ITE CA2 physiology

Question 1

Post-ROSC acute coronary syndrome guidelines include:

Answer 1

Post-ROSC acute coronary syndrome guidelines include:

• Rapid performance of an ECG, which is both diagnostic and permits the establishment of pre-intervention baseline.
• Determination of indication for coronary angiography and cardiac catheterization
• Continuation of other post-ROSC care such as therapeutic hypothermia as indicated

Question 2

The force-velocity relationship demonstrates that the greater the afterload, the (faster/slower) the velocity of shortening.

Answer 2

The force-velocity relationship demonstrates that the greater the afterload, the slower the velocity of shortening.

Question 3

What is the main physiologic factor in water resorption

Answer 3

AVP (Arginine vasopressin or antidiuretic hormone) is the main physiologic factor in water resorption. It is released from the pituitary in response to hyperosmolality, reduced effective circulating volume, angiotensin II, stress, pain, nausea, hypoglycemia, pregnancy, and certain drugs.

Question 4

Where is AVP released and why

Answer 4

AVP is the main physiologic factor in water resorption. It is released from the pituitary in response to hyperosmolality, reduced effective circulating volume, angiotensin II, stress, pain, nausea, hypoglycemia, pregnancy, and certain drugs (nicotine).

Question 5

Factors that inhibit release of AVP

Answer 5

Factors that inhibit its release are hypoosmolality, increased effective circulating volume, cortisol, and drugs such as caffeine.

Question 6

AVP mechanism

Answer 6

AVP stimulates water resorption by increasing intracellular levels of cyclic adenosine monophosphate (cAMP) and activating protein kinase A. It also stimulates vasoconstriction by activating G protein and phospholipase C, which releases calcium from the sarcoplasmic reticulum. There are two classes of AVP receptors: V1 receptors present in vascular smooth muscle and V2 receptors present in the distal and collecting tubules of the kidney.

Question 7

AVP metabolism and half life

Answer 7

AVP is metabolized by the kidneys and liver after its release into the plasma. Its half-life is 15-20 minutes.

Question 8

ADH hypersecretion occurs in ______ deficiency

Mechanism

Answer 8

ADH (AVP) hypersecretion occurs in cortisol deficiency. Cortisol deficiency results in increased hypothalamic secretion of corticotropin-releasing hormone (CRH), an ADH secretagogue (a substance which promotes secretion). Cortisol feeds back negatively on CRH and ACTH, an inhibitory effect that is removed with adrenal insufficiency. Both cortisol and antidiuretic hormone are released in response to surgical stress, but it should be noted that cortisol appears to directly suppress ADH secretion.

Question 9

Renin pathway

Answer 9

A decrease in blood pressure stimulates the release of renin into the serum from the renal tubules. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by ACE. Angiotensin II causes an increase in blood pressure by direct vasoconstriction, enhancing the sympathetic nervous system, and causing an increase of aldosterone.

Aldosterone also acts on the kidneys to decrease the urinary excretion of sodium and water. This ultimately leads to an increase in blood volume and therefore blood pressure.

Question 10

Renin secretion can be caused by 3 different mechanisms:

Answer 10

Renin secretion can be caused by 3 different mechanisms: a decrease in serum NaCl concentration sensed by the kidneys, a decrease in blood pressure sensed by kidney baroreceptors, or activation of renal B1 receptors by norepinephrine

Question 11

How are static and dynamic compliance measured?

Answer 11

Static compliance measures the lung at a fixed volume unlike dynamic compliance, which measures the lung during normal rhythmic breathing.

Question 12

Atrial contraction normally contributes approximately ____% of the preload.

Answer 12

Atrial contraction normally contributes approximately 15% of the preload. In patients with poor left ventricular filling, as in diastolic dysfunction, the atrial contraction becomes very important.

Question 13

The Sinus Nerve of Hering

Answer 13

The Sinus Nerve of Hering is a branch of the glossopharyngeal nerve that innervates the carotid sinus which is responsible for control of the carotid baroreceptors, not the carotid body chemoreceptors. Increases in activity of the carotid sinus actually can impair ventilation.

Question 14

Carotid body
does what
under what conditions
via what pathway
impaired by what

Answer 14

The carotid body chemoreceptors increase ventilation when PaO2 (not PAO2, CaO2 or SaO2) decreases through afferent impulses via the glossopharyngeal nerve to CNS ventilation centers. Their function is impaired by opioids, benzodiazepines, volatile anesthetics (as low as 0.1 MAC), and bilateral carotid endarterectomy.

Question 15

How does CO2 affect ventilation

Answer 15

Ventilatory increase by alterations in PaCO2 is controlled primarily via central chemoreceptors, not peripheral chemoreceptors. These receptors have little contribution to hypoxic ventilatory drive. The central chemoreceptors are located in the ventral medulla in approximation with CSF. These areas are not actually sensitive to PaCO2 but to increases in H+ concentration. CO2 has the ability to cross the BBB and once there is converted to carbonic acid by carbonic anhydrase. The H+ ion concentration increases result in a steady increase in respiratory rate and tidal volume. Metabolic acidosis will not have the same effect as hydrogen ions cannot cross the blood-brain barrier and are readily buffered by body fluids. The brain, on the other hand, has no buffering capacity, therefore H+ becomes trapped in the CSF and levels increase quickly. It is true that the medications mentioned in the previous paragraph also impair central chemoreceptor response to PaCO2. In patients with chronic CO2 retention (e.g. COPD, OSA), CSF pH is normalized by passage of HCO3 into the CSF in the arachnoid villi and thus a greater PaCO2 is required to stimulate an increase in ventilation.

Question 16

Normal response to hypoglycemia

Answer 16

The normal response to hypoglycemia is an increase in sympathetic discharge, cortisol release, and glucagon release with symptoms of diaphoresis, tachycardia, hypertension, altered mental status, and possibly even seizures

Question 17

What is only symptom seen in patient who is hypoglycemic and on beta blockers? And what mediates it?

Answer 17

Diaphoresis is mediated by sympathetic stimulation via release of acetylcholine and stimulation of muscarinic receptors and is the only symptom that may be seen in a patient who is hypoglycemic and on beta blockers.

Question 18

Where does sympathetic nervous system arise

Answer 18

The sympathetic nervous system is composed of preganglionic neurons located in the lateral horn of the spinal cord from T1-L2.

Question 19

beta 2 effect in eye

Answer 19

beta-2 mediated relaxation of the ciliary muscle of the lens which improves distance, not near vision

Question 20

parasympathetic nervous system

Answer 20

The parasympathetic nervous system originates from the brainstem and sacral spinal cord and uses acetylcholine at all synapses. Acetylcholine binds to nicotinic receptors at the autonomic ganglia and muscarinic receptors at the effector site.

Question 21

SNS neurotransmitters

Answer 21

Within the ANS, all preganglionic neurons are cholinergic and release acetylcholine. Postganglionic neurons in the PNS are also cholinergic. Most postganglionic neurons in the SNS are adrenergic and release norepinephrine; however, those innervating sweat glands are cholinergic.

The postganglionic neuron then projects axons to effector organs and releases norepinephrine with stimulation of alpha or beta receptors. The exception is with sweat glands and the chromaffin cells of the adrenal medulla, both of which are stimulated by acetylcholine via muscarinic (sweat glands) and nicotinic (chromaffin cells) receptors. The adrenal medulla is essentially a modified postganglionic sympathetic neuron.

Question 22

What diseases affect compliance and how

Answer 22

A few diseases that are associated with a decreased compliance include acute respiratory distress syndrome, pulmonary fibrosis, and pulmonary edema. These will shift the pressure-volume curve to the right and will cause it to flatten out. Emphysema causes an increased compliance and shifts the pressure volume curve to the left and causes it to become steeper.

Question 23

Goals for patients presenting with acute stroke include

Answer 23

Goals for patients presenting with acute stroke include normothermia, normotension, euvolemia, normal blood glucose levels, avoidance of hypoxemia (SpO2 < 94%), avoidance of hyperoxia (SpO2 100% on oxygen), and, most importantly, rapid fibrinolysis.

Question 24

A urine-to-plasma osmolar ratio (UOSM : POSM) >x indicates prerenal oliguria (generally secondary to hypovolemia)

Answer 24

A urine-to-plasma osmolar ratio (UOSM : POSM) >1.5 indicates prerenal oliguria (generally secondary to hypovolemia)

Question 25

Carbon dioxide is transported in the blood as…

Answer 25

Carbon dioxide is transported in the blood as dissolved CO2, bicarbonate, and carbamino compounds.

Question 26

eccrine and apocrine sweat glands
innervation
Neurotransmitter
Type of receptors Pre and post ganglionic

Answer 26

Both eccrine and apocrine sweat glands are innervated by postganglionic sympathetic fibers. Eccrine glands are responsible for the majority of sweat gland secretion and use acetylcholine as the neurotransmitter. The preganglionic neurons synapse and release ACh on nicotinic receptors. The postganglionic neurons differ from other sympathetic postganglionic neurons in that they release acetylcholine to act on muscarinic receptors; all other muscarinic receptors function under the parasympathetic nervous system

Question 27

Autonomic nervous system
Preganglionic length
Neurotransmitters
Receptors

Answer 27

The autonomic nervous system consists of the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). The PNS is responsible for the “rest-and-digest” processes in the body, and activation of target receptors causes salivation, lacrimation, urination, digestion, and defecation. The preganglionic fibers are long compared to the SNS, and release ACh to act on nicotinic receptors. The shorter postganglionic fibers release ACh to muscarinic receptors resulting in the above effects.

The SNS is responsible for the “fight-or-flight response”. The preganglionic fibers are short as compared to the PNS, and release ACh to nicotinic receptors. The longer postganglionic fibers release norepinephrine (NE) to the heart and blood vessels via alpha/beta receptors, ACh to sweat glands via muscarinic receptors and dopamine to renal vessels via dopamine receptors. The adrenal glands have no postganglionic fibers, and release NE and epinephrine directly into the blood stream.

Question 28

Sweat gland secretion

Answer 28

Sweat gland secretion is increased as part of both the adrenergic (apocrine) and cholinergic (eccrine) responses via alpha-1 and muscarinic receptors respectively. The major neurotransmitters for apocrine glands are catecholamines; whereas, for eccrine glands, the major neurotransmitter is acetylcholine. The cholinergic response (i.e. eccrine gland) is responsible for the majority of increased sweat gland secretion.

Question 29

IGE mediated allergic reactions

Answer 29

IgE-mediated symptoms include: urticaria, angioedema, dyspnea, dysphagia, bronchospasm, and anaphylaxis.

Severe non-IgE-mediated reactions include: Stevens-Johnson syndrome or toxic epidermal necrolysis (mucosal lesions, bullous or exfoliative skin lesions, evidence of other organ involvement such as renal failure or hepatic failure), DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) syndrome, interstitial nephritis, and hemolytic anemia.

Question 30

severe Non-IgE mediated reactions

Answer 30

IgE-mediated symptoms include: urticaria, angioedema, dyspnea, dysphagia, bronchospasm, and anaphylaxis.

Severe non-IgE-mediated reactions include: Stevens-Johnson syndrome or toxic epidermal necrolysis (mucosal lesions, bullous or exfoliative skin lesions, evidence of other organ involvement such as renal failure or hepatic failure), DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) syndrome, interstitial nephritis, and hemolytic anemia.

Question 31

Uremia effect on coagulation

Answer 31

Uremia interferes with platelet activation and aggregation (primarily via effects on vWF and GPIIb-IIIa) and leads to increased production of platelet inhibitors (e.g. prostacyclin and nitric oxide).
(Impportant reason for dialysis prior to surgery)

Question 32

Respiratory alkalosis causes what electrolyte abnormalities

Answer 32

hypocalcemia
hypokalemia
hypophosphatemia
(Hypocalcemia is caused by increased calcium binding to negatively charged plasma proteins as the proteins release hydrogen ions to restore physiologic pH

A rising cellular pH stimulates the glycolytic pathway, enhancing sugar-phosphate production. This triggers increased cellular uptake of phosphorus, thus decreasing serum phosphorus concentration.

Hydrogen-potassium transporters pump hydrogen ions out of cells in the setting of alkalosis in order to restore physiologic pH. Simultaneously, potassium is pumped intracellularly to ensure electroneutrality, thus leading to hypokalemia.)

Question 33

Hydrocortisone in septic shock
when to use it
how to dose
when not to use it

Answer 33

Patients with septic shock not responsive to fluid resuscitation and vasopressors may benefit from corticosteroid replacement. Hydrocortisone 200 mg IV per day should be administered; it can then be tapered once vasopressors are no longer required. Steroids are NOT recommended for patients with septic shock responsive to fluids or vasopressors nor are they indicated for sepsis in the absence of septic shock.

Question 34

DIC lab test

Answer 34

The triad most expected in DIC is an increased PT/aPTT with decreased platelets and fibrinogen levels; however, this is often altered in pregnancy

Disseminated intravascular coagulation is associated with an elevated prothrombin time. However, it may not become apparent until significant disease has occurred. Therefore, if a prolonged PT is seen, it is very likely the patient has significant consumption of clotting factors.

Question 35

Carotid body chemoreceptors

Answer 35

Carotid body chemoreceptors are primarily responsive to reductions in arterial partial pressure of oxygen (PaO2)
Kick in when below 60-65

Question 36

carotid body afferent nerve

Answer 36

afferent glossopharyngeal nerve branches

Question 37

cAMP causes
heart muscle
vascular muscle

Answer 37

In somewhat of a contradiction, cAMP causes heart muscle to contract more and vascular muscle to contract less. This explains the inodilator effect of milrinone, dobutamine, and low dose epinephrine. Relaxation of smooth muscle also explains bronchodilation with albuterol and tocolysis with terbutaline.

Question 38

adaptations to altitude

Answer 38

Short-term adaptations (first several hours) to hypoxemia at altitude include increased minute ventilation and cardiac output.

Intermediate adaptations (hours to days) include a rightward then leftward shift of the oxygen-hemoglobin dissociation curve, CSF bicarbonate loss, and enhanced renal bicarbonate excretion.

A long-term adaptation (weeks) is increased hemoglobin concentration from increased erythropoietin secretion.

These adaptations ultimately result in a normal blood pH, decreased PaCO2, decreased blood bicarbonate concentration, and increased oxygen delivery to tissues despite a decreased PaO2.

Question 39

VACTERL association

Answer 39

VACTERL association: Vertebral, Anal, Cardiac, Tracheal, Esophageal, Renal, and Limb.

If TEF, most common association is cardiac defect

Question 40

mediastinal widening ass’d with what biologic agent

Answer 40

bacillus anthracis (anthrax)

Question 41

In what patients can sux cause hyperkalemia with potassium coming from the GI tract rather than skeletal muscle?

Answer 41

Severe hyperkalemia can occur in hypovolemic patients with severe metabolic acidosis who receive succinylcholine. In these patients, potassium comes from the gastrointestinal tract rather than skeletal muscle. Consider correction of acidosis with sodium bicarbonate administration and hyperventilation prior to use of succinylcholine in these patients.

Question 42

Greatest source of evaporative heat loss in surgery

Answer 42

Most evaporative heat loss can be attributed to tissue exposure from the surgical incision.

Question 43

Cardiovascular changes in the elderly include

Answer 43

Cardiovascular changes in the elderly include decreased compliance of the arterial and venous vasculature, increased afterload, desensitization to β-receptor stimulation, LV hypertrophy and reduced ventricular compliance, diastolic LV dysfunction (negative lusitropy), reduced parasympathetic nervous system tone, and fibrosis of the cardiac conduction system.

Question 44

Peripheral neuropathy in diabetes mellitus is related to

Answer 44

Peripheral neuropathy in diabetes mellitus is related to microangiopathy (ischemia in axonal nerve tissue)

Question 45

phospholipoprotein produced where

Answer 45

Pulmonary surfactant, also known as phospholipoprotein, is produced by type II alveolar cells and functions to reduce alveolar surface tension. Reduction in surface tension increases pulmonary compliance, prevents atelectasis at end expiration, and facilitates recruitment of collapsed airways.

Question 46

Type III alveolar cells

Answer 46

Type III alveolar cells, also known as alveolar macrophages, are an important element of immunologic lung defense. Their migratory and phagocytic activities permit ingestion of foreign materials within alveolar spaces. Type III alveolar cells do not produce surfactant.

Question 47

Type I alveolar cells

Answer 47

Type I alveolar cells are flattened, thin-walled, squamous cells that cover approximately 80% of the alveolar surface. These cells provide the surface suitable for gas exchange. Type I cells are highly differentiated and metabolically limited, which makes them highly susceptible to injury. When type I cells are damaged severely (during acute lung injury or adult respiratory distress syndrome), type II cells replicate and modify to form new type I cells. Type I alveolar cells do no produce surfactant.

Question 48

old people sympathetic vs parasympathetic

other cardiovascular changes:

Answer 48

Elderly patients have a decrease in parasympathetic tone and increase in sympathetic tone at rest. Other cardiovascular changes occurring in the elderly include a reduction in ischemic preconditioning and worsening diastolic dysfunction with increased left atrial pressures. Systolic function is often preserved in the otherwise healthy elderly patient.
Decreased beta-receptor responsiveness and decreased vagal tone result in a lessened response to pharmacologic agents including exogenous catecholamines and vagolytic agents.

Question 49

normal mixed venous blood sat

Answer 49

Normal values of SvO2 range between 65 and 80%.

Question 50

Total body water percentage by age

Answer 50

Total body water percentage is highest as a neonate and normalizes by teenage years. This percentage is offset in old age due to increased fat content.

Question 51

In a healthy human adult, total body water (TBW) comprises

Answer 51

In a healthy human adult, total body water (TBW) comprises approximately 55-60% of lean body mass in men and 45-50% in women. Although most body tissue is 70-80% water, this is offset by bone (20% water) and fat (10-15% water). TBW is made up of 1/3 extracellular fluid and 2/3 intracellular fluid. Extracellular fluid volume is further subdivided into 3/4 interstitial fluid and 1/4 plasma fluid.

Question 52

Normal CVP ranges

Answer 52

Normal CVP ranges from 1-5 mmHg with an average value of 3 mmHg in a healthy individual.

Question 53

The respiratory centers in the brain are located in the

Answer 53

The respiratory centers in the brain are located in the cerebral medulla, including both dorsal (inspiration) and ventral (expiration) respiratory groups.

TrueLearn Insight : Mnemonic: “DIVE” for dorsal = inspiration, ventral = expiration.

Question 54

dorsal respiratory group further controlled by

Answer 54

The baseline respiratory rhythm originates in the cerebral medulla, in the dorsal & ventral respiratory groups. The dorsal group is active during inspiration, which the ventral group is active during expiration.

The dorsal group is further controlled by two specific pontine areas; the lower pontine center (apneustic) is excitatory, while the upper pontine center (pneumotaxic) is inhibitory. Respirations are further affected by central and peripheral chemo- and baroreceptors.

Question 55

Patients with myotonic dystrophy have an increased risk of pulmonary aspiration due to

Answer 55

Patients with myotonic dystrophy have an increased risk of pulmonary aspiration due to gastric atony and delayed emptying, intestinal hypomotility, and pharyngeal muscle weakness.

Question 56

Clinical manifestations of myotonic dystrophy are a result of _____
type 1
Type 2

Answer 56

Clinical manifestations of myotonic dystrophy are a result of delayed skeletal muscle relaxation after voluntary contraction. Two subtypes exist. Myotonic dystrophy type 1 is more common and can be congenital, child-onset, or most typically, autosomal dominant with adult-onset. Type 2 is rarer than type 1 and is typically associated with milder symptoms.

Question 57

• Muscle degeneration
• Cataracts
• Premature balding
• Diabetes mellitus
• Thyroid dysfunction
• Adrenal insufficiency
• Gonadal atrophy
• Cardiac abnormalities (e.g., conduction dysfunction, cardiomyopathy, and mitral valve prolapse).

Answer 57

Symptoms and associated findings of myotonic dystrophy include:

• Muscle degeneration
• Cataracts
• Premature balding
• Diabetes mellitus
• Thyroid dysfunction
• Adrenal insufficiency
• Gonadal atrophy
• Cardiac abnormalities (e.g., conduction dysfunction, cardiomyopathy, and mitral valve prolapse).

Question 58

where and how is acetylcholine synthesized

Answer 58

Acetylcholine (ACh) is synthesized in the presynaptic terminal by acetylation of choline with acetyl-CoA via choline acetyltransferase in the cytoplasm.

Question 59

acetylcholine recycling process

Answer 59

Acetylcholine is rapidly broken down by acetylcholinesterase in the synapse into acetate and choline. Choline is recycled back into the presynaptic neuron. Unlike norepinephrine, there is no reuptake of acetylcholine and it must be synthesized constantly.

Question 60

The Haldane effect

Answer 60

The Haldane effect states that deoxygenated hemoglobin has a higher affinity for CO2. Once the deoxygenated hemoglobin reaches the lungs, the high O2 concentration decreases this affinity and the CO2 is released.

Question 61

The Bohr effect states that

Answer 61

The Bohr effect states that in areas of high CO2, the hemoglobin has less affinity for O2 which is more readily released for consumption by the tissues.