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Quick Study Final Flashcards

1
Q

Ventrolateral medulla

A

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

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2
Q

Internal intercostals

A

Expire

T-1 to T-11.

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3
Q

Hyperoxia

A

PCR sensitive to dissolved O2, decrease firing rate

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4
Q

Compliance of the lung

A

Less compliant at the apex than the base

Increase gravity, increase effect of base pulling on apex, decrease compliance

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5
Q

ANGII on HCO3- reabsorption

A

Increases reabsorption by stimulating Na-H+ exchanger (Na+ in, H+ out)

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6
Q

Renal Lobe

A

Medically pyramid and the cortical tissue at its base and sides (1/2 renal column)
Number of lobes=number of pyramids

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7
Q

Renal Lobule

A

Medullary Ray in the center of the lobule and the surrounding cortical material
Represents a renal secretory unit

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8
Q

Renal secretory unit

A

Collecting duct and a group of nephrons that drain into that duct

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9
Q

Filtration Apparatus of Kidney

A

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

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10
Q

Clara Cells

A

Prevent luminal adhesion if the airway wall collapses

Line the bronchioles

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11
Q

True Vocal Cords vs. False Vocal Cords

A

True-stratified squamous epithelium, vocalis ligaments, vocalis muscle

False-respiratory epithelium, seromucous glands, ventricle let

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12
Q

Renal Lobe

A

Medically pyramid and the cortical tissue at its base and sides (1/2 renal column)
Number of lobes=number of pyramids

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13
Q

Renal Lobule

A

Medullary Ray in the center of the lobule and the surrounding cortical material
Represents a renal secretory unit

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14
Q

Renal secretory unit

A

Collecting duct and a group of nephrons that drain into that duct

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15
Q

Filtration Apparatus of Kidney

A

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

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16
Q

Clara Cells

A

Prevent luminal adhesion if the airway wall collapses

Line the bronchioles

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17
Q

True Vocal Cords vs. False Vocal Cords

A

True-stratified squamous epithelium, vocalis ligaments, vocalis muscle

False-respiratory epithelium, seromucous glands, ventricle let

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18
Q

Clinical S/S of IEM

A

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

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19
Q

Amino acid disorders unable to break down

A

Protein

Acute presentation or chronic presentation

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20
Q

Organic acid disorders unable to break down

A

Protein and fat

Acute presentation or chronic presentation

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21
Q

Fatty acid oxidation disorders

A

Unable to break down fats

Energy defect disorder

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22
Q

Carbohydrates disorders unable to break down

A

Carbohydrates

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23
Q

Energy Defect diseases

A

Fatty acid oxidation disorder, glycogen storage diseases, mitochondrial disorders

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24
Q

Acute Intoxication disorder

A

Metabolic crisis: poor feeding, vomiting, irritability, altered mental status, no focal neurological deficits.
AAD
OAD

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25
Chronic presentation
Failure to thrive, developmental delays, intellectual disabilities, hearing loss AAD, OAD
26
Complex Molecule Defects
More complex presentation Dysmorphic features Lysosomal strange diseases, proviso all diseases
27
AGMA Numonic
MUDPILES A CAT MUDPILES
28
Metabolic Acidosis with normal anion gap
Diarrhea ``` RTA Topi rampage Intoxications Renal Failure Inhalant use Toluene ```
29
Test for Metabolic Acidosis
Blood lactate, pyruvate, ammonia, and glucose levels
30
Most likely to lead to a metabolic acidosis with an increased anion gap
Organic Acid Disorders
31
Normal anion gap and no significant acidosis
Amino acid disorders, urea cycle defects, maple syrup urine disease
32
Most carbohydrate disorders (yes/no) metabolic acidosis
NO. Except fructose 1,6, bisphsophatase
33
Increased AG and metabolic acidosis
Glycogen storage disorders Mitochondrial disorders Pyruvate dehydrogenase complex deficiency Ketone utilization defects
34
Ketosis
Permanant--ketone utilization defect | Ketosis + other metabolic abnormalities--mitochrondrial metabolism (OAD, Mito-RCD)
35
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
36
PAC
organic acid disorders and fatty acid disorders
37
Urine Organic Acids and urine acylglycine
OAD and FOAD
38
Plasma and ketone bodies
KUD ketone utilization defects
39
Phase 4 Nodal Cell AP
Funny Na--influx K+ out T-type Ca2+--calcium in
40
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
41
Repolarization depolarization of myocytes
Depolarization-opening of fast Na+ | Rapid repolarization-slow voltage gated K+ channels
42
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
43
Ca2+ blockers and myocytes
Less time for cross bridge cycling | Less Ca++ TnC binding=fewer myosin binding sites uncovered
44
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,
45
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
46
ACh in heart
Decreases If and Ica conductance a Increase Ik conductance Decreases Ca permeability and raises threshold
47
NE on heart
Increase Funny Na and increase Ca through membrane | Lowers threshold potential
48
DC counter shock
Phase 4 of myocytes AP to get the as many closed fast Na+ to open in order to create an AP.
49
SA node
Ik, Ica, If | Basal heart rate
50
Interatrial pathway
Neural like cells, right to left atrium quickly to synchronize contraction Fast Na for this, Ik, Ica, If
51
Internodal pathway
Fast Na, K, Ca, and Funny
52
Bundle of His
fast Na
53
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
54
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
55
Purkinje Fibers
Subendocardium, fastest rate | Cell to cell conduction through myocardium because Purkinje fibers interdigitate with ordinary contractile fibers
56
Depolarization direction
Endocardium to epicardium due to Purkinje fibers | Right completely depolarized before left because it is much thinner
57
Gap junctions of intercalated disks
Allow ions to flow rapidly from one myocytes to the next without a decrease in amplitude
58
Duration of AP for epicardium vs endocardium
Longer for endocardium Wave of repolarization is epicardium to endocardium Slower due to myocytes and no Purkinje
59
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
60
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
61
P-R segment
Conduction delay in the AV node | Segments include the humps, so that would be the AV delay
62
PR interval
Time between atrial depolarization and ventricular depolarization
63
Isovolumic relaxtion
End of of T wave | When the aortic valve closes
64
S1 sound
Occurs when is isovolumic contraction starts
65
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
66
Restoration of myocardial infarction after MI
K+ washed out of interstitium, RMP more negative (back to normal)
67
Increasing K+ permeability
More negative RMP, decrease slope of line to prepotential, decrease HR
68
First Degree
All components are normal except PR interval is greater than 20 seconds but constant
69
WPW syndrome
Delta wave due to early dep of ventricular prior to activation of AV node, there is a new pathway.
70
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
71
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
72
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
73
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
74
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)
75
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
76
PNA on coronary flow rate
Decreased PNA will increase HR which will increase coronary flow and coronary rate
77
Heart work
SV X MAP | Increase either, increase heart work, increase coronary flow by increasing adenosine
78
Adenosine
Dilates coronary VSM | Increased heart tissue accumulation of adenosine with increased HW
79
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
80
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
81
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
82
Histamine in the lungs
Systemic=dilation | Lungs=constriction

NBS1 (9 decks)

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