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103 Cards in this Set

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EKG findings for 1st, 2nd, and 3rd degree blocks
1= increased PR (norm -.12-.2)
2= Q with P, but PR increases; P not always with Q
3= p without A, Q without P
Enchancement of S2
Enchancement of S2 by delaying pulmonic valve closure
How does Ach Effect the heart
Ach -> Sa and AV nodes, increasing PR interval
effects mediated by modification of phase 4 slope
Phase 0, 3 and 4 in SA node
Phase 0 (upstroke) - ca influx
Phase 3 (downstoke) - K+
Phase 4 (slow upstroke) - Na funny
Inspiration and Systemic Arterial Pressure
Insp decreases SAP by decreasing LV output
Cushing's Response
Increased ICP leads to increased Systemic arterial pressure (via VMC) in order to maintain cerebral blood flow. There may be profound bradycardia (via Baroreceptors)
LaPlaces Law
wall tension = T*P*r/thickness
Control of Breathing
Basic rhythym set at Dorsal Medulla
Input comes from apneustitic centers in pons; and pnemotaxic centers (nucleas parabronchialis)
FeV1 and Vital Capacity
FeV1 is usually 85% VC
Alveolar Volume Eqn
Va=Vt-Vdead Times Frequency
relation between Alveolar oxygen, and inspired oxygen
PAo2 = PiO2-PaCo2/.8
What happens to pCo2 in V/Q mismatch
with V/Q mismatch you see a decrease in PCo2 as a result of in an increase in ventilation due to the drop in P02
V/Q ration in the normal lung: where is it highest
in the apex (low lung compliance b/c the artery is big)
Central vs. Peripheral Chemoreceptors
Central respond only to Pco2 (main) and pH

Peripheral respond to pC02, pH, O2 (less than 60 mmHg)
Hering-Breuer Reflex
Lung stretch receptors -> inh inspiration
muscle that contracts during inspiration
external intercostals
Define DlCO
amt of O2 that pass per 1 mmHg of gradient of O2
HyperKalemia and paralysis
HyperK decreases the gradient for K+, thus DEpolarizes the membrane and leads to sodium channel inactivation
Dihydropyridine Receptors
Voltage gated ion Ca channels in striated muscle that aid in excitation-contraction coupling
Excitation contraction coupling in smooth muscle and cardiac cells
Cardiac -> Ca opens SR
SM -> IP3
Phospholamban
inhibits ryanodine receptor Ca pump... inhibition of phospholamban leads to increased calcium sequestration (this occurs via PKA phosphorylation
Mg2+ and muscle contraction
Mg2+ inhibits it
Calcium and muscle excitabilty
decreased calcium leads to increased excitability (I believe this is because Na gets activated)
Capacitance and conduction velocity of neurons
decreased capcitance leads to increased velocity (less electrons must flow)
Light Rxn with Eye
Light hits Rods, causes increased hydrolysis of cGMP (via more all trans) which hyperpolarizes cell leads to decreased inh NT release on bipolar and ganglion
Substance P
Subs P is released pain fibers (C-delta) on spinal cords
Molecular effects of epinephrine on smooth muscle
epi increase PLC which increases Ip3
PKA and Phospholamban
PKA phosphorylates Phospholamban, increasing Ca sequestration (and decreases SM contractility)
A, C, V waves
W and Y decents
a wave -> atrial contraction
c wave -> tricuspid be pushed back by contracting ventricle
x decent -> continued atrial relaxation during systole
v wave -> atrial filling against closed mitral valve
y descent -> rapid ventricular filling
Organ with highest AV gradient
the heart
pressure gradient between aorta and ventricle
think aortic stenosis
How much blood is in your arteries and veins vs. Pulmonary Circulation at a given time
Arteries and veins -> 2/3 blood
Pulmonary circulation -> 10% of blood
How do you keep PDA open?

How does it close?
keep open with prostaglandins

Closure: Oxygen -> bradykinin -> closure DA (pharmacologically closed with indomethicin)
Why do the lungs have lots of lymph?
High lymph b/c of high levels of interstitual proteins
Coorelation of turbulence and vessel size, blood velocity, blood density, and blood viscosity
Reynolds Eqn: http://www.cvphysiology.com/Hemodynamics/H007.htm

more turbulence with bigger vessel, higher velocity, high blood density and LOWER viscosity (velocity and viscos should be inversely related)

Don't get caught up on the diameter thing though, because increased diameter also leads to decreased velocity which reduces turbulence and the likelihood of seeing turbulence
compare CO and met actvity of kidney
Kidney si unique in that it receives 20% of CO with relatively low metabolic activity (most in cortex, where Na reabs occurs
TPR and Pulm BF changes at Birth
TPR increases with loss of placenta

PBF increases as pulm resistance decreases
Major contractility pattern during digestive phase? How is it activated?
Segmentation, which is activated by wall distention
Role of Ca2+ in B12 absorption
IF-B12 bind to enterocytes via interaction with calcium
effect of VIP, ACh, Sub P, and Dopamine of Smooth Muscle (GI)
VIP -> relaxation (VIPoma presents with diarrhea)

ACh, Sub P, and Dopamine -> contraction
Where is most water and Na reabsorbed?
most H2o/Na reabs occurs in the small bowel (jejunem = #1 site, duodeum = #2)
Motilin
MMC hormone
Amino Acid absorption
occurs in the jejunum
Vitamin synthesized by bacteria, and is abosorbed by humans (humans still will get it form other sources however)
folic acid

vit K, B6, thiamine are also synthesized by bacteria, however not absorbed in appreciable amounts
Aldosterone and the colon
Na/K under it's control (net K= secretion?)
Bicarb and the colon
Hco3- is secreted in the colon (think diarrhea gives you met acidosis-- norm anion gap)
Two things needed for Absorption of fat soluable vitamins (besides intact bowel)
1) Bile
2) Pancreatic Lipases
Absorption of fructose glucose and galactose
fructose -> facilitated diffusion
Glucose and Galactose -> Na-dep active transport
pH of Saliva
Saliva has HCo3-, thus it it basic
What is the effect of sulfonylation of Bile Acids
aids in excretion
How are Bile Acids conjugated
With Taurine and Glycine. Bile acids are secreted conjugated with these amino acids
Caffiene and EtoH on stomach pH
Both stimulate the secretion of Gastric Acid
2 regulators of Pancreatic enzyme secretion
Neural (vagus-Ach)

Hormonal (CCK; secretin -> Hco3- and water secretion, not enzyme)
Where are secondary Bile acids formed?
in the small intestine
Enterogasterone
released by SI. Acts to inhibit antrul Gastrin release
Where is most renal Na reabsorption occur?
In the cortex

Na reabso is proportional to O2 consumption
What does the Tmax for glucose refer to?
Tmax refers to the maximal reabosprion rate of glucose (mg/min)
What are the 2 things that regulate Aldosterone
1) Ang II

2) K+ (high leads to it's secretion)
What percent of TBW is Plasma?
plasma is 8%, or 1/4 of ECF, which is 1/3
What things increase Renin secretion?

Decrease it?
Renin Secretion increased by sym. stimulation; adenosine from macula densa increases it too

Decreased by: Ang II and ANF
How is Na reaborbed in the Proximal Tubule? Where are the transporters?
Na/K on basolateral

Na/H, Na/glucose, etc. on apical
Anion Gap
Na-(Cl+Hco3-)
Importance of PAH
PAH clearance is a good indicator of RPF, since all of it is secreted
Filtered Load
FL=GFR*plasma conc
Net Acid Excretion
NAE= NH4 + TA- bicarb

TA is mostly Po4-
What is the normal amount of fixed acid load
70-100 meq of acid
Why is there a lower pH and higher Na gradient in the distal neph when compared with the proximal
distal has more tight jxns
Aldosterone and H+ secretion
Aldosterone increases Na/K exchanger, decreasing the activity of the Na/H exchanger... this increases H+ secretion
Sympathetic stimulation of kidney and protein excretion
Sym Stim increases protein excretion (I think it's secondary to vasocontriction)
Prostaglandins and Renin
PG's stimulate Renin release (like adenosine)
Volume depletion and Hyperaldo on systemic pH
Volume depletion and Hyperaldo create met ALKALOSIS (both lead to increased Na reabsorption which created increased proton excretion)
Trophic Effects of ACTH
ACTH -> GC andSex hormones, not Aldosterone (zona glomerulosa)
Distal Tubule, acid secretion, and potassium
In situations of hypoKalemia, H+ goes inside of cell instead of K+, leading to increased K+ secretion
Glutamine and the kidney
Glutamine uptake used to make NH4+-> H+ secretion
Which arteries bath Loop of henle
Vaso Recta
Supraoptic and Paraventricular Nuclei
Supraoptic -> ADH

Paraventricular Nuclei ->oxytocin
FSH and LH in spermatogensis
pulsatile GnRH -> FSH and LH

FSH -> Sertoli cells -> meiotic and mitotic division of sperm

LH -> testerone release by leydig cells
Hormone of fetal Adrenal Cortex
fetus makes primarily DHEA (they lack 3beta-hydroxy steroid DH)
Hormone sensitive Lipase
the hormone is epinephrine and glucogon, not insulin

epinephrine and glucogon -> increased cAMP -> phosphorylates Lipase -> increased TG's breakdown in fat
Of the 3 effects of PTH, which is predominant?
the effect on bone (reabs)
Ang II and thrist
Ang II activates subfornical organ in Diencephalon
Heat Intolerance and Thyroid hormones
Heat intolerance = hyperthyroid
cold -> hypo
Cabbage and turnips
have goitrogens (increase thyroid size)
L-arg
stimulates GH release
Melatonin
syn by Pineal Gland; in dark, synthesis increases via norepi from postgang sym fibers; fxns include inhibition of GHRH

IS NOT ASSOCIATED WITH SKIN COLOR (that is melanin)
Anti-inflammatory actions of cortisol
1) decreases vasc permeability
2) decreases IL-1 secretion
3) stabilizes lysozomal membranes
4) inhibits PPLA2
Ductal and glandular growth in breast
Estrogen -> ductal
Progesterone -> Glandular
Effect of progesterone and estrogen on cervical mucosa
Est -> thinner, more fernlike
Progest -> thicker (blocks sperm)
Milk Let-down
associated with oxytocin
Secretion of Pancreatic polypeptide
Secreted by F cells in Islet
Near Vision
near vision = increased refractive power= contraction of ciliary body
Spindle fibers
Spindle -> Ia fibers -> length and velocity
Golgi tendon
Golgi tendon -> Ib fibers -> tension of muscle
Tetany and contraction strength. Why?
Tentany (or increased firing rate) -> increased contraction b/c of increased cross bridge cycling time (not b/c of increased intracellular calcium)
gamma motor fibers
maintain Ia spingle activity during contraction of muscle
Raffini ending
= tonic receptors-- pressure sensors in the skin
Pacacian (?Sp) Receptors
Deeper, detect skin deformation (vibration)
Muscle Recruitment for activity
Small MU before Large
Spacticity
spasticity is associated with loss? of corticoreticular fiber that inhibit vesttibular spinal and reticulospinal neurons. These act on Ia fibers, and cause spacticity...

GET BETTER EXPLANATION
Primary Fxn of cerebellum
Posture
EEG: alpha and delta waves
alpha- normal, awake with shut eyes, 8-12 waves/min?

delta- sleep, slow and big
Vibration of basilar mem in cochlea
High Freq-> base (oval and round window)

Low -> apex of cochlear
Babinski Reflex
Rep UPM damage

due to damage of CST in pyramids to spinal cord