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NBS1 > Quick Study Final > Flashcards

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
Q

Chronic presentation

A

Failure to thrive, developmental delays, intellectual disabilities, hearing loss
AAD, OAD

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26
Q

Complex Molecule Defects

A

More complex presentation
Dysmorphic features
Lysosomal strange diseases, proviso all diseases

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27
Q

AGMA Numonic

A

MUDPILES

A CAT MUDPILES

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28
Q

Metabolic Acidosis with normal anion gap

A

Diarrhea

RTA
Topi rampage
Intoxications
Renal Failure
Inhalant use
Toluene
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29
Q

Test for Metabolic Acidosis

A

Blood lactate, pyruvate, ammonia, and glucose levels

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30
Q

Most likely to lead to a metabolic acidosis with an increased anion gap

A

Organic Acid Disorders

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31
Q

Normal anion gap and no significant acidosis

A

Amino acid disorders, urea cycle defects, maple syrup urine disease

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32
Q

Most carbohydrate disorders (yes/no) metabolic acidosis

A

NO. Except fructose 1,6, bisphsophatase

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33
Q

Increased AG and metabolic acidosis

A

Glycogen storage disorders
Mitochondrial disorders
Pyruvate dehydrogenase complex deficiency
Ketone utilization defects

34
Q

Ketosis

A

Permanant–ketone utilization defect

Ketosis + other metabolic abnormalities–mitochrondrial metabolism (OAD, Mito-RCD)

35
Q

Lactic Acidosis

A

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
Q

PAC

A

organic acid disorders and fatty acid disorders

37
Q

Urine Organic Acids and urine acylglycine

A

OAD and FOAD

38
Q

Plasma and ketone bodies

A

KUD ketone utilization defects

39
Q

Phase 4 Nodal Cell AP

A

Funny Na–influx
K+ out
T-type Ca2+–calcium in

40
Q

Depolarization and repolarization of the heart nodal cell

A

Depolarization–decreased permeability to K+, increased funny Na+, T-type

Repolarization-increased permeability to K+, closer to K+ equilibrium potential

41
Q

Repolarization depolarization of myocytes

A

Depolarization-opening of fast Na+

Rapid repolarization-slow voltage gated K+ channels

42
Q

Calcium channel blockers on nodal cells

A

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
Q

Ca2+ blockers and myocytes

A

Less time for cross bridge cycling

Less Ca++ TnC binding=fewer myosin binding sites uncovered

44
Q

Sympathetics vs Parasympathetics to the heart

A

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
Q

Factors that influence pacemaker depolarization rate

A

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
Q

ACh in heart

A

Decreases If and Ica conductance a
Increase Ik conductance
Decreases Ca permeability and raises threshold

47
Q

NE on heart

A

Increase Funny Na and increase Ca through membrane

Lowers threshold potential

48
Q

DC counter shock

A

Phase 4 of myocytes AP to get the as many closed fast Na+ to open in order to create an AP.

49
Q

SA node

A

Ik, Ica, If

Basal heart rate

50
Q

Interatrial pathway

A

Neural like cells, right to left atrium quickly to synchronize contraction
Fast Na for this, Ik, Ica, If

51
Q

Internodal pathway

A

Fast Na, K, Ca, and Funny

52
Q

Bundle of His

A

fast Na

53
Q

AV node conduction velocities

A

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
Q

RBB vs LBB

A

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
Q

Purkinje Fibers

A

Subendocardium, fastest rate

Cell to cell conduction through myocardium because Purkinje fibers interdigitate with ordinary contractile fibers

56
Q

Depolarization direction

A

Endocardium to epicardium due to Purkinje fibers

Right completely depolarized before left because it is much thinner

57
Q

Gap junctions of intercalated disks

A

Allow ions to flow rapidly from one myocytes to the next without a decrease in amplitude

58
Q

Duration of AP for epicardium vs endocardium

A

Longer for endocardium
Wave of repolarization is epicardium to endocardium
Slower due to myocytes and no Purkinje

59
Q

Inotropic agents (CO, SV, RAP)

A

Increase contractility, increase CO, increase SV, decrease RAP (because more blood is ejected from the heart on each beat), decreased ESV

60
Q

Atrial Systole

A

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
Q

P-R segment

A

Conduction delay in the AV node

Segments include the humps, so that would be the AV delay

62
Q

PR interval

A

Time between atrial depolarization and ventricular depolarization

63
Q

Isovolumic relaxtion

A

End of of T wave

When the aortic valve closes

64
Q

S1 sound

A

Occurs when is isovolumic contraction starts

65
Q

Myocardial Infarction

A

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
Q

Restoration of myocardial infarction after MI

A

K+ washed out of interstitium, RMP more negative (back to normal)

67
Q

Increasing K+ permeability

A

More negative RMP, decrease slope of line to prepotential, decrease HR

68
Q

First Degree

A

All components are normal except PR interval is greater than 20 seconds but constant

69
Q

WPW syndrome

A

Delta wave due to early dep of ventricular prior to activation of AV node, there is a new pathway.

70
Q

Myocardial infarction cardiac myocytes

A

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
Q

Systolic current of injury

A

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
Q

Diastolic Current of Injurt

A

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
Q

NO for MI

A

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
Q

Factors that shift filtration curve up and to the right (promoting edema)

A

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
Q

SNA and coronary flow

A

Decreased SNA= decreased coronary blood flow

Increased SNA=increase heart contractility, SV, and heart work, which increase coronary flow and coronary flow rate

76
Q

PNA on coronary flow rate

A

Decreased PNA will increase HR which will increase coronary flow and coronary rate

77
Q

Heart work

A

SV X MAP

Increase either, increase heart work, increase coronary flow by increasing adenosine

78
Q

Adenosine

A

Dilates coronary VSM

Increased heart tissue accumulation of adenosine with increased HW

79
Q

SNA and AVAs of skin

A

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
Q

Cerebral circulation

A

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
Q

Pulmonary Edema

A

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
Q

Histamine in the lungs

A

Systemic=dilation

Lungs=constriction

NBS1 (9 decks)

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