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Explain the traditional view of all nephron units are diseased and the intact nephron hypothesis of chronic renal failure.
**Intact Nephron Hypothesis- yes nephrons are delicate and vulnerable but when something happens to the nephrons in the kidney, not all are affected- some are left unaffected, or intact.
Define glomerular filtration rate
GFR is the amount of plasma that is circulated through the kidney every 20 minutes. Each kidney has approx 1 million nephrons in each kidney. The more loss of nephrons, the more cricital the renal failure.
Define cystitis and acute pyelonephritis.
cystitis(infection into bladder)
pyleonephritis(infection of kidneys).
Identify the most common organisms causing UTI’s.
80% of UTIs, the causative organism is E-Coli(gram neg rods). 10% of UTIs, causative organism crotiois(gramm neg rod). 90% probability that the UTI is from a gram-negative rod. Portal of entry is ALWAYS the urethera.
Explain why PG increases the incidence of UTI.
Pregnancy there is an increased risk of UTI. This is because as pregnancy continutes the progesterone goes up, progesterone relaxes smooth muscles. The smooth muscle is what surround the urethera. Since the muscle is relaxed, it allows a wider opening to the urethera. Nature makes the bladder smaller to compenstae for this.
Explain the role of leukocidins in acute GN.
Define rapidly progressive GN.
more intense. Lots of hematuria, big time proteinuria, and azotemia(BIG TIME retention of Nitrogenous Substances- more severe than uremia) Foods with nitrogen = PROTEINS. Protein is broken down to ammonia, which is then broken down to urea, which is toxic that's why it is exrected through the urine.
Explain chronic GN.
incidious. Characterised by a slow atrophy of the nephrons. Kidneys normally weight 250grams a piece and are the size of the first. In chronic glomerularnephritis, the kidney is half the size of the first and weight about 50 grams a piece.
Explain the relationship between hypertension of chronic renal failure.
maintaining fluid and electrolyte and nitrogen is the measure of the function of the kidney- also a function of the blood pressure.The glomerularis is basically a capillary- able to handle about 60-70 mm/hg pressure. The problem with HTN is the pressure is so great that it blows out the glomeruli.
To Fix this problem the kidney constricts the afferent renal arteriole and dialtes the efferent renal arteriole to decrase the increase pressure on the nephrons.
To fix the low pressure coming in to nephrons the kidney will dialte the afferent arteriole and constrict the efferent.
-Maculodensa cells produce renin. Renin is squeeze out of the cells and picked up in the vascular system. Renin activates angiotension I, angiotension I is acted on by an enzyme in the lungs- which causes angiotension II. Angiotension II is a powerful vasoconstrictor, which increases the blood pressure. The kidney does this to increase the pressure to the kidneys.
Renin also causes the adrenal glands to increase production of aldosterone. When aldosterone is increased then sodium is unable to be excreted- retain sodium and water- this increase blood volume- which increases blood pressure.
Give the most likely cause of renal artery stenosis.
the artery is blocked by plaque, when the kidney isn't profused, it always assumes that the the bp needs to be increased. This high blood pressure activates the inflammatory process to fix the “plaque” which it thinks is a damaged vessle. Then deposits calcium- stenosis of the artery occurs.
ALWAYS, ALWAYS, check the renal artery first when dealing with HTN.
Explain renal tubular acidosis in terms of H+ and HC03.
-Classic- Distal- Type I- not a problem with blood pressure or glomerular filtration rate- will have a problem with dealing with hydrogen ions and bicarb ions. Have the inability to acidify urine- cannot make urine acid- cannot pee out hydrogen ions. If hydrogen ions cannot be excreted then the blood ph will go up-more acidic. ALKALINE URINE.
More common in children and females.
What is proximal Renal Tubular Acidosis.
- type II-have ALKALINE URINE. There is an inability to reabsorb bicarb back into the vascular system. Cannot reabsorb the bicarb to buffer the hydrogen.
Explain how chronic renal failure may lead to secondary gout.
Secondary gout- decrease in uric acid excretion in chronic renal failure. Uric acid is excreted by the kidneys. If the the kidneys cannot excrete uric acid then gout occurs. Early lead intoxication is thought to increase risk of high uric acid.
Explain toxic nephropathy.
drugs or chemical injested that decrease renal function.Whatever is in the blood stream, the kidney is exposed to it every 20 minutes. The kidneys are a portal of exit. Kidneys are very vulnerable to toxic stuff.
Distal Tubule- females are more likely to be invovled in analgesic abuse. And the distal tubule is the blunt site for analgesic abuse.
Classic profile- female, middle aged- history of chronic backpain or chronic headache.
Explain the effects of led on the kidney.
lead is incorporated into the bone first, leeched out of the bones, and then affects the tubular part of the kidney- it destroys the tubular part of the kidney. Can come from paint, pipes, toys. Every year the incidence of lead poisioning increases in kids. Slow progressing disease, but will lead to renal failure.
Explain uremic syndrome in terms of GFR
means that you only have 5-10% of the GFR ability left OR this patient has lost 90-95% of their GFR ability.
Explain how renal failure leads to metabolic acidosis.
(if the kidneys are good functioning, then the kidneys have a great handling of K+. ) This person has lost 95% of their ability to pee out K+ and H+. If you cannot excrete H+ then the blood ph is going down(acid) and the K+ is going up.---seen in the T wave of EKG.
Cardiac problems occur when the potassium level is in the neighborohood of 7-8. Fatal dysarythmias will occur.
Explain the effects of sodium imbalance in uremic syndrome.
will have a decreased output of sodium, so there will be an increase in the sodium levels. Water is not excreted which increases blood volume which increases blood pressure.
If the heart cannot compenstate for the increase blood volume then CHF results(HTN, Edema, CHF)
Explain the Hematologic problems associated with uremic syndrome.
Normochromic, Normocytic anemias- production problem or a loss problem. In the case with renal failure it is a production problem. This is because the kidneys are not producing erythropoietin- the bone marrow can produce RBC with out erythopoietin but not as affective. When the bone marrow produces RBCs without erythopoietin then the RBCs will have a life, half of the normal. These red cells are exposed to acidic, high potassium, enviornment- causing less than a life span of half the normal.
Explain the skin discoloration associated with uremic syndrome.
Skin will be pale, waxy feel, and straw colored- not just totally white.
Severly anemia and increase of urochrome will cause these sx to appear.
Urochrome- is the pigments that give urine it's color- straw color. Since the patient has a decreased urine output the urochrome is not being removed from the vascular system so the skin has the yellow color.
Explain the reasons for CNS disturbances in uremic syndrome.
parallels azotemia, or the more nitrogenous substances that are retained the greater the increase of CNS involvement.
Irritable-> convulsions-> coma
retention of nitrogenous substances are very neurologically toxic.
Explain the reasons of skeletal disorders in uremic syndrome.
Skeletal Disorders- normally vitamin D, made from the UV light/skin exposure, is activated by the kidneys so calcium is absorbed. Kidney function is decline- so therefore vitamin D is not activated, calcium is not absorbed- bones become weak-osteomalacia is the same as osteroporosis, pretty much only from renal failure.
Rickets can result from the lack of renal function.
measuring the urea in the blood. High protein diets will affect this. Dehydration will also effect the BUN. (BUNs are hydration dependent and dietary influent.)
Creatine- product of muscle metabolism. Creatine is excreted from the kidney. Not influenced from protein or hydration. Measuring creatine is more accurate than BUN. The Creatine Clearance- collection of a 12 hour urine specimen. Serum creatine and urine creatine should be the same. The degree of difference tells us how much the kidneys are affected.
acute renal failure; occurs quickly
characterized by oliguia- urine output of less than 400 ml/day.
Affects about 5% of all hospitalized patients.
prerenal- things that are occuring to the blood before it gets to the kidneys.
Hemorrhages, burns, MI, pulmonary embolus.
Postrenal- on the other side of filtration. The problem is getting the urine out of the bladder. Could be caused from a tumor, mechanical obstruction.
Renal- intrinsically renal problem. Something has damaged the kidney. This is more likely to not be reversible. Reaction to contrast dyes, antibiotics, heavy metal poisioning, could be a child who are drank antifreeze- antifreeze urine will glow under the light of a black light- pretty good indicator that antifreeze is the cause.
Transverse fracture- break directly across the bone. Tend to be pretty stable and are often re-aligned without surgery. Typically can be done with closed reductions
Oblique fracture- one that is across the angel, sticking out of skin. Not stable, need surgery, pins need to stablize bones.
Spiral fracture- fractures that spiral up the bone. Indicator of abuse.
Impaction fracture- compression fractures. These are fractures that occur when two bones crush a third bone. Seen in the vertebra.
Stress fractures- typically see in people who are doing some real active sport- increase activity level. Classicly seen in runner- become bitchy beacause they are having a drug withdrawl from the lack of endorphins. Usually cannot detect these with an x-ray initally, only way to heal is to quit the activity. When the fracture begins to heal you can then sometime spot them on an xray.
Avulsion- is the sepeation of a fragment of bone, at the site of tendon or ligament insertion. A chip off the bone. Nothing you can do about it. It will heal, requires nothing.
Explain the four R’s of fractures.
recognition- have patient describe what happen
reduction- manipulating the broken pieces of bone back to their normal location- then put in traction- stabilize.
Retention- Closed reductions are retained with cast(cast goes above and below the cloest joint). Open reductions are usually retained in surgery and then traction.
Dislocation- there is no touching of mating and articular cartilage.
Classically seen in the shoulder- ask if patient can tense/move deltoid: if they say no then this means that they tore their axiallary nerve.- ask patient is the can abduct and aduct: if they say no, then this means they have ripped ulnar nerve. Patient will need to have surgery. Airplane cast is what they will be held in. the shoulder will never work like it use to.
Subluxation- refers to a devation in the normal relationship between mating(touching/fused) and articular(joint) cartilage- slight dislocation.
Scoliosis- latter curvature of the spine that may also include rotation of the spine.
Pre-Teens- primarily seen in this population.
nonstructural- not the spine that is causing the spine- it is something else that is causing the spine to curve or rotate(posture, leg length)
structural- the spine is the problem. The spine inheritantly is curver or rotated. When there is rotation- definetly in brace- have to wear the brace until the appearance of Risser's sign(couple of small little bones that develop off the base of the spine and stops the roatation of the spine, still may be curved but will not rotate). Curvature- maybe in the brace.
Risser's sign(couple of small little bones that develop off the base of the spine and stops the roatation of the spine, still may be curved but will not rotate). Curvature- maybe in the brace.
Multiple Myeloma- maligancy involving plasma cells(precursor to B cells- involved in antibody production). Multpile Tumors are developing in the bone. More common in males than in females, 2:1. rare to see in a person under the age of 40.
Giant Cell Tumors-usually occur in young adults, more common in males. Occur at the end of long bones. Removed, yet there is still a strong occurancy for them to reoccur. The are benign. Their presentation is very similar to ostogenic sarcoma.
Osteogenic sarcoma- occur in long bone, occur in younger population. Maligant. Most common bone cancer in individuals between the ages of 10-25. Look very similar to giant cell tumor. Only diagnosed with biopsy. Tumor is removed but a portion of the extremity is also removed.
Degenerative Joint Disease
Explain the pathology of osteoarthritis.
more common in females,10:1. Estorgen is related to this disease. Disorder of moveable joints, slow progressive disorder. Characteristised by a deteroation of bone and cartilage in the joint. Coorelated with age(older the more likely), not an inflammatory disease- rather losing cartilage in joint tissue. Tends to run in the family, gentic? High incidence in people who are doing repetitive motion, for example- secretary typing.
Heberden's Nodes- large swollen joints, painful.
No specific tx that will halt the loss of cartilage.
Explain the pathology of rheumatoid arthritis.
Rheumatiod Arthritis- involves bones and joints but is autoimmune. More common in females by 2.5 times. Progressive joint deteroiating but also inflammation. Probability increases with age, but the disease can start very early. Produce hydrolytic enzymes, produce protenase enzyme, collagenase enzyme, and these three are the components of synovial joint fluid. The synovial fluid begins to be replaced with panesous tissue, a granular, rough tissue.
WBC are hardly ever present in the healthy individual, but very high amounts in the RA patient(15,000-25,000) they also have a high level of IgM antibodies. Proteins, water, and collagen are located in other areas than the joints, so this disease involves multiple systems. No Tx.
Explain the pathology of SLE discussing arthritis, butterfly rash, Raynaud’s syndrome and antinuclear antibody.
more common in females, 10:1. 40% will have butrerfuly rash, 40% raynaud's, 95% antinuclear antibody will be positive. High incidence of osteoarthritis- present arthritis pain in symmetry; example, both knees, both wrist, etc. often times its the arthritis that presents before lupus.
uncommon connective tissue disease.
Characteristed- by a fibrous growth that occurs in connective tissue.
More common in females
Very correlated with raynaud's disease
Present with- stretched looking skin on body, tight skin. No wrinkles. Can't make their face wrinkle because the fibrous tissue growths are pushing the skin out. Fibrous growths are located in organs as well, not just under the skin.
Explain the basic pathology of gout.
Gout- nine different kinds of gout, that all end up at the same point. Increase in uric acid. Primary gout is exclusively a male problem.
Primary gout is exclusively a male problem.
Pain is located almost always in the joint of the big toe.
Uric acid has a tendcy to crystalize and responds to gravity; hence joint of big tone. Uric acid crystalizes in the joint and cut into the joint.
Uric acid kidney stones
Primary gout tends to run in the family. Can be exacerbated by alcohol particular beer and wine. Also exacerbated by certain foods, prepackaged luncheon meats(nitrates)
Explain the reasons for giantism and acromegaly.
Giantism- excess amounts of growth hormone from the pituitary gland. Seen in children and young adults
Acromegaly- bones grow thicker, and wider.
Explain the differences between graves disease and toxic nodular goiter.
Grave's disease- more common in females, much more so than males. Sx- fatigue, heat intolerance, increase sweating, increase appetite, wide eye(expothalamus-fatty/lymphocyte deposits behind eyes). Will not be over weight, may be under weight.
Toxic Nodular Goiter- tends to be in older people. Slow growing, not usual to see.
Thyroid Storm- from physiologic stress- results in tachycardia, fibrillation.
All occur in hyperthyroidism.
Explain the differences between primary and secondary hypothyroidism.
primary hypothyroidism- means the problem is in the thyroid. TSH is increased and the t3 and t4 are down.
secondary hypothyroidism- problem is in the pituitary. TSH is down and T3 and T4 are down.
Explain papillary follicular carcinoma of the thyroid.
Papillary Carcinoma- most common*
makes up 80% of thyroid cancers in both adults and children. Very similar to follicular carcinoma. Both follicular and papillary are slow growing, located on the outside of thyroid gland, do not metastise quickly.
Medullary carcinoma- occurs in the middle of the thyroid. Tends to be slow growing, given that its in the middle of the gland- where the secreting of the gland is, there is secretion of the cancer cells. Metastis early.
Explain the role of parathyroid hormone in hypercalcemia
above 10.5- most likely reason is parathyroid hormone excess, and more likely reason for this is benign adenoma on the parathyroid gland.
Calcium and phorsphous are always inversly related. Calcium is increased, phosphrous is decreased.
Tend to see sx: HTN, EKG changes- changes in the heart, can develop multiple bone cyst because the calcium is going to be deposited in the bone.
hypocalcemia- decrease 9.0mg- this occurs from either lack of parathyroid OR idopathic hypoparathyroidism(unknown reason for a hypoparathyroid).
Sx: tetany-like muscle contractions, seizures, cardiac changes, memory problems, confusion.
Sx: hyperglycemia because of this glucose produciton from a non-carbohydrate source. Edema, puffiness of tissues. Decreased immune functioning. Facial hair production in female population.
Less production of ACTH. More common than Cushing's. Think this may be autoimmune. Usually see all the adrenal hormones decreased. Not enough Salt, Sugar, Sex.
Peeing out sodium and water, Increase in hydrogen and Potassium, decrease in blood ph-acidosis.
Increased cell sensitivity to insulin- hypoglycemic. Decrease in aldosterone means peeing out sodium and water- loss of blood volume- loss of bp- potassium goes up, blood ph goes down(acidotic). Loss of androgens in males, don't really see the effect. In females when there is a loss of androgens, females will lose body hair.
places in the body that do not have insulin receptors because they don't need them(eyes, peripheral tissue, etc). Develop hardening lesions in retinas, kidney, peripheral nerves, peripheral blood vessels.
This damage can occur in a type II diabetic, but is going to be slower.
Large concern with overweight children, because by the time they are in their 20's they are going to have severe complicaitons.
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