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intracellular compartment (ICF)
fluid within cells, 2/3 of body water
site of K+
intracellular compartment
moderate amounts of Mg 2+
intracellular compartment
extracellular compartment (ECF)
fluid within cells, 1/3 of body water
found in interstitial/tissue spaces, within blood cells
extracellular compartment
site of Na+, Cl-, moderate amounts of HCO3-
extracellular compartment (ECF)
third space =
when transcellular compartment contains large amounts of fluid
capillary filtration pressure
pushes water out of capillary to interstitium
capillary colloidal osmotic pressure
pulls water back into capillary
interstitial hydrostatic pressure
opposes outward water movement
tissue colloidal osmotic pressure
pulls water out of capillary
lymphatic system
accessory route to return interstitial fluid to the circulation
compulsive water drinking
psychogenic polydipsia
psychogenic polydipsia is seen in people with
psychiatric disorders
neurogenic DI (diabetes insipidus)
defect in synthesis/release of ADH
nephrogenic DI (diabetes insipidus)
kidneys don’t respond properly to ADH
syndrome of inappropriate secretion of ADH (SIADH)
ADH secreted despite normal OSM, decreases urine output, transient or chronic condition, dilution hypoatemia
hypertonic (translocational) hyponatremia
water shifts from ICF to ECF with hyperglycemia
hypotonic (dilutional) hyponatremia
caused by water retention, water intoxication
hypovolemic hypotonic hyponatremia
sweating in hot weather (lose water + salt)
euvolemic hypotonic hyponatremia
retain water with dilution of Na+ while maintaining ECF (e.g., SIADH)
hypervolemic hypotonic hyponatremia
seen with edema-associated disorders, e.g., heart failure, cirrhosis, renal disease
where is most fluid found?
intracellular compartment
primary source of water loss
urine
Na+ (sodium) regulates
extracellular fluid volume and osmolarity
Na+ (sodium) is regulated by
aldosterone and antidiuretic hormone (ADH)
Calcium, Ca2+ is regulated by
PTH
Regulate K+
insulin, epinephrine, aldosterone, and glucocorticoids
respiratory acidosis acute disorders of ventilation
problem with respiratory center of medulla, lung disease, respiratory muscle weakness, airway obstruction
respiratory acidosis choric disorders of ventilation
bronchitis, emphysema
respiratory acidosis increased CO2 production
exercise fever, sepsis
functions of the main electrolytes (ions)
transmit nerve signals, and contract muscles including the heart
causes of edema
increase in capillary filtration pressure, decrease in capillary colloidal osmotic pressure, increase capillary permeability, obstruction to lymph node
LDL
1° carrier of cholesterol
HDL
50% protein, little cholesterol
VLDL
higher amounts triglycerides, lower amounts of cholesterol
lipoproteins are made in the small intestine
chylomicrons
transport absorbed fats to skeletal muscle and adipose
chylomicrons
small, spherical dilation of vessel at bifurcation, eg circle of willis
berry aneurysm
involves entire circumference of vessel; gradual, progressive dilation of vessel
fusiform aneurysm
extends over part of circumfernce of vessel and appears sac like
saccular aneurysm
false aneurysm resulting from tear in intima layer of aorta the creates a blood filled cavity
aortic dissection
inflammatory injury and necrosis of blood vessel walls, may result in injury from direct injury to vessel
vasculitides
small vessel vasculitides
arterioles, venules, capillaries
small vessel vasculitides
mediated by type III immune complex hypersensitivity reaction, commonly involve the skin
medium sized vessel vasculitides
produce necrotizing damage to medium sized muscular arteries of major organ systems
large vessel vasculitides
involve large elastic arteries, involve infiltration of vessel wall with giant cells and mononuclear cells
Thromboangiitis obliterans (Buerger disease)
affects medium sized arteries, usually plantar and digital vessels
Buerger disease is common in
male smokers, 25-40 years, tobacco may trigger immune response
Buerger disease
pain associated with intermittent claudication, sensitivity to cold; area can become cyanotic
Raynaud disease
vasospasm of arteries & arterioles in fingers (& toes), seen in healthy young women, begins with stress or cold
venous thrombosis (thrombophlebitis)
presence of thrombus in vein with accompanying inflammatory response in vessel wall, more common in lower extremities, associated with blood stasis and vessel wall injury
a symptom of peripheral arterial disease
claudication (calf pain with walking)
stable angina
angina pectoris
angina pectoris
symptomatic paroxysmal chest pain/pressure associated with transient
prinzmental angina is caused by
spasms of coronary arteries; mechanism uncertain
silent myocardia ischemia
absence of anginal pain
silent myocardia ischemia is seen in patients that are otherwise
asymptomatic, with previous MI, with recurring angina episodes, or with
autonomic neuropathy (diabetics)
ST segment elevation
transmural injury
ECG changes
T wave inversion due to altered myocardial repolarization
ST segment elevation
transmural injury
Depression
subendocardial injury
abnormal Q wave
no depolarizing current conduction after injury
mitral valve prolapse
floppy mitral wave
mitral valve prolapse is
mucinous degradition of mitral valve leaflets to become floppy so that they balloon back into L-atrium during systole
mitral valve stenosis
incomplete opening, commonly the result of rheumatic fever
mitral valve stenosis results in
left atrium dilation and pulmonary congression
mitral valve regurgitation
incomplete closure, associated with rheumatic fever, rupture of chordae tendinae/papillary muslces
dialated cardiomyopathies
result in progressive cardiac hypertrophy and dialation with lower pumping ability of one or both ventricles, can result from infections, alcohol/toxic agents, neuromuscular or immunological disorders, genetic influences
hypertrophic cardiomyopathies
excessive ventricular growth/hypertrophy
restrictive cardiomyopathies
not common in western countries, ventricular filling is restricted because of rigidity of ventricular walls
peripiartum cardiomyopathy risk factors
maternal age, african-american, multifetal pregnancy, preeclampsia and gestational hypertension
peripartum cardiomyopathy is similar to
dialated cardiomyopathy
in most cases of peripartum cardiomyopathy
½ cases heart returns to normal within 6 mos; remainder of cases can result in maternal death with another pregnancy
kawaskai disease
mucocutaneous lymph node syndrome; acute febrile disease affecting skin, brain, eyes, joints, liver, lymph nodes & heart; results in vasculitis (inflammation of blood vessels)
coarctation of the aorta
narrowing of the aorta proximal of distal to the ductus arteriosus
coarctation of the aorta symptoms
disparity in pulsations and BP in arms bounding and legs (weak), surgically remediation between 2-4 years
transposition of the great vessels
aorta originates in right ventricle/pulmonary artery originates in left ventricles
transposition of the great vessels survival depends
on communication between R/L sides of heart via patent ductus arteriosus or septal defect
patent ductus arteriosus
persists after birth should close after 24-72 hours and become permanetely sealed by 2-3 weeks, treated surgically or with drugs that prevent prostaglandin synthesis
endocardial cushion defects
cushions form the AV canals, upper part of ventricular septum and lower part of atrial septum, common in Down’s syndrome children, may be partial or complete AV canal defects
Four asociated conggenital heart defects that are present in tetralogy of fallot
Ventricular septal defect, dextroposition or shifting to the right of aorta so that it overrides the right ventricle, narrowing of pulmoary outflow channel, hypertrophy of right ventricle
function of heart is supra-normal but inadequate because of high metabolic demands
high output
inadequate because of disordes that impair pumping abilty of heart
low out put
imparied ejection
systolic failure
imparied filling
diastolic failure
congestion in peripheral circulation
right side failure
congestion in pulmonary circulation
left side failure
AV node block
partial or complete interruption of impulse transmission from the atria to the ventricles
tachycardia
your heart is beating much faster than normal,
bradycardia
heart is beating slower than normal
heart flutter
heart palpitations
renin-angiotensin-aldosterone system
increases Na+ absorption and decreases GFR
myoglobin
released quickly, elevated within 1 hour of myocardial cell death, not cardiac specific
creatine kinase MB
isoenzyme specific for myocardial tissue, rises within 4-8 hours of injury, returns to normal within 2-3 days
troponin I & T
rise within 3 hrs of MI, remainc elevated for 7-10 days
cause of cardiac tamponda
increased fluid, blood or pus in pedicardial sac, due to tramua, surgrey, cancer, uremia, cardiac repture with MI
cardiac tamponade relief
echocardiogram can evaluate condition, to remove fluid from pericardial sac
stenosis
narrowing of a valvular orifice, failure of valve to open properly