vignettes physio Flashcards
hypoxemia at high altitude stimulates the peripheral chemoreceptors
to increase ventilation, causing arterial Pco2 to decrease and arterial pH to rise (respiratory alkalosis)
Botulinum toxin inhibits the release of acetylcholine from…
alpha motoneurons by blocking one of the proteins responsible for the fusion of the synaptic channel with the presynaptic membrane
calcium ions are the regulators of contraction of skeletal muscle. calcium is actively sequestered in sarcoplasmic reticulum
by an ATP pump during relaxation of muscle. Nervous stimulation leads to the release of calcium into the cytosol and raises the concentration from less than 1 mM to about 10mM.
the calcium binds to troponin C. the calcium-troponin complex undergoes a conformational change, which is transmitted to tropomyosin and causes
tropomyosin to shift position. the shift of tropomyosin allows actin to interact with myosin, and contraction proceeds.
hypothermia increases hemoglobin’s affinity for oxygen, causing the oxyhemoglobin dissociation curve
to shift to the left. with a leftward shift, the saturation of hemoglobin with oxygen is greater than normal at any Po2, as denoted by a lower P50 value than normal. acidosis, hypercapnia (increased Pco2), and an increase in erythrocyte 2,3-BPG all cause rightward shifts of the oxyhemoglobin dissociation curve.
a patient has a tendency to have elevated blood pressure and heart rate, which can be controlled in part by a calcium channel blocker. the effects of neurotransmitters upon calcium currents in heart muscle cells is enhanced by the release of
norepinephrine, which acts through beta-adrenergic receptors. this effect is additionally mediated by modulation of the K+ current, which serves to keep the action potential of the muscle cells constant. the pacemaker current is also affected by this process since its threshold is decreased as a result of activation of the beta-receptors. lowering the threshold serves to increase the HR
When circulating antibodies against the postsynaptic nicotinic acetylcholine receptors on the motor end plate, destroy the receptors and prevent acetylcholine from binding, the resulting end plate potential
is decreased at the neuromuscular junction, causing weakness and fatigue in the skeletal muscle. Patients with this autoimmune disease have a 75% incidence of concurrent thymic hyperplasia, and may benefit from thymectomy. Other treatments for Myasthenia gravis include administration of acetylcholinesterase inhibitors, immunosuppressive agents, and plasmapheresis or intravenous immunoglobulin.
A 56 year old woman presents with a flat red rash on the face and upper trunk with erythematous rash on the knuckles and in the shape of a V on the neck and anterior chest. She also complains of muscle weakness with difficulty getting out of a chair and combing her hair. laboratory findings include an increased creatine phosphokinase (CPK), positive antinuclear antibody, and anti-Mi2 dermatomyositis-specific antibodies. in addition to oral prednisone, physical therapy is ordered with the goal of improving muscle strength, and thus the ability to preform activities of daily living. Repetitive stimulation of a skeletal muscle fiber will cause an increase in contractile strength due to
an increase in duration of cross bridge cycling. each time a skeletal muscle fiber is stimulated by an alpha-motoneuron, enough Ca2+ is released from its sarcoplasmic reticulum to fully activate all the troponin within the muscle. therefore every cross bridge can contribute to the generation of tension. however, the transmission of force from the cross bridge to the tendon does not occur until the series elastic component (SEC) of the muscle is stretched.
35 female, neurology consult for muscle weakness. physician suspects myasthenia gravis, and confirms the diagnosis by administering a drug that increases the force of muscle contraction in patients with myasthenia gravis ! use caution when administering the drug to patients with heart disease due to profound bradycardia! the ability of the drug to increase the force of muscle contraction in patients with myasthenia gravis results from
decreasing the metabolic breakdown rate of acetylcholine. drug used to test for myasthenia gravis is an acetylcholine esterase inhibitor. by preventing the breakdown of acetylcholine, the increase results show an increase in time that acetylcholine remains in the synaptic cleft. acetylcholine can bind to end-plate receptors for a longer time, the magnitude of the end-plate potential increases, increasing the probability of in generating an action potential.
healthy, 32 year old male lifts weights as part of his workout. in one of the biceps muscle fibers at rest, the length of the I band is 1.0mm and the A band is 1.5mm. contraction of that muscle fiber results in a 10% shortening of the length of the sarcomere. the length of the A band after the shortening by the muscle contraction measures
1.50mm. during contraction, the sarcomere (distance between Z lines) decreases in length and the length of the A band is almost constant. however, as the degree of overlap of thick and thin filaments is altered, the thin filaments, which form the I band are anchored to the Z line, are pulled toward the center of the sarcomere. as this occurs, the I band decreases in length and the H band is no longer visible. the filaments themselves do not decrease in length, they slide past one another in the sliding filament model of muscle contraction.
62 year old male history of diabetes and HTN arrives in er with substernal chest pain lasting an hour. he is given intravenous nitroglycerin to help reduce the pain. what is expected following the use of nitrates?
myocardial oxygen demand is decreased from systemic vasodilation and subsequent decrease in left ventricular wall stress as a result of the reduction in venous return
A man drinks 2 L of water to replenish the fluids lost by sweating during a period of exercise. Compared with the situation prior to the period of
sweating,
His intracellular fluid volume will be greater Sweat normally contains about 40 to 60 meq of sodium per liter of fluid. Thus, approximately 100meq of sodium will be lost from the extracellular fluid during the exercise period, and when the lost water is replenished, the extracellular fluid will become hypotonic. The hypotonic extracellular fluid will equilibrate with the intracellular fluid and make it hypotonic as well. Because the extracellular fluid volume is dependent on the amount of sodium, the loss of sodium will result in a decreased extracellular fluid volume and an increased intracellular fluid volume after water is replaced.
Several days following a myocardial infarction, a 51-year-old male develops the sudden onset of a new pansystolic murmur along with a diastolic
flow murmur. Workup reveals increased left atrial pressure that develops late in systole and extends into diastole. These abnormalities in this individual are most likely the result of
Rupture of a papillary muscle
Cardiac rupture, whether of free wall, septum, or papillary muscle, occurs in only 1 to 5% of cases
following acute myocardial infarction. It occurs usually within the first week of infarction, when there is maximal necrosis and softening (4 to 5
days) and is very rare after the second week. Rupture of the free wall results in pericardial hemorrhage and cardiac tamponade. Rupture of the interventricular septum causes a left-to-right shunt. Serious mitral valve incompetence results from rupture of anterior or posterior papillary muscles. This valve incompetence can produce signs of mitral regurgitation, including a new pansystolic murmur along with a diastolic flow murmur. Indeed, the onset of a new murmur following a myocardial infarction should raise the possibility of papillary rupture.
A medical student presents to the emergency room with a two-day history of severe vomiting and orthostatic hypotension. What kind of metabolic abnormalities would you expect?
Hypokalemic, hypochloremic, metabolic alkalosis.
Analysis of serum electrolytes reveals low potassium (hypokalemia), low chloride (hypochloremia), and metabolic alkalosis. These abnormalities arise from two sources. First, gastric juice contains potassium and chloride in concentrations higher than found in the plasma. Loss of gastric juice through vomiting or drainage leads to depletions of these electrolytes from the
plasma. Second, the metabolic abnormalities are exacerbated by the student’s dehydration. Contraction of the vascular volume leads to orthostatic hypotension and the activation of renal mechanisms important for conserving volume. As a result, water, sodium, and bicarbonate are reabsorbed at the expense of increased potassium and hydrogen excretion.
A medical student presents to the emergency room with a two-day history of severe vomiting and orthostatic hypotension. What kind of metabolic abnormalities would you expect?
Analysis of serum electrolytes reveals low potassium (hypokalemia), low chloride (hypochloremia), and metabolic alkalosis. These abnormalities arise from two sources. First, gastric juice contains potassium and chloride in concentrations higher than found in the plasma. Loss of gastric juice through vomiting or drainage leads to depletions of these electrolytes from the
plasma. Second, the metabolic abnormalities are exacerbated by the student’s dehydration. Contraction of the vascular volume leads to orthostatic hypotension and the activation of renal mechanisms important for conserving volume. As a result, water, sodium, and bicarbonate are reabsorbed at the expense of increased potassium and hydrogen excretion.
A medical student presents to the emergency room with a two-day history of severe vomiting and orthostatic hypotension. What kind of metabolic abnormalities would you expect?
Analysis of serum electrolytes reveals low potassium (hypokalemia), low chloride (hypochloremia), and metabolic alkalosis. These abnormalities arise from two sources. First, gastric juice contains potassium and chloride in concentrations higher than found in the plasma. Loss of gastric juice through vomiting or drainage leads to depletions of these electrolytes from the
plasma. Second, the metabolic abnormalities are exacerbated by the student’s dehydration. Contraction of the vascular volume leads to orthostatic hypotension and the activation of renal mechanisms important for conserving volume. As a result, water, sodium, and bicarbonate are reabsorbed at the expense of increased potassium and hydrogen excretion.
A 70-year-old female is treated with sublingual nitroglycerin for her occasional bouts of angina. Which of the following is involved in the action
of nitroglycerin?
a. α-adrenergic activity
b. Phosphodiesterase activity
c. Phosphorylation of light chains of myosin
d. Norepinephrine release
e. cGMP
cGMP
Nitric oxide is thought to be enzymatically released from nitroglycerin. It can then react with and activate guanylyl cyclase to increase GMP, a vasodilator due to its effect on increasing calcium efflux. It also indirectly causes the dephosphorylation of the light chains of myosin. These actions lead to the vasodilator effect of nitroglycerin. Reaction of nitric oxide occurs withprotein sulfhydryl groups. Tolerance may develop in part from a decrease in available sulfhydryl groups. Autonomic receptors are not involved in the primary response of nitroglycerin, but compensatory mechanisms may counter the primary actions
After a mild hemorrhage, compensatory responses initiated by the baroreceptor reflex keeps blood pressure at or close to its normal value. Which one of the following values is less after compensation for the hemorrhage than it was before the hemorrhage?
a. Venous compliance
b. Heart rate
c. Ventricular contractility
d. Total peripheral resistance
e. Coronary blood flow
Venous compliance The fall in blood volume and pressure produced by hemorrhage elicits the baroreceptor reflex. The reflex increases the activity of the sympathetic nervous system and decreases the activity of the parasympathetic nerves innervating the heart. Sympathetic stimulation of the smooth muscle surrounding thevenous vessels decreases their compliance, causing end-diastolic volume (EDV) to increase. However, the EDV does not increase above the levels observed prior to the hemorrhage. Heart rate, ventricular contractility, and total peripheral resistance are all increased above their prehemorrhage levels by sympathetic stimulation. The coronary blood flow increases to meet the increased energy requirements of the heart beating at a higher rate with increased contractility.
A 70-year-old female is treated with sublingual nitroglycerin for her occasional bouts of angina. Which of the following is involved in the action
of nitroglycerin?
a. α-adrenergic activity
b. Phosphodiesterase activity
c. Phosphorylation of light chains of myosin
d. Norepinephrine release
e. cGMP
cGMP
Nitric oxide is thought to be enzymatically released from nitroglycerin. It can then react with and activate guanylyl cyclase to increase GMP, a vasodilator due to its effect on increasing calcium efflux. It also indirectly causes the dephosphorylation of the light chains of myosin. These actions lead to the vasodilator effect of nitroglycerin. Reaction of nitric oxide occurs withprotein sulfhydryl groups. Tolerance may develop in part from a decrease in available sulfhydryl groups. Autonomic receptors are not involved in the primary response of nitroglycerin, but compensatory mechanisms may counter the primary actions
After a mild hemorrhage, compensatory responses initiated by the
baroreceptor reflex keeps blood pressure at or close to its normal value.
Which one of the following values is less after compensation for the hemorrhage
than it was before the hemorrhage?
a. Venous compliance
b. Heart rate
c. Ventricular contractility
d. Total peripheral resistance
e. Coronary blood flow
Venous compliance
The fall in blood volume and pressure produced by hemorrhage elicits the baroreceptor reflex. The reflex increases the activity of the sympathetic nervous system and decreases the activity of the parasympathetic nerves innervating the heart. Sympathetic stimulation of the smooth muscle surrounding thevenous vessels decreases their compliance, causing end-diastolic volume (EDV) to increase. However, the EDV does not increase above the levels observed prior to the hemorrhage. Heart rate, ventricular contractility, and total peripheral resistance are all increased above their prehemorrhage levels by sympathetic stimulation. The coronary blood flow increases to meet the increased energy requirements of the heart beating at a higher rate with increased contractility.
A patient in heart failure improves markedly after using a drug that increases the inotropic state of her heart. Which one of the following changes is primarily responsible for the improvement in her condition?
a. A reduction in heart rate
b. A reduction in heart size
c. An increase in end-diastolic pressure
d. An increase in wall thickness
e. An increase in cardiac excitability
A reduction in heart size
The most obvious deleterious effect of a failing heart is the inability to pump enough blood to satisfy the energy requirements of all the tissues. Among the compensatory mechanisms that develop in response to heart failure is an increase in retention of fluid by the kidney. Increased retention of fluid causes the end-diastolic volume
of the heart to increase, which, by the Starling mechanism, increases the strength of the heartbeat. However, two deleterious effects result from an increase in end-diastolic volume. A larger than normal end-diastolic volume causes an increase in end-diastolic pressure, which can lead to pulmonary edema. In addition, the large end-diastolic volume increases the wall stress
that must be developed by the heart with each beat, and this increases the myocardial requirement of oxygen. The increase in contractility that results from the administration of a positive inotropic drug such as digoxin will allow the heart to produce the same force at a lower volume and thus eliminate the need for an increase in volume of fluid.
A 65-year-old man is diagnosed with a form of a peripheral neuropathy.
This individual will likely display
a. A loss in motor function, but sensory functions will remain largely intact
b. A reduction in conduction velocity of the affected nerve
c. An increase in the number of Ranvier’s nodes
d. Degeneration of myelin but the axon will typically remain intact
e. Signs of an upper motor neuron (UMN) paralysis
A reduction in conduction velocity of the affected nerve
In a peripheral neuropathy, there may be damage to either the myelin or the axon directly, although, more often, there is damage to the myelin Because of myelin (or axonal) damage, there is a reduction (or loss) of conduction velocity. The
disorder may affect both sensory and motor components of the peripheral nerve, thereby causing dysfunction in both the sensory and the motor processes associated with that nerve. Because there is peripheral neuronal damage, the motor loss will be reflected in a weakness, paralysis, or reflex activity associated with the affected muscle, as well as impairment of sensation.
The individual is likely to be suffering from
a. Multiple sclerosis (MS)
b. Amyotrophic lateral sclerosis (ALS)
c. Myasthenia gravis
d. Combined system disease
e. Muscular dystrophy (MD)
The likely basis for this disorder is the result of
a. The production of excessive quantities of acetylcholine (ACh)
b. The production of antibodies that act against nicotinic ACh receptors
c. A minor stroke involving the motor strip of the cerebral cortex
d. A vitamin B deficiency
e. Viral encephalitis
Myasthenia gravis / The production of antibodies that act against nicotinic ACh receptors
Myasthenia gravis is an autoimmune disease that causes cranial nerve and limb muscle weakness by producing antibodies that act against the nicotinic receptor at the neuromuscular junction. The result is that the action of nerve fibers that innervate skeletal muscle are affected, producing loss of the effects of ACh at the neuromuscular junction. The net result is a reductionof the size of the action potential in the muscle, producing a weakness in the affected muscle. This disorder is reversed by administration of drugs that inhibit the enzyme, acetylcholinesterase, that degrades ACh. Multiple sclerosis, ALS, and combined system disease (see the chapter entitled “The Spinal Cord”) involve damage to axons and/or nerve cells within the CNS, producing much more profound damage to motor functions and, in the case of combined system disease, damage to both motor and sensory systems. Muscular dystrophy is typically characterized, in part, by progressive
weakness of muscles and degeneration of the muscle fibers. The other disorders listed all involve disorders affecting the CNS, and thus, the
symptoms associated with these disorders differ significantly from those described in this case. Excessive release of ACh is not a realistic event that is likely to occur (except from the bite of a black widow spider). In theory, if it were to occur, there is no reason to believe that muscular weakness would be a symptom. Instead, there would be some rigidity and muscle spasms
A 59-year-old male with a history of rheumatic heart disease is found to have atrial fibrillation (AF), for which he is treated with digoxin
Treatment with digoxin converts his AF to a normal sinus rhythm and most likely results in a decrease in which of the following?
a. The length of the refractory period
b. The velocity of shortening of the cardiac muscle
c. The conduction velocity in the atrioventricular (AV) node
d. The atrial maximum diastolic resting potential
The answer is c. (Hardman, pp 813–814.) Digoxin is used in AF to
slow the ventricular rate, not usually the AF itself. Digoxin acts to slow the
speed of conduction, increase the atrial and AV nodal maximal diastolic
resting membrane potential, and increase the effective refractory period in
the AV node, which prevents transmission of all impulses from the atria to
the ventricles. It exerts these effects by acting directly on the heart and by
indirectly increasing vagal activity.
