin binding sites on actin

Smooth

1) Ca++ binds Calmodulin
2) Ca++/Calmodulin increase MLCK
3) MLCK increases Myosin ATPase
4) Phosphorylated myosin binds actin

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7
Q

What is different between contraction of skeletal muscle & smooth muscle?

A

1) In smooth muscle ECF Ca++ is the PRIMARY source of Ca++, NOT SR Ca++ as in skeletal muscle
2) MLCK is only present in smooth muscle
3) Myosin ATPase is constitutively active in skeletal muscle; smooth muscle, this is regulated

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8
Q

What are the signs and symptoms of Type II DM?

A

1) Asymptomatic initially
2) Infections become more frequent b/c of the energy (glucose) source for microorganisms
3) Neuropathy
4) Classic severe insulin deficiency signs occurs late in the progression of symptoms
5) Obesity & metabolic syndrome

*****#4, note that type II DM becomes apparent when the Beta-cells are no longer able to compensate for increased resistance to insulin

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9
Q

What are the distinguishing features between Type I and Type II DM related to B-cell function?

A

Type I= absolute beta cell destruction leading to beta cell destruction
- Decrease in beta-cell mass

Type II= insulin resistance followed by an insulin secretory defect
- Increase in beta-cell mass

*Note that there are 2x subtypes of DM-I, a & b. A= autoimmune, B= idiopathic–diagnosis is based on NOT finding autoantibodies

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10
Q

What are the distinguishing features between Type I and Type II DM related to insulin sensitivity?

A
  • In type-II DM the body is NOT responding to insulin i.e. a decrease in insulin sensitivity, which initially results in an INCREASE in insulin secretion–a compensatory mechanism
  • Type I, the body simply is NOT producing insulin
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11
Q

What are the therapeutic strategies employed & rationale for these strategies in treating Type I DM?

A

1) Diet i.e. balanced carbs, fat, and protein

2) Patient education on:
- Carb counting
- Insulin action
- Blood glucose targets

3) Insulin ABSOLUTELY required it must be non-PO route b/c insulin is a peptide that will be degraded in the GI tract

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12
Q

What are the therapeutic strategies employed & rationale for these strategies in treating Type II DM?

A

First, remember that potential therapies for the DM may have a negative impact on the overall Metabolic Syndrome in DM-II, which presents a challenge to treating DM-II

1) Diet
2) Patient education
3) Pharmacologic strategies

*Insulin is used ONLY when other agents DO NOT allow for achievement of therapeutic goals

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13
Q

What are the acute complications potentially experienced by DM patients? How are these addressed?

A

Hypoglycemia (e.g. insulin overdose)

  • Glucose
  • Glucagon

DKA

  • Restore plasma volume
  • Reduce blood glucose
  • Correct acidosis
  • Replenish electrolytes
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14
Q

Outline the different pharmacological strategies that are used to treat DM-II.

A

1) Increase insulin secretion
2) Increase insulin action
3) Inhibit gluconeogenesis
4) Inhibit glucose digestion & absorption from the GI tract
5) Suppress glucagon secretion

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15
Q

How can you pharmacologically increase insulin secretion in DM-II?

A
  • GLP1 analogs are used to activate GLP1 receptors to promote insulin secretion
  • DPP4 (enzymes that breaks down GLP1) inhibitors, which indirectly promote insulin secretion
  • Inhibition of ATP-sensitive K+ channels on B-cells to eventually cause insulin release
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16
Q

What is the relationship between flow, velocity or flow, and cross-sectional area in the vascular system?

A

v= Q/A

v= velocity of flow (cm/sec)
Q= flow (mL/sec)
A= cross-sectional area (cm2)

*Velocity is slower in larger vessels

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17
Q

What is Ohm’s law as it relates to the vascular system?

A

Q=dP/R

Q= flow (mL/min)
dP= pressure difference mmHg 
R= resistance

*Thus, flow increases with pressure & decrease with increasing resistance–main source of resistance is arterioles.

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18
Q

What is Poiseuille’s Law?

A

R= 8nl/pir4

R= resistance 
n= viscosity of blood 
l= length of BV 
r4= radius raised to 4th power
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19
Q

What is TPR? How does TPR systemic compare to TPR pulmonic?

A

TPR= dP/CO

TPR-systemic= Psystemic-RAP/CO
TPR-pulmonic= Ppulmonic-LAP/CO

*****Note, CO= HR x SV
Also, TPR ~MAP/CO

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20
Q

TEMPERATURE INCREASE–Explain temperature-induced changes in skin blood flow, sweating, shivering, thermogenesis, & piloerection.

A

Generally, remember that the temperature regulating center is located in the anterior hypothalamus. In response to temperature increase, mechanisms are activated to increase heat-loss:

1) Vasodilation= warm blood from core at surface–>heat loss to environment
- Alpha-1 adrenergic inhibition
2) Sweating leads to evaporation & heat loss
- SNS CHOLINERGIC stim.
3) Shivering, thermogenesis, piloerection are INHIBITED

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21
Q

TEMPERATURE DECREASE–Explain temperature-induced changes in skin blood flow, sweating, shivering, thermogenesis, piloerection.

A

Generally, remember that the temperature regulating center is located in the anterior hypothalamus. In response to temperature increase, mechanisms are activated to increase heat-loss:

SNS:

1) Vasoconstriction= decreased thermal conductivity
- Alpha-1 mediated/ NOREPINEPHRINE
2) Thermogenesis= metabolic generation of heat
- Beta-adrenergic mediated/ EPINEPHRINE
- PNS–>TRH–>TSH–Thyroxine

Posterior Hypothalamus
3) Shivering= skeletal muscle heat generation

Sweating is inhibited

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22
Q

What are the differences between myelinated & unmyelinated nerves? Specifically, where are the voltage-gated Na+ channels? Which conducts more rapidly? Which conducts more efficiently?

A

Myelinated nerves are myelinated & non-myelinated ones are not.

  • Nodes of Ranvier
  • Myelinated neurons BOTH conduct more rapidly & are more efficient
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23
Q

How does myasthenia gravis affect synaptic transmission? is the problem pre-synaptic or post-synaptic? Is this an autoimmune disease?

A
  • Autoimmune
  • Post-synaptic
  • Antibodies against NAChR, an important mediator of EPPs
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24
Q

How does Eaton-Lambert Syndrome affect synaptic transmission? is the problem pre-synaptic or post-synaptic? Is this an autoimmune disease?

A
  • Often occurs in patients with small-cell carcinoma of the lung (& breast cancer)
  • Patients have antibodies to voltage gated Ca++ channels
  • Autoimmune & pre-synaptic
  • Less Ca++ enters pre-synaptic terminals; thus, less ACh is released, which results in muscle weakness
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25
Q

How does botulinum toxin affect synaptic transmission? is the problem pre-synaptic or post-synaptic? Is this an autoimmune disease?

A
  • Botulinum toxins cleave SNARE proteins*
  • Vesicles will not properly dock to pre-synaptic membrane
  • ACh will not be released
  • Symptoms:
    1) NMJ paralysis
    2) Muscle weakness

*As does tetanus toxin, but tetanus causes tetanic contraction.

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26
Q

How does a-bugarotoxin affect synaptic transmission? is the problem pre-synaptic or post-synaptic? Is this an autoimmune disease?

A
  • A peptide from the venom of a banded krait (snake)
  • Irreversibly blocks NAChR
  • Post-synaptic
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27
Q

What is the difference between GPIba, GPVI, GPIIb/IIIa

A
  • GPIba binds vFW to mediate platelet tethering
  • GPVI binds collagen for strong platelet adhesion & activation
  • GPIIb/IIIa binds fibrinogen, forming the platelet plug
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28
Q

What is the P2Y12 receptor? What drug antagonises this receptor?

A

Is the receptor for ADP on platelets, which leads to platelet activation

*Plavix is a P2Y12 antagonist

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29
Q

What are PARs? Why are PARs important?

A

PAR stands for “Protease activated receptors,” which are GPCRs on the surface of platelets that are activated by thrombin

*Activation of PARs leads to further platelet activation & is important because this links the platelet & coagulation systems

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30
Q

What is the Thromboxane A2 receptor?

A

A platelet receptor

Thromboxane A2 works in an autocrine fashion, increasing platelet activation; it also is a vasoconstrictor

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31
Q

What are Collagen, vWF, and fibrinogen ligands for?

A 
Collagen= GPVI 
vFW= GPIba 
Fibrinogen= GPIIb/IIIa
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32
Q

What are Thromboxane A2, ADP, & thrombin ligands for?

A

TXA2R
P2Y12R (plavix antagonist)
PARs

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33
Q

Outline the vascular response to tissue damage. Specifically address the functions of ADP, 5-HT, and Thromboxane A2.

A

1) Damaged tissue secretes factors that cause vasoconstriction
2) Platelets become activated
3) Activated platelets secrete Thromboxane A2 & Serotonin, leading to further vasoconstriction

Vasoconstriction prevents blood loss & slows flow to give platelets a better chance of adhering.

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34
Q

Describe the effects of constricting either the afferent or the efferent arteriole on renal blood flow (RBF).

A 
Afferent= decrease RBF 
Efferent= decrease RBF
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35
Q

Describe the effects of constricting either the afferent or the efferent arteriole on GFR.

A 
Afferent= decreased GFR 
Efferent= increased GFR
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36
Q

How could you increase the glomerular hydrostatic pressure by constricting the efferent or afferent arterioles?

A

Constricting the efferent arteriole

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37
Q

What is the source of fibroblast growth factor 23 (FGF 23).

A

Osteoblasts and osteocytes in bone

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38
Q

What is FGF23?

A

“fibroblast growth factor 23”

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39
Q

What are the effects of FGF23 on the kidney?

A

1) Decreased reabsorption of phosphate

2) Decreases the production of calcitriol

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40
Q

What stimulates the secretion of FGF23?

A

1) Elevated phosphate levels

2) Calcitriol i.e. active Vitamin D

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41
Q

What are the relationships between FGF23 and parathyroid hormone and calcitriol and their actions?

A

Vitamin D= increased reabsorption of Ca++ & phosphate

FGF23= decreased reabsorption of Ca++ & phosphate

PTH= increased absorption of Ca++. decreased absorption of phosphate

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42
Q

How does the autonomic nervous system differ from the somatic nervous system in terms of neruons?

A
  • In the somatic nervous system, there is one large neuron that synapses directly on the effect cell
  • In the ANS, there are two neurons (preganglionic & post ganglionic, with an intervening ganglia)
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43
Q

How do the sympathetic & parasympathetic nervous systems differ organization of the neurons?

A
  • Sympathetic= Short pre-ganglionic & long post-ganlgionic fiber
  • Parasympathetic= Long pre-ganglion & short post-ganglionic

*Note that the the ganglia of the PNS are clustered within the walls of visceral organs

44
Q

What is the alternate name for the sympathetic nervous system?

A

Thoraco-lumbar division

45
Q

What is the intermediolateral cell column?

A
  • Lateral horn of the spinal cord

- Location of the cell bodies of autonomic ganglia

46
Q

Describe the path of sympathetic outflow.

A

1) Cell body in the intermediolateral column
2) Preganglionic axon exits the spinal cord via the ventral root w/ somatic motor neurons
3) Diverge from somatic & enter the white rami communicantes

47
Q

Describe cranial outflow.

A
  • Preganglionic fibers follow certain cranial nerves
  • Ganglia lie very close to target organs

Specific cranial nerves= oculumotor, fascial, glossopharyngeal, & vagus

48
Q

Describe sacral outflow.

A
  • Parasymathetic fibers emerge from the spinal cord in a bundle known as the nervi erigentes
  • Synapse with pelvic ganglia
  • Short postganglionic fibers to target organs
49
Q

What is the enteric nervous system?

A

Two ganglia sandwhiched between the layers of the gut:

  • Myenteric (Auerbach’s)
  • Submucosal (Meissner’s)
50
Q

Specifically, where is the myenteric plexus located? What does the myenteric plexus control?

A
  • Between the external longitudinal & deep circular smooth muscle layers
  • Motility
51
Q

Specifically, where is the submucosal plexus located? What does the submocosal plexus control?

A
  • Between the circular muscularis mucosae

- Ion & fluid transport

52
Q

What NT is released from all of the preganglionic fibers?

A

ACh

*Regardless of system, all preganglionic fibers release ACh

53
Q

What do the postganglionic fibers of the PNS release?

A

ACh

54
Q

What do the postganglionic fibers of the SNS release?

A

NE/Epi or DA

55
Q

What is the exception to postganglionic fibers of the SNS releasing NE/Epi or DA?

A

Thermoregulatory sweat glands, which posses muscarinic receptors & respond to ACh

56
Q

What neurotransmitter do postganglionic fibers to the renal vascular smooth muscle release?

A

DA

57
Q

What NTs are released by the adrenal medulla?

A

Epi & NE

58
Q

What receptors are present in the target organs of the PNS?

A

Muscarinic ACh

59
Q

What receptors are present in the thermoregulatory sweat glands?

A

Muscarinic ACh

60
Q

What receptors are present in the target organs of the SNS? What are the two exceptions to this?

A
  • Alpha & Beta Adrenergic
  • Exceptions:
    1) thermoregulatory sweat
    2) renal vasculature
61
Q

What receptors are present in the renal vasculature?

A

DA-1

62
Q

What receptors are present in skeletal muscle?

A

Nicotinic ACh

63
Q

How is ACh synthesized?

A

1) Uptake of choline from the ECF via the Na+ dependent choline transporter (CHT)
2) Conjugation by ChAT (AcetylCoA + Choline)
3) Final product: ACh

Note that acetylcholine is synthesized in BOTH the cytoplasm & in the mitochondria. ChAT= choline acteyltransferase

64
Q

What drug can block the choline transporter (CHT)?

A

Hemicholiniums

*Note that these are not used clinically.

65
Q

How is ACh stored?

A

Once ACh is synthesized, it is transported into the storage vesicle via the “vesicle assocaited transporter” (VAT)

66
Q

What drug blocks VAT?

A

Vescamicol

67
Q

How is ACh released?

A

1) Depolarization of nerve
2) Voltage-dependent Ca++ entry
3) Ca++ binds Calmodulin, activating “vesicle associated membrane proteins,” VAMPs & “synaptosome-assocaited proteins,” (SNAPs)
4) Exocytosis

68
Q

What is the function of the VAMPs & SNAPs?

A
  • Docking storage vesicles on the inner surface of the nerve terminal facing the synapse
  • Fusion of the synaptic vesicle with the neural membrane
69
Q

What does botulinum toxin block?

A

VAMPs & SNAPs

*Botulinum toxin enzymatically removes two amino acids from one or more of these fusion peptides

70
Q

How is ACh action terminated?

A

1) Rapid hydrolysis of ACh via acetylcholine esterase (AChE)
2) Choline re-uptake into terminals
3) ACh interaction with ACh autoreceptors

71
Q

What does acetylcholine esterase break ACh into?

A

Choline & Acetate

72
Q

What drug blocks Acetylcholine esterase? What happens at the synapse in response to these drugs? Give an example of an AChE inhibitor.

A
  • AChE inhibitors
  • Increase ACh concentrations & over-stimulation of receptors

*Neostigmine is an AChE inhibitor

73
Q

How are catecholamines synthesized?

A

1) Tyrosine is converted to DOPA via Tyrosine Hydroxylase*
2) DOPA is converted to Dopamine
3) Dopamine is converted to Norepinephrine

Note that this is the rate-limiting step

74
Q

What drug blocks tyrosine hydroxylase? What step of the catecholamine synthesis process does this drug block?

A
  • Metyrosine

- Conversion of Tyrosine to DOPA

75
Q

What part of catecholamine synthesis only occurs in the adrenal medulla?

A

Norepinephrine is converted to Epinephrine

76
Q

What is tyramine?

A

Tyramine is a naturally occurring monoamine compound, and a trace amine derived from the metabolism of tyrosine (alternative to DOPA)

77
Q

What causes an increase in Tyramine?

A

Ingested of naturally occurring fermented cheese

78
Q

What is Tyramine a precursor of?

A

Norephinephrine

79
Q

How are catecholamines stored?

A

Synthesized catecholamines are transported into vesicles for storage via the “Vesicular Monoamine Transporter (VMAT)”

*Note that the conversion of norephinephrine to epinephrine occurs in the vesicle, if the converting enzyme is available.

80
Q

What blocks VMAT? What is the mechanism of action?

A

Reserprine, blocks VMAT & causes a depletion of catecholamine stores

Still used today for “resistant hypertension

81
Q

How are the catecholamines released?

A

Similar exocytosis mechanism as ACh

82
Q

What drug blocks VAMP?

A

Bretylium

83
Q

How is catecholamine transmission terminated?

A

1) Diffusion into the circulation & metabolized by liver COMT (catechol-O-methyl transferase)
2) Binding to an autoreceptor on the pre-synaptic nerve terminal
3) Neuronal Re-uptake via NET1 (NE transporter on the presynaptic nerve terminal), where:
- Repackaged in vesicles
- Metabolized by mitochondiral monoamine oxidase (MAO)
4) Extraneuronal uptake via extraneuronal transporters (ENT or NET2)

84
Q

What is the mechanism of action of cocaine & tricyclic antidepressants?

A

NET1 antagnoists that leads to an increase in NE in the synaptic cleft

85
Q

What is the effect of MAO antagonists? How are they related to Tyramine?

A

MAO is a mitochondrial enzyme that metabolizes catecholamines

  • Irreversible MAO antagonists enhance the availability of Tyramine
  • Can lead to hypertensive crisis
86
Q

What is the rate-limiting step in catecholamine synthesis?

A

Conversion of Tyrosine to DOPA via Tyrosine Hydroxylase

87
Q

What are the muscles of inspiration?

A

Diaphragm
External intercostals
Scaleni
SCM

88
Q

What are the muscles of expiration?

A

Abdominal wall muscles

89
Q

What is FVC?

A

Forced vital capacity= total amount of air that can be forcibly expired after maximal inspiration

90
Q

What is FEV1?

A

The volume of air that can be forcibly expired in the first second

*Speed

91
Q

Why is the FEV1/FVC ratio important?

A

It is a reflection of RESISTANCE to airflow

  • Big ratio= small resistance
  • Small ratio= big resistance (obstructive)

.75- 0.8= normal

92
Q

What is FEF 25, 50, & 75?

A

Forced expiratory flow rate at varying volumes of air out

93
Q

How does the FEV1/FVC ratio change in obstructive lung disease? Why?

A

Less than 0.7

  • FCV & FEV1 decreased, but FEV1 is decreased more than FVC
94
Q

How does the FEV1/FVC ratio change in restrictive lung disease? Why?

A

Greater than 0.8

FVC & FEV1 are decreased, but FEV1 is decreased less than FVC

95
Q

Draw the flow volume curve curve in obstructive lung disease.

A

N/A

96
Q

Draw the flow volume curve curve in restrictive lung disease.

A

N/A

97
Q

Draw the flow volume curve curve in upper airway obstruction.

A

N/A

98
Q

How does restrictive lung disease effect FEV1, FVC & FEV1/FVC ratio?

A

asdf

99
Q

How does obstructive lung disease effect FEV1, FVC & FEV1/FVC ratio?

A

asdf

100
Q

What are the three most prevalent obstructive lung disorders?

A

Asthma
Chronic Bronchitis
Emphysema

101
Q

What are the main differences between asthma, chronic bronchitis, and emphysema?

A
  • Asthma is the most reversible of obstructive lung diseases
  • Chronic bronchitis is hallmarked by increased sputum production
  • Emphysema involves the most damage to the alveolar wall
102
Q

Outline the pathophysiology of allergic asthma.

A

In response to an allergen, a myraid of inflammatory cells release inflammatory mediators that result in:

1) Bronchoconstriction
2) Plasma exudation
3) Edema
4) Vasodilation
5) Mucus hypersecretion
6) Activation of sensory nerves

Chronic inflammation leads to structural changes including:

1) Thickening of the basement membrane
2) Smooth muscle hypertrophy & hyperplasia
3) Angiogenesis
4) Hyperplasia of mucus-secreting cells

103
Q

What are the therapeutic options in asthma?

A

Acute reliever

Controller

104
Q

What are the receptors for rescue treatments?

A
  • B-2 adrenergic (bronchodilation)

- Anticholinergics (M3)

105
Q

List the controller treatments used for asthma.

A 
Inhaled corticosteroids
Antileukotrienes 
Long-acting B-agonists
Theophylline
Systemic corticosteroids
Anti-IgE
106
Q

How is asthma manifested on PFT?

A

Decreased airflow rates throughout the vital capacity

  • Decreased PEFR
  • Decreased FEV1
  • Decreased MMEFR

Medical Physiology (74 decks)

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