Quick Study Final Flashcards
Ventrolateral medulla
Senses changes in H+ in intersitial fluid that are a result of hypoxia (anaerobic metabolism)
Responsible for most of the ventilators response to hypercapnia
Response=increase ventilation
Internal intercostals
Expire
T-1 to T-11.
Hyperoxia
PCR sensitive to dissolved O2, decrease firing rate
Compliance of the lung
Less compliant at the apex than the base
Increase gravity, increase effect of base pulling on apex, decrease compliance
ANGII on HCO3- reabsorption
Increases reabsorption by stimulating Na-H+ exchanger (Na+ in, H+ out)
Renal Lobe
Medically pyramid and the cortical tissue at its base and sides (1/2 renal column)
Number of lobes=number of pyramids
Renal Lobule
Medullary Ray in the center of the lobule and the surrounding cortical material
Represents a renal secretory unit
Renal secretory unit
Collecting duct and a group of nephrons that drain into that duct
Filtration Apparatus of Kidney
Fenestrations of endothelium—small proteins, thick, negative charged glycocalyx
Glomerular Basement Membrane–size and ion selective, repels anions and restricts movements of cation
FIltration slit Membrane-true size selective barrier, NEPHRIN (transmembrane protein), and modified adherens junctions
Clara Cells
Prevent luminal adhesion if the airway wall collapses
Line the bronchioles
True Vocal Cords vs. False Vocal Cords
True-stratified squamous epithelium, vocalis ligaments, vocalis muscle
False-respiratory epithelium, seromucous glands, ventricle let
Renal Lobe
Medically pyramid and the cortical tissue at its base and sides (1/2 renal column)
Number of lobes=number of pyramids
Renal Lobule
Medullary Ray in the center of the lobule and the surrounding cortical material
Represents a renal secretory unit
Renal secretory unit
Collecting duct and a group of nephrons that drain into that duct
Filtration Apparatus of Kidney
Fenestrations of endothelium—small proteins, thick, negative charged glycocalyx
Glomerular Basement Membrane–size and ion selective, repels anions and restricts movements of cation
FIltration slit Membrane-true size selective barrier, NEPHRIN (transmembrane protein), and modified adherens junctions
Clara Cells
Prevent luminal adhesion if the airway wall collapses
Line the bronchioles
True Vocal Cords vs. False Vocal Cords
True-stratified squamous epithelium, vocalis ligaments, vocalis muscle
False-respiratory epithelium, seromucous glands, ventricle let
Clinical S/S of IEM
Too much substrate is bad (intoxication)–damage to the body
Too little primary product is bad (energy defects; other pathway deficiencies)–lack substrate for other processes
too much alternative product (intoxication)
Too much substrate, too much alternative product
Too little primary product
Amino acid disorders unable to break down
Protein
Acute presentation or chronic presentation
Organic acid disorders unable to break down
Protein and fat
Acute presentation or chronic presentation
Fatty acid oxidation disorders
Unable to break down fats
Energy defect disorder
Carbohydrates disorders unable to break down
Carbohydrates
Energy Defect diseases
Fatty acid oxidation disorder, glycogen storage diseases, mitochondrial disorders
Acute Intoxication disorder
Metabolic crisis: poor feeding, vomiting, irritability, altered mental status, no focal neurological deficits.
AAD
OAD
Chronic presentation
Failure to thrive, developmental delays, intellectual disabilities, hearing loss
AAD, OAD
Complex Molecule Defects
More complex presentation
Dysmorphic features
Lysosomal strange diseases, proviso all diseases
AGMA Numonic
MUDPILES
A CAT MUDPILES
Metabolic Acidosis with normal anion gap
Diarrhea
RTA Topi rampage Intoxications Renal Failure Inhalant use Toluene
Test for Metabolic Acidosis
Blood lactate, pyruvate, ammonia, and glucose levels
Most likely to lead to a metabolic acidosis with an increased anion gap
Organic Acid Disorders
Normal anion gap and no significant acidosis
Amino acid disorders, urea cycle defects, maple syrup urine disease
Most carbohydrate disorders (yes/no) metabolic acidosis
NO. Except fructose 1,6, bisphsophatase
Increased AG and metabolic acidosis
Glycogen storage disorders
Mitochondrial disorders
Pyruvate dehydrogenase complex deficiency
Ketone utilization defects
Ketosis
Permanant–ketone utilization defect
Ketosis + other metabolic abnormalities–mitochrondrial metabolism (OAD, Mito-RCD)
Lactic Acidosis
Hyperlactatemia–increase in blood lactate without metabolic acidosis
Lactic acidosis–persistently increased blood lactate level in association with metabolic acidosis
CSF lactate
Blood lactate and pyruvate
Postprandial lactate
PAC
organic acid disorders and fatty acid disorders
Urine Organic Acids and urine acylglycine
OAD and FOAD
Plasma and ketone bodies
KUD ketone utilization defects
Phase 4 Nodal Cell AP
Funny Na–influx
K+ out
T-type Ca2+–calcium in
Depolarization and repolarization of the heart nodal cell
Depolarization–decreased permeability to K+, increased funny Na+, T-type
Repolarization-increased permeability to K+, closer to K+ equilibrium potential
Repolarization depolarization of myocytes
Depolarization-opening of fast Na+
Rapid repolarization-slow voltage gated K+ channels
Calcium channel blockers on nodal cells
Decrease slope of phase 4, decreased heart rate
Decrease slope of phase 0, depolarize slowly, extend heart rate
Decreased peak potential, decreasing conduction rate of AP between cells, less voltage-gated K+ channels open, slower repolarization
Ca2+ blockers and myocytes
Less time for cross bridge cycling
Less Ca++ TnC binding=fewer myosin binding sites uncovered
Sympathetics vs Parasympathetics to the heart
Symp–NE, increased cAMP, increased HR and contractility, decreased ESV and EDV
Para–ACh, decreased cAMP, ACh-dependent K+ hyperpolarize cell, more negative maximum diastolic potential increase in prepotential, slower heart rate,
Factors that influence pacemaker depolarization rate
Phase 4–NE increases by increasing Ca+ perm, ACh decreases by increasing K
MDP-ACh hyperpolarizes, making more negative, slowing HR
Threshold potential–cardiac depressants and CICR-RYR sensitivity
ACh in heart
Decreases If and Ica conductance a
Increase Ik conductance
Decreases Ca permeability and raises threshold
NE on heart
Increase Funny Na and increase Ca through membrane
Lowers threshold potential
DC counter shock
Phase 4 of myocytes AP to get the as many closed fast Na+ to open in order to create an AP.
SA node
Ik, Ica, If
Basal heart rate
Interatrial pathway
Neural like cells, right to left atrium quickly to synchronize contraction
Fast Na for this, Ik, Ica, If
Internodal pathway
Fast Na, K, Ca, and Funny
Bundle of His
fast Na
AV node conduction velocities
Slower than any other region of the heart
Complete atrial contraction and ejection before ventricles contract
AN–atrial muscle, nodal
N-nodal only, slowly changing prepotential
NH-nodal and bundle of his, rapid rate of depolarization and large amplitude
RBB vs LBB
RBB-right side of IV, connect with Purkinje in the apex of RV
LBB-larger, divides into anterior and posterior division
Anterior-wall of IV septum and apex
IV depolarized from left to right, shorter LBB
Posterior-posterior free wall of LV along base of heart–papillary muscles
Purkinje Fibers
Subendocardium, fastest rate
Cell to cell conduction through myocardium because Purkinje fibers interdigitate with ordinary contractile fibers
Depolarization direction
Endocardium to epicardium due to Purkinje fibers
Right completely depolarized before left because it is much thinner
Gap junctions of intercalated disks
Allow ions to flow rapidly from one myocytes to the next without a decrease in amplitude
Duration of AP for epicardium vs endocardium
Longer for endocardium
Wave of repolarization is epicardium to endocardium
Slower due to myocytes and no Purkinje
Inotropic agents (CO, SV, RAP)
Increase contractility, increase CO, increase SV, decrease RAP (because more blood is ejected from the heart on each beat), decreased ESV
Atrial Systole
Increase in atrial pressure causes an A wave in JVP curve
Causes 4th heart sound (abnormal)
Left atrial pressure and left ventricular pressure increasing
Aortic pressure decreasing
P-R segment
Conduction delay in the AV node
Segments include the humps, so that would be the AV delay
PR interval
Time between atrial depolarization and ventricular depolarization
Isovolumic relaxtion
End of of T wave
When the aortic valve closes
S1 sound
Occurs when is isovolumic contraction starts
Myocardial Infarction
Increased K+ in intersitium, decreased efflux of K+, more positive RMP, less magnitude action potential, vent depolarization is not isoelectric i.e. ST segment is not isoelectric
Restoration of myocardial infarction after MI
K+ washed out of interstitium, RMP more negative (back to normal)
Increasing K+ permeability
More negative RMP, decrease slope of line to prepotential, decrease HR
First Degree
All components are normal except PR interval is greater than 20 seconds but constant
WPW syndrome
Delta wave due to early dep of ventricular prior to activation of AV node, there is a new pathway.
Myocardial infarction cardiac myocytes
RMP less negative, fewer of the Na+ channels have reset to closed.
Less rapid depolarization
Inside of cell is still negative during plateau phase
Systolic current of injury
Normoxic–inside of cells are slightly positive and outside slightly more negative
Ischemic-remains negative (due to fewer Na+ channels set to closed due to higher K+ inside of cell) on inside and outside remains positive (due to
Diastolic Current of Injurt
K+ outside increased due to ATPase deceased activity and leak of K+, reducing the concentration gradient for K+, decreasing K+ efflux, which causes partial depolarization of the cell. This partial depolarization results in a less negative inside, so the outside is less positive, elevating the ST segment
NO for MI
Dilation of coronary vessels to produce cGMP inside vascular smooth muscle cells in the wall of coronary arteries.
Myosin phosphatase is activate, dephosphorylating regulatory MLCK– vasodialation
Act on Beta
Factors that shift filtration curve up and to the right (promoting edema)
Severe hypertension–>Increase CHP
Right heart failure–>increase Right atrial pressure–>increase Pv–>increase Pv
Increased blood volume (excess aldosterone)–>increase MCFP and PV–> increased filtration
Histamine, bradykinin, increase protein permeability (reduce oncotic pressure)
SNA and coronary flow
Decreased SNA= decreased coronary blood flow
Increased SNA=increase heart contractility, SV, and heart work, which increase coronary flow and coronary flow rate
PNA on coronary flow rate
Decreased PNA will increase HR which will increase coronary flow and coronary rate
Heart work
SV X MAP
Increase either, increase heart work, increase coronary flow by increasing adenosine
Adenosine
Dilates coronary VSM
Increased heart tissue accumulation of adenosine with increased HW
SNA and AVAs of skin
SNA contract AVAs to the deep plexus and to reduce blood flow to the superficial vascular plexus.
Less heat lost
No SNA, AVAs are open, and heat loss.
SNA dilates cutaneous Arterioles
Only myogenic regulation
Cerebral circulation
Regional flow changes with changes in regional activity
Change in SNA has little effect
Controlled solely by local metabolism
Large fluctuations of around 10% give little change in flow, get to 20% you will increase SNA, increase SV, increase MAP
CO2, H+, K+ elevation increase flow
50% O2 loss increase flow
Pulmonary Edema
Low capillary hydrostatic pressure, net force for reabsorption along entire capillary
Increase pressure, increase resistance leads to pulmonary edema
Increase RAP, increase PCP, but still reabsorbing
LEFT VENTRICULAR HEART FAILURE, LEFT AP INCREASES=pulmonary edema
Histamine in the lungs
Systemic=dilation
Lungs=constriction
