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1
Q

Calcitriol MOA

A

acts on intestines, bone, kidney, and parathyroid gland

In intestines - enhances the absorption of Ca and Phosphate at the level of the enterocyte

In bone - promotes bone formation and mineralization by regulation of proteins produced by osteoblasts

Parathyroid gland - inhibits synthesis of PTH

calcitriol acts w/ PTH to increase Ca

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2
Q

Diastolic heart failure is due to….

A

primary impairments of ventricular relaxation, filling, or compliance or secondary to diseases of the pericardium

(ie HCM)

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3
Q

What happens in response to hypoxemia if there weren’t any carotid body receptors?

A

Hypoxemia would depress respiration

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4
Q

Equation to calculate corrected Na

A

= Na(measured) + 1.6 ( [measured glucose - normal glucose] / 100)

for every measured 100 mg/dl increase in BG, the measured serum sodium increase by 1.6 if < 400

If BG > 400 use correction factor of 2.4

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5
Q

List mediators that cause vasodilation

A

Prostacyclin

NO

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6
Q

In CHF, how do positive inotropes affect the frank-starling curve

A

Shifts it upwards (improves cardiac output)

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7
Q

What is the free water deficit?

A

= 0.6 * BW * ([ current Na patient / normal Na patient] -1)

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8
Q

Describe the renin-angiotensin-aldosterone system

A

Decreased blood flow and BP to the kidney results in activation of the renin-angiotension-aldosterone system

Renin is release from the juxtaglomerular cells in response to decreased baroreceptor activity, sympathetic activity, or decreased tubular chloride as sensed by the macula dense.

Generation of angiotensin II causes vasoconstriction (direct by triggering vascular smooth muscle contraction) and indirect (stimulation of sympathetic activity and release of vasopressin)

Antiogensin II promotes Na and water rendition in the proximal tubule and alters glomerular filtration through preferential constriction of the efferent arteriole.

Aldosterone release results in K excretion and Na retention in the cortical collection duct

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9
Q

How does sudden correction of arterial hpoxemia cause further hypercapnia?

A

(1) depression of formerly hypoxic-driven peripheral chemoreceptors
(2) relief of hypoxic pulmonary vasoconstriction in poorly ventilated lung regions that further reduces the ability of these units to eliminate CO2
(3) significant correction of hypoxemia causes better saturation of Hgb so that previously buffered protons on oxyhemoglobin are released w/ subsequent generation of new CO2 from stores (Haldane effect)

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10
Q

Vasopressin receptors?

A

V1 - vasoconstriction and increase in SVR

V2 - renal collecting duct promotes water retention to help support blood volume and preload

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11
Q

Mechanism of pulmonary edema secondary to HCM

A

b/c of elevated filling pressure caused by diastolic dysfunction

cats rarely develop systolic dysfunction and positive inotropes are actually contraindicated

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12
Q

Where in the brain are the generation centers for respiration?

A

Medullary respiratory center
Apneustic center
Pneumotaxic center

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13
Q

How does Cushing’s result in a hyper coagulable state

A

elevated fVIII and vWF

Elevated PAI-1

Elevated IX, XI, XII

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14
Q

Describe the baroreceptor system

A

Fall in stretch - identified by carotid sinus and aortic arch, stimulus to the vasomotor center of the medulla is decreased

Result is an increase in sympathetic
Decrease in parasympathetic outflow

leads (via catecholamines) to vasoconstriction (increase in SVR) and increased HR and contractility (and thereby CO)

…all functioning to raise BP back to normal

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15
Q

What is early after depolarization and delayed afterdepolarization and which electrolyte changes induce these?

A

Triggered activity results from small membrane depolarizations that appear after an are dependent on the upstroke of the action potential.

Early afterdepolarizations - occur during the process of depolarization
- hypokalemia and drug-induced prolongation of the QT segment increases the risk of EADs

Delayed after depolarizations - occur after full depolarization
- occur secondary to intracellular calcium overload associated with sustained tachycardia and digoxin toxicity

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16
Q

Describe the MOA of ADH

A

Stimulus for ADH release = low circulating volume and elevated plasma osmolality

(baroreceptors sense low stretch w/ decreased ECV and send impulses to the pituitary gland that simulate ADH release)

in the absence of ADH - renal tubular cells cannot reabsorb water –> ADH is responsible for activating the V2 receptor on the renal collecting tubular cell (aquaporin-2 molecules are inserted into the cell’s luminal membrane)

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17
Q

Define the ATT scoring system

A

Six categories

  1. Perfusion
  2. Cardiac
  3. Eye/muscle/integument
  4. Nervous
  5. Skeletal
  6. Respiratory

Scoring 0-3 w/ 3=severe injury

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18
Q

What type of immune reaction is a reaction to a RBC transfusion and why won’t Benadryl be of help?

A

Type II - antibody mediated

diphenhydramine results in decreased histamine and histamine plays a role in a type II hypersensitivity reaction

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19
Q

How do ammonia and glutamine cause seizures in HE?

A

Glutamine and ammonia result in overstimulation of the NMDA receptor by glutamate and ammonia

..in part b/c of free radical formation

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20
Q

What serves as a counterregulatory process to RAAS and SNS

A

natriuretic peptide system (ANP, BNP)

Circulating ANP and BNP is increased in dogs/cats with heart disease, roughly in proportion to disease severity

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21
Q

Define PaCo2 by using minute ventilation and VCO2

A

PaCO2 ~ VCO2 / VA

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22
Q

what is the definition of diffusion impairment?

A

Thickened respiratory membrane

ie ARDS, oxygen toxicity

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23
Q

Calculate the dosing for albumin replacement

A

Albumin deficit (grams) = 10 * (desired albumin - patient albumin) * weight * 0.3

HSA is a 25% solution (25 grams in 100 mls = 2.5 g/ml)

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24
Q

There are 3 characteristic shapes of ventilator waveforms - name them and include what they mean

A

Square - indicated that a given parameter changes abruptly but is then held constant for a period of time

Ramp - indicate that a parameter is changing gradually over time

Sine - patient efforts such as seen w/ spontaneous breaths in CPAP or SIMV

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25
Effect of diuretics on the frank-stalling heart curve
Reduce preload, shift to the left
26
What is the main site for Mg resorption
Loop of henle
27
What are the three characteristic shapes of ventilator waveforms?
Square Ramp Sine
28
Fxn of endothelin
Postent vasoconstrictor produced by vascular endothelial cells in response to sheer stress, angiotensin II, and other various cytokines Directly alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes
29
How is urea removed from the CNS
no urea cycle removed by transamination of glutamate into glutamine in astrocytes (glutamine [ ] in HE are elevated in dogs w HE and are frequently correlated w neurons dysfxn) Glutamine is then exchanged across the BBB for tryptophan (leading to increased tryptophan and increased tryptophan metabolites (serotonin) Glutamine is also transported from astrocytes into neurons, where it is converted to glutamate Overstimulation of the NMDA receptors by glutamate and ammonia can cause seizures and neurotoxicity, in part b/c of free radical formation
30
How does TBI, cardiomyopathies and neoplasia result in increased coagulability?
Increased TF
31
List effective vs ineffective osmoles
Effective: Na, Cl, HCO3, K, Glucose Ineffective: BUN
32
How is venous admixture calculated and what is considered normal?
Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2) Normal is considered less than 5% Values > 10% are considered to be increased and may increase to more than 50% in severe, diffuse lung disease
33
What senses a change in plasma osmolality and what are the two major physiologic mechanisms for controlling plasma osmolality?
Hypothalamic osmoreceptors ADH system and thirst
34
What is the mechanism of negative pressure pulmonary edema?
Pathogenesis not clearly understood - but high pressure and increased permeability mechanisms have been suggested and both seem plausible. During UA obstruction, extreme sub atmospheric intrathoracic pressures are generated that then acute pulmonary vascular pressure overload, an increase in vascular return, and preload. Exacerbated by sympathetic stimulation associated w hypoxia causing an increase in afterload. **both hydrostatic pressure edema and resultant microvascular damage** **endothelial cell injury and vascular leak cause the permeability edema**
35
List electrolyte disturbances that occur with massive transfusions
Hypomagnesemia Hypocalcemia Hyperkalemia
36
Describe the chemoreceptor system
Reflex originating in chemoreceptor organs (carotid and aortic bodies) responds to: - decrease in tissue oxygen tension - increase in CO2 - decrease in pH Reflect a decrease in blood flow or oxygen delivery rather than a change in blood pressure per se. Cause increased signaling from the chemoreceptors and serve to excite the vasomotor center and promote sympathetic outflow.
37
What is responsible for most of the respiratory response to carbon dioxide?
Central chemoreceptors
38
What is the main action of PTH?
increases blood Ca levels through... - increased tubular reabsorption of calcium - increased osteoclastic bone resorption - increased production of calcitriol **acts to increase Ca in states of low Ca**
39
How does IMHA result in a hyper coagulable state
Circulating TF procoagulant
40
At what pulmonary venous pressures would you expect to see CHF
Pulmonary venous pressures greater than 25 mmHg Systemic venous pressure greater than 20 mmHg
41
What is the blast theory
Seen in neurogenic pulmonary edema ..it is thought that massive, neuronal, sympathetic activity results in a sequence of events causing both hydrostatic and increased permeability edema - this is known as the blast theory. Initially, hydrostatic pressure edema occurs, but at very high pulmonary hydrostatic pressures, endothelial cell injury and vascular leak result in RBC and protein leakage into the alveolus. Sympathetic stimulation also causes vascular effects that can result in acute cardiac insufficiency.
42
Define paradoxical intracellular acidosis
occurs after Na bicarbonate administration Bicarbonate cannot freely cross cell membranes, but the CO2 produced as bicarbonate is metabolized can freely enter cells. Once intracellular the CO2 combines w/ water, leading to H ion release and causing an intracellular acidosis.
43
What center is responsible for terminating respiration?
Pneumotaxic center Located in the upper pons, sends inhibitor impulses to the inspiratory center - terminating in aspiration and thereby regulating inspiratory volume and RR
44
How does doxopram stimulate respiration
via peripheral chemoreceptors at higher dosages -stimulates the medullary respiratory center --> causing an increase in TV and RR
45
How does PLN result in a hyper coagulable state?
Platelets are hyperaggregable (increased markers of activation) Increases in fVIII and fibrinogen concentrations (+/- vwf and fV increases) low AT activity
46
Equation to calculate osmolality and effective osmolality
Osmolality = 2*Na + (BUN/2.8) + (Glucose/18) Effective osmolality = 2*Na + (Glucose/18)
47
What ar ether main contributors to anion gap?
Albumin and phosphorus **AG not reliable in hypoalbunimeic patients**
48
What regulates vasopressin release?
Released from the anterior pituitary regulated by changes in blood osmolarity. In face of significant hypotension - release of vasopressin can increase significantly, independent of osmolarity.
49
What is the equation of motion?
Muscle pressure + ventilator pressure = (tidal volume / compliance) + (resistance x flow)
50
Calculate amount of blood to give an anemic patient
volume (ml) of whole blood = 2 * PCV rise desired (%) * body weight
51
What are the axes of the frank-starling curve
``` y-axis = Cardiac Output x-axis = preload ```
52
What does the apneustic center control?
Located in the lower pons Is responsible for coordinating the speed of inhalation and exhalation
53
Effects of ammonia in the brain
down-regulates NMDA receptors blocks chloride extrusion from the postsynaptic neuron, decreasing inhibitory neurotransmitters
54
What is responsible for the moment to moment regulation of blood pressure?
Baroreceptor reflex system
55
What is exclusively responsible for the increase in ventilation secondary to hypoxemia?
Peripheral chemoreceptors | **hypoxemia has NO action on central chemoreceptors**
56
what is plateau pressure
Airway pressure measured at the end of an inspiratory pause
57
What is the only underlying cardiac disease that predisposes to infective endocarditis?
sub aortic stenosis
58
Calculate Na deficit
= 0.6 8 BW * (target Na - patient Na) **select a target Na concentration of no more than 10-15% higher than the patient's current Na Calculated Na deficit determines the amount of hypertonic saline to be infused to raise plasma Na no water than 2 meq/L/hr
59
MOA of hypernatremia w/ activated charcoal and mannitol
Hypertonic cathartic draws electrolyte-free water into the GI tract Osmotic diuresis w/ mannitol causes an electrolyte-free water loss and thus can cause hypernatremia
60
Where are peripheral chemoreceptors located?
Carotid bodies at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch Carotid bodies are responsible for the majority of the peripheral chemoreceptor control of ventilation, whereas the aortic bodies tend to have a greater role in the regulation of the circulation
61
Name the four phases of the respiratory cycle
Inspiratory flow Inspiratory pause Expiratory flow Expiratory pause
62
What are the specific areas of the dorsal and ventral respiratory groups?
Dorsal - located in the region of the nucleus tracts solitaires - where visceral afferents from cranial nerves IX and X terminate. This area is responsible for inspiration. Ventral - comprises 4 nuclei (nucleus retroambiguus, nucleus para-ambiguous, nucleus retrofacialis, pre-Botzinger complex). Ventral group controls voluntary forced exhalation and acts to increase the force of inspiration.
63
Briefly describe the cell-based method of coagulation
Initiation phase = on TF-bearing cells; TF-initiated generates small amounts of thrombin (TF = membrane protein). Plasma fVII binds to TF and is activated --> generating small amounts of thrombin, this activates platelets that are adhered to the site of vascular damage. Amplificationa nd Propagation - on platelets - Amplification: platelets are activated and have activated cofactors V and VIII bound to their surfaces. Thrombin amplifies the initial signal Propagation phase - complexes are assembled on the surface of the activated platelet.
64
Calcitonin MOA
**reduces blood Ca levels** Decreases renal tubular reabsorption of Ca Acts on bone to inhibit osteoclastic bone resorption activity
65
Where are central chemoreceptors located?
Ventral surface of the medulla in close proximity to the dorsal and ventral respiratory neurons
66
List mediators that cause vasoconstriction
``` Catecholamines (NE, epi) Vasopressin Angiotensin II Endothelian I Thromboxane ```
67
Wha causes vasodilation in sepsis?
Nitric oxide - unregulated via TNF-alpha, IL-1beta, IL-6 Upregulation of ATP-sensitive K channels Depletion of vasopressin stores Vascular insensitivity to catecholamines
68
How are EtCO2, PaCO2, and PvCO2 related
EtCO2 < PaCO2 < PvCO2 **all by 5 mmHg**
69
What are the 4 gases in the alveoli? ...and what are their values (breathing room air at sea level)
Nitrogen = 560 mmHg CO2 = 40 mmHg O2 = 105 mmHg Water vapor = 50 mmHg
70
What is the most important factor to control breathing?
PCO2 Feedback for CO2 depends primarily on central chemoreceptors Small increases in PCO2 produce large increases in breathing Central chemoreceptors sense changes in CO2 and/or pH and provide a tonic drive to the network of respiratory neurons and a feedback on the blood levels of CO2 and therefore the adequacy of ventilation for the metabolic needs Peripheral chemoreceptors cause a minimal increase in ventilation secondary to increased arterial PCO2 and decreased pH
71
List the 3 main anticoagulant proteins and their MOA
Antithrombin - inhibits thrombin and Xa, lesser inhibitory effects on IX and fVVa-TF complex - is most effective when bound to heparin-lie GAGs of the glycocalyx or when exposed to heparins Protein C - inhibits factors Va and VIIIa, is activated to aPC when trace amounts of thrombin bind TM located on the endothelium TFPI - released from Ecstatics and acts to inhibit fVIIa-TF complexes and factor Xa (all components of the extrinsic pathway)
72
Fxk of protein S
is a co-factor for the inhibition of Xa by TFPI

Hopper's CCM Book (1 decks)

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