Valley Review Book Flashcards
How much body water is in the ECF? ICF?
TBW = 42L
ECF (1/3)= 14L
ICF (2/3)= 28L
Components of phospholipids in the phospholipid bilayer
Hydrophobic head (+ charge) Hydrophilic tail
Major Intercellular Ions
K, Mg, PO4
Major extracellular ions
Na, Cl, Ca, HCO3
Examples of ligand gated ION channels
5-HT3, GABA(A), Glutamate
Examples of GPCR
Muscarinic ACh receptors & most adrenergic receptors
Function of Na-K ATPase (pump)
3 Na OUT and 2 K IN
Example of something that stimulates the Na-K Pump
Insulin and Beta-2 agonists (aka ritodrine, terbutaline)
The 4 major categories of receptors
- Ligand gated ion Channels
- GPCR
- Calalytic
- nuclear receptors
Effect of increased cAMP in cardiac muscle
Increases contractility (d/t inc Ca) (Beta-1)
Effect of increased cAMP in bronchial muscle
relaxes bronchial smooth muscle(d/t dec Ca) (Bronchodilation) (Beta 2)
What kind of receptors are beta adrenergic receptors
Gs: stimulate increased cAMP
Subunits of the GPCR
heterotrimeric:
Gamma
Beta
Alpha
List the common second messengers
cAMP cGMP Ca Calmodulin Inositol Phosphate (IP3) Diacylglycerol (DAG)
Metabolizes cAMP into AMP
PDE
cAMP simulates
Protein Kinase A
Activates cGMP
NO, NTG, Nitroprusside, Nitric Oxide Donors
Function of phospholipase C
create IP3
Normal serum osmolality
300 mOsm/kg (270-310)
Most electrolytes are reabsorbed in what part of the nephron?
Proximal Tubule
Site of action of carbonic anhydrase inhibitors
Proximal Tubule
Function of the descending loop of henle
Reabsorbs H2O (Impervious to Na)
Site of action of loop diuretics
Ascending Thick LOH
Function of Ascending Thick LOH
NA/K-Cl Pump
Site of action of ADH
Collecting Ducts
MOA of ADH
Inserts Aquaporins (V2) into the collecting duct to facilitate reabsorption of H2O
The site of action of aldosterone
collecting duct (primarily) and Late Distal Tubule
MOA of aldosterone
Facilitates Na (therefore H2O) reabsorption and K+ excretion
Site of action of hydrochlorothiazide (HCTZ)
Early Distal Tubule
Site of action of Spironolactone (K sparing)
Late Distal Tubule
The peritubular capillaries of the LOH
Vasa Recta
Components of the nephron found in the cortex
Glomeruli, proximal tubules, distal tubules
Components of the nephron found in the medulla
LOH and Collecting Ducts
CO delivered to kidneys
1.25L/min (25%)
What establishes the osmotic gradient in the medulla of the nephron?
Loop of Henle
Where is glucose reabsorbed in the nephron
Proximal Tubule
Where is vasopressin synthesizes? Released?
Synthesized in the paraventricular and supraoptic nuclei of the hypothalamus
Released from the posterior pituitary (Neurohypophysis)
What stimulates ADH release?
Increase plasma osmolarity (also Stress, hypotension Pain, CPAP, PEEP, VA)
Normal urine osmolarity
1200-1500 mOsm (AVP level low 0.5mg/kg/hr)
Urine osmolarity seen with high levels of AVP/ADH/Vasopressin
50-100 mOsm (AVP level 2-25 mg/kg/hr)
Causes of SIADH
Intracranial Tumor, Hypothyroidism, Porphyria, small Oats cell carcinoma of the lung
the major determinant fo extracellular fluid volume
Sodium content
Most important HORMONE for regulation of extracellular fluid volume
Aldosterone
Things that increase Na excretion
increased GFR, increased ANP, decreased aldosterone
Things that decrease Na excretion
decreased GFR, increased aldosterone, decreased ANP
Where is aldosterone produced
Zona Glomerulosa of the adrenal cortex
Where in the nephron is most of the sodium reabsorbed
proximal tubule (active process requiring energy)
Where in the nephron is most of the potassium reabsorbed?
Proximal Tubule 60%; Ascending LOH 25%
What factors increase K+ excretion?
- Aldosterone secretion
- Increased Distal Tubular flow rate: Increased flow rate seen with Lasix
- BiCarbonate Concentration in Tubular Fluid: increase urine alkalinity increases K+ excretion
List some loop diuretics
(ide) furosemide bumetanide Torsemide Ethacrynic acid
What is the target for loop diuretics?
Inhibition of the Na-K-2Cl symporter: inhibit the reabsorption of these ions (located in the Thick Ascending LOH)
Side effects of loop diuretics
Hypokalemia, Fluid volume deficit, Otho Hypo, reversible deafness
MOA of thiazide diuretics
Inhibit Na reabsorption in the early distal tubule
Examples of Thiazide diuretics
Chlorothiazide, Hydrochlorothiazide, Chlorthalidone, Metolazone
MOA of potassium-Sparing Diuretics
Decrease Na reabsorption form the late distal tubule and collecting duct
MOA of Spironolactone
Competitively inhibits aldosterone:
- therefore inhibits sodium reabsorption in the late distal tubule and collecting duct
Side effects of thiazide diuretics
Hypokalemia due to increased K+ secretion
Side effects of potassium-sparing diuretics
Hyperkalemia
MOA of carbonic anhydrase inhibitor
Inhibits the enzyme carbonic anhydrase in the proximal tubule which inhibits bicarb reabsorption
Example of carbonic anhydrase inhibitor
Acetazolamide
Actions of carbonic anhydrase inhibitors
Dec Bicarb reabsorption
Dec sodium reabsorption
-> these cause diuresis
-> hyperchloremic metabolic acidosis
One of the principal therapeutic uses of acetazolamide
Decrease IOP by decreasing formation of aqueous humor
Side effects from osmotic diuretics
Hypokalemia (K+ secretion is increased secondary to flow through the distal tubule and collecting duct)
Prerenal causes of perioperative oliguria
Decreased RBF
Hypovolemia
Decreased CO
Renal causes of perioperative oliguria
Renal Tubular Damage (acute tubular necrosis)
Renal Ischemia
Nephrotoxic Drugs
Release of HgB or Myoglobin
Postrenal causes of perioperative oliguria
Obstruction
Bilateral ureteral obstruction
Extravasation due to bladder rupture
Tests to differentiate prerenal from renal failure
Renal failure (Aka acute tubular necrosis, ATN)) has high fractional excretion of sodium (FENa) > 0.03 (3%) Prerenal failure FENa < 0.01 (1%)
Normal GFR
125 ml/min
GFR for renal insufficiency
12-50 mL/min
Pathophysiology of CKD
Chronic anemia Pruritus Coagulopathies Hyperkalemia Hypocalcemia Hypermagnesemia HTN Pericardial Dz Metabolic acidosis
Treatment options for hyperkalemia
give Ca Give HCO3 Hyperventilate Loop Diuretics Give insulin-glucose Administer B2 agonist (terbutaline) Kayexelate Dialysis
Where is most of the HCO3 absorbed?
In the proximal Tubule (90%)
Formula for anion Gap
([Na]+[K])-([Cl]+[HCO3])
Normal anion gap
12mM
What is the definition of anion gap?
total of unmeasured anions (-) such as Proteins, HPO4, & SO4
Ion responsible for RMP in nerve? Depolarization? REpolarization?
RMP = K Depolarization= Na INTO cell Reploarization = K OUT of cell
Motor neurons are what kind of nerve fiber?
A-alpha fibers (Large, myelinated, fast conduction velocity)
Receptors found in the motor end plate
Nm (nicotinic ACh receptors)
What affect does ACh binding to PREsynaptic Nicotinic receptors in the NMJ have?
Positive feedback: increases release of ACh
This accounts for fade seen with NDMB and phase II blocks with succ
Ions that diffuse across NMJ as a result of ACh binding to nicotinic receptors
Ca and Na IN K OUT (Hyperkalemia with succ)
What subunit does ACh (and succ) bind to on the Nicotinic receptor in the NMJ
2 Alpha subunits (one ACh to each)
MOA of NDMB
Competitive inhibition of ACh- binding sites (Alpha subunits) in the NMJ
How long after succ does myalgia occur?
24-48 hours
Characteristics of NDMBs
aka Phase II Block: Competitive inhibition Fade after high frequency stimulation Exhibits post-tetatinc facilitation Antagonized by anticholinesterases NO fasciculations
Metabolism of succinylcholine
Plasma cholinesterase ( false, pseudo, non-specific, or type-II)
Characteristics of depolarizing muscle blockers
AKA Phase I Block:
- decreased single twitch hight
- response to high frequency stimulation is maintained
- minimal or No fade after TOF
- Antagonized by non depolarizers
- potentiated by anticholinesterase
- Fasciculations precede block
Intermediate action NMBs
(30-45min) (CAR-V) Cisatracurium Atracurium Rocuronium Vecuronium
Define DOA of NMBs
The time from injection to return of 25% twitch height
The amino steroid NMB
“curonium”
Rocuronium
Vecuronium
Pancuronium
The benzylisoquinoline NMB
“curium”
Atracurium
Cisatracurium
Mivacurium
What are some properties of NMBs?
100% ionized at physiologic pH
VERY highly protein bound
Do NOT cross BBB/Placenta (d/t ionization)
excreted in urine (d/t ionization)
NMB with primarily biliary excretion
Vec and Roc
Metabolism is the primary route of elimination for which NMBs
Succ, atracurium, Cis, mivacurium
the “curiums” + Succ
NMB which is metabolized by hofmann elimination
Cisatricurium
Atracurium ( and ester hydrolysis by non-specific esterase’s)
NMB’s that elicit the release of histamine
Succ, Miv, atra …
Why does succinylcholine elicit bradycardia
Mimics the action of ACh at muscarinic receptors in the SA node
NMB that is a direct vagolytic
Pancuronium ( aka antimuscarinic actions)
Potassium changes seen with succinylcholine
Increases plasma K by 0.5 mEq/L in healthy
5-10 mEq/L in Burn, trauma or head injury
Why is the twitch response greater on the paralyzed size of a hemiplegic patient?
Due to up-regulation of ACh receptors
Signs of malignant hyperthermia
Increased EtCO2, Pyrexia, Tachycardia, Cyanosis, Rigidity, or master spasm (trismus)
Serum abnormalities seen in MH
increased H, K, Ca, and CO2
Decreased O2
What defect is present that causes MH
Mutation in ryanodine receptor (RyR1)
One of the earliest, most sensitive and specific signs of MH
Elevation in EtCO2
Antibiotics that increase the degree of blockade with NDNMBs
Neomycin, streptomycin
LAs that increase the degree of blockade with NDNMBs
Amides (dec dose by 1/3 to 1/2)
Effect of VAA on degree of blockade from NDNMBs
increased blockade
Lithiums effect on NMBlockade
increases degree of block
Effect of myasthenia graves on succinylcholine
block DECREASED
Clinical response to 75-80% blockade
TV > 5mg/kg; single twitch as strong as baseline
Clinical response for 90% blockade
ABD relaxation adequate for most and surgeries (1 twitch on TOF)
Clinical response for 70-75% Blockade
No palpable fade, sustained tetany for 5 seconds, VC at least 20 mL/kg ( reliable indicator for recovery)
Clinical response for 50% blockade
Neg insp test -40cm H2O, Head Lift for 5 seconds, sustained strong hand grip, SUSTAINED BITE, (reliable indicator of recovery
When does a phase II block occur with succinylcholine
Treatment with higher doses, and/or prolonged exposure (this is diagnosed by the presence of FADE)
The predominant neurotransmitter in the periphery
ACh
Where is NE released in the periphery
From all sympathetic POST-ganglionic nerves (the exception is sweat glands)
The adrenal medulla is innervated by
Sympathetic Preganglionic Neurons that release ACh
Where are muscarinic receptors found
peripherally in tissues innervated by parasympathetic postganglionic neurons
List the nerve fiber types and their transmitted sensation
A-alpha: Muscle contraction & proprioception A-beta: Proprioception, touch, pressure A-gamma: Skeletal muscle tone A-delta: Pain, Temperature, Touch B-Fibers: Autonomic sC-Fibers: Autonomic dC-Fibers: Pain, Temperature, Touch
Origin of the sympathetic nervous system
Thoracolumbar: T1-L2 or T1-L3
Origin of cardiac accelerators
T1-T4
Origin of the stellate ganglion
Inferior cervical and first thoracic ganglia
Signs and symptoms of Horner Syndrome
(Stellate ganglion block) Ipsilateral Miosis Ptosis Enophthalamos Flushing Increased Skin Temp Anhydrosis Nasal Congestion
All sympathetic preganglionic fibers pass through the _______
White Ramus located from T1-L2
Function of grey rami
Allow for coordinated mass discharge of the SNS
What is the function of presynaptic Alpha 2 receptors
Negative feedback for the release of NE
Pathway for the synthesis of NE
Tyrosine-> L-Dopa-> Dopamine (DA) -> NE -> Epi
What is the % of NE and Epinephrine in the adrenal medulla?
20% NE; 80% Epi
What metabolizes NE
MAO in the nerve terminal; COMT in the plasma
80% of NE is not metabolized but undergoes reuptake from the synaptic cleft
Drugs to avoid in patients taking MAOI’s
Indirect acting sympathomimetics (ephedrine) and Meperidine: They may lead to hypertensive crisis Meperidine > ephedrine
Effect of Beta 1 stimulation on the heart
Increased HR(SA node) , Contractility (muscle fibers), and conduction speed (AV node)
Effect of Beta 2 stimulation on the lungs
increased secretions and bronchodilation
Beta receptor of the kidney
Beta 1: increases renin release -> Increase BP
Beta receptor of the liver
Beta 2: Gluconeogenesis and glycogenolysis
Effect of Beta stimulation on the uterus
Beta 2: relaxation (Ritodrine)
Resting BP is controlled mainly by _______
Renin (85%)
Where is renin released
Juxtaglomerular cells of the AFFERENT arteriole
Function of Renin
Converts angiotensinogen to Angiotensin I
Where is ACE found
On the endothelial surface of capillaries especially in the PULMONARY Capillaries (this is why it causes cough)
The two most important stimuli for aldosterone release
Angiotensin II and High serum potassium
Function of aldosterone
Increase potassium excretion and sodium reabsorption (Promotes volume expansion)
What causes Renin release
Dec RBF
Inc SNS stimulation or [Cl-]
Why do we see a decrease in MAP and Diastolic BP with low dose EPI
Beta 2 mediated vasodilation (decreased SVR)
Anatomical landmark for T4
Nipple
What are some side effects of ritodrine?
Hyperglycemia, Hypokalemia, tachycardia
Origin of the parasympathetic nervous system
Craniosacral
Cranial Nerves: oculomotor CN III, facial CN VII, glossopharyngeal CN IX, and Vagus CN X
Sacral nerves S2-S4
Drug that can cause cholinergic crisis
Physostigmine (i.e. excess acetylcholine)
Symptoms of cholinergic crisis
DUMBBELL STPD (accessive AcH) Diarrhea, Urination, Miosis, Bradycardia, Bronchoconstriction, Emesis, Lacrimation, Lethargy, Salivation, & Seizures. Treatment Atropine, Pralidoxamine, and Diazepam
Which antimuscarinic least crosses the BBB
Glycopyrolate (d/t charged ammonium group)
Signs of anticholinergic syndrome
delirium, dry mouth, flushed skin, blurred vision, tachycardia, rash, hypotension
(mad as a hatter, Dry as a bone, Red as a beet, Blind as a bat….)
Treatment for anticholinergic syndrome
Physostigmine
Bronchodilation is promoted by stimulation of which receptor
Beta 2 Adrenergic
MOA of leukotriene antagonists?
competitive antagonists of leukotriene
What is the function of the reticular activating system (RAS)
functions to maintain alert/awake state
What is the purpose of SSEP monitoring
Monitor for posterior chord ischemia or brain ischemia
Site of SSEP stimulation at the ankle
Tibial Nerve
Indicators of damage in nerve being monitored surging SSEP
DECREASE in amplitude
INCREASE in latency
Motor evoked potentials are used to monitor for
Ischemia to the anterior (ventral) cord
BAEP monitor the integrity of
CN VIII
VEPs monitor the integrity of
The optic nerve CN II
Order the evoked potentials according to their sensitivity to anesthetic agents
VEP (Very)
SSEP (Somewhat)
BAEP (Barely)
Where is the substantial gelatinous located
In Lamina II & III of the dorsal horn
Major neurotransmitter of A-delta fibers
Glutamate which binds to AMPA and NMDA
Major neurotransmitter for C Fibers
Substance P which binds to NK-1 receptors
What is the function of the dorsolateral tract
(descending tract) modulates pain
What is the function of the lateral spinothalamic tract?
Carry pain and temperature
What is the function of the ventral spinothalamic tract
crude touch and pressure
Root associated with clavicle dermatome
C4
Root associated with nipple dermatome
T4
Root associated with xiphoid dermatome
T6
Root associated with umbilicus dermatome
T10
Root associated with tibia dermatome
L4-L5
Root associated with perineum dermatome
S2-S5
What decreases the release of substance P from C-Fibers
Enkephalin (Modulates Pain)
Spinal opioid analgesia is mediated through what receptor
Mu-2 primarily (S in Spinal looks like 2)
Name the hydrophilic opioids
Morphine
Name the lipophilic opioids
fentanyl, alfentanil, sufentanil
Site of action of IV opioids? Intrathecal/Epidural?
- IV: Periventricular/periaqueductal grey
- Spinal/Epidural: Substantia Gelatinosa
Supraspinal analgesia is mediated by
Mu-1 (primarily), Delta, and Kappa receptors
Side effects from Mu-1 receptors
Bradycardia and Euphoria
Opioid receptor responsible for physical dependence and respiratory dependence
Mu-2
Kappa receptors are responsible for
sedation and dysphoria
Competitive opioid antagonist
Naloxone (narcan)
Naltrexone (trexate)
Nalmefene
White rami carry _______
myelinated sympathetic preganglionci neurons
List the Cranial Nerves
Oh Oh Oh To Touch And Feel A Girls Vagina Ahh Heaven Olfactory Optic Oculomotor Tochlear Trigeminal Abducens Facial Acoustic (Vestibulococclear) Glossopharyngeal Vagus Accessory Hypoglossal
Site of formation of CSF
Choroid Plexus of the Lateral, Third, and Fourth ventricles
Site of reabsorption of CSF
Arachnoid Villi and arachnoid granulations (both are part of the arachnoid membrane
List the flow of CSF in the brain
Choroid plexus -> Lateral Vent -> Foramina of Munro -> Third Ventricle -> Aqueduct of Sylvius -> Fourth vent -> Foramina of Lusaka & Magendie -> Subarachnoid Space -> Brain -> Arachnoid Villi
Major vessels that supply the circle of willis
Internal Carotid arteries and the basilar artery
What is stump pressure
measures the pressure transmitted through the circle of willie back to the carotid artery
Desired stump pressure
> 40 mmHg
Effects of VAA on CBF? CMRO2
Dec CMRO2
Increased CBF
Effects of IV anesthetics in CBF & CMRO2?
Decrease both (Except ketamine which increases both)
Arterial blood supply to the spinal cord
(1) one anterior spinal artery
(2) two posterior spinal arteries
(3) small segmental spinal arteries
Major source of blood to the spinal cord
75% via the anterior spinal arteries
Origin of the artery of adamkiewicz
From the left side in the lower thoracic (T8-T12 75%) or upper lumbar region (L1-L2 10%)
Decorticate rigidity is cause by
Damage to the brain above the cerebellum and brainstem aka supratentorial (upper ext flexion lower ext extension with feet turned medial)
Decerebrate rigidity is caused by
Extensive damage to the brainstem or cerebral lesions that compress the thalamus and brainstem
Mechanical ventilation is required for which form of rigidity
Decerebrate d/t damaged brainstem which contains vital responses centers
What is the normal ICP?
< 15 mmHg
Components of Cushing’s triad
Increased BP (MAP)
Decrease in HR
Irregular respiration
Cushing’s triad is the result of
increased intracranial pressure
What is the correct placement of the single orifice catheter
- 0 cm ABOVE the junction of the SVC and atrium
2. 0cm Below for MULTI orifice catheters
At what age does the anterior fontanelle close
18 months
Which fontanelle closes last
Posterolateral
The P wave correlates with what cardiac event
Atrial depolarization
The PR Interval correlates with what cardiac event
Atrial systole & AV nodal delay
The QRS Complex correlates with what cardiac event
Ventricular Depolarization (and atrial repolarization)
The QT interval correlates with what cardiac event
Ventricular systole
The T wave correlates with what cardiac event
Ventricular depolarization
Phases in the SA node action potential
Phase 4: Diastole (K+ OUT & some Na IN) (Ca is in the last 1/3)
Phase 0: Slow depolarization (Ca & Na INTO cell)
Phase 3: Depolarization (K+ OUT of the cell)
Phase 4: Diastole (Na/K Pump restores Na and K lvls)
On what phase for the nodal action potential do CCB work?
They slow the rate of Phase 4 depolarization
On what phase of the cardiac action potential do CCB work?
The work on Phase 2 (Plateau)
RMP of cardiac ventricular cells
-90 mV
What happens when gates Na channels are inactivated?
Cell enters the absolute refractory period
Diagnosis of RBBB on the ECG
Look at leads V1 & V6
V1 = rSR’ (broad R’ wave)
V6= qRS
Diagnosis of LBBB on the ECG
Look at leads V1 & V6
V1= Loss of R wave
V6= Wide R wave with a notch
Diagnosis of 1st degree heart block
PR interval > 0.20 seconds
Diagnosis of 2nd degree AV block Type I
Progressive increase in PR interval until a beat is skipped
Diagnosis of 2nd degree AV block Type II
Appearance of a NON-CONDUCTED P-wave (No progressive prolongation of PR)
Diagnosis of 3rd Degree AV block
Independent P-wave (atrial) and QRS wave (Ventricular) activity
What is the cause of Heart rate increase from Right atrial stretching
Bainbridge Reflex
Indication of myocardial ischemia on ECG
Subendocardial ischemia = ST depression > 1mm
Transmural Injury = ST elevation > 1mm
What part of the ventricular action potential correlates with the QRS complex?
Phase 0
What part of the ventricular action potential correlates with the T wave?
Phase 3
What part of the ventricular action potential correlates with the QT Interval?
Phase 2
EKG changes for hyperkalemia
Peaked or tented T waves