Term
| 1. Explain the traditional view of all nephron units are diseased and the intact nephron hypothesis of chronic renal failure |
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Definition
• All nephron hypothesis (Traditional view): because the nephrons are so delicate that when they are insulted or diseased, all are diseased or insulted to some degree- nephrons can’t really escape insult
• Intact nephron hypothesis: nephrons are delicate and when nephrons are diseased they are destroyed but some nephrons are unaffected by insult. |
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Term
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Definition
| when the total number of nephrons is below a point where we can maintain fluid and electrolyte balance uremia is the result |
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Term
| 2. Define glomerular filtration rate |
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Definition
rate plasma (blood) flows though the nephrons per minute
• Entire blood volume circulates through kidneys every 20 minutes |
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Term
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Definition
• Cystitis
• Lower urinary tract infection: urethra and/or bladder
• Symptoms:
• Frequency of urination
• Burning |
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Term
| Define acute pyelonephritis |
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Definition
| • Infection has gone up urethra, into bladder, out the ureters and in the renal pelvis portion of the Kidneys are infected (very serious) |
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Term
| 4. Identify the most common organisms causing UTIs |
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Definition
| • 90% are Gram Negative Rods (urethra and bladder) (E. coli) |
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Term
| 5. Explain why PG increases the incidence of UTI |
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Definition
| • Progesterone relaxes smooth muscle around urethra, gets bigger = easier for bacteria to get in |
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Term
| 6. Explain the role of leukocidins in acute GN |
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Definition
• Immune system develops Ab to kinase and the Ab misreads Ab and get GN as start loosing nephrons, GFR will decrease, can’t excrete Na in vascular system and H2O = BL volume increases and BP increased. Also, H2O causes edema
• Leukocidins: substances that are toxic to leukocytes, especially exotoxins produced by some pathogenic staph and strep – destroy leukocytes by lysis of the cytoplasmic granules and are partially responsible for the pathogenicity of the organisms |
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Term
| 7. Define rapidly progressive GN |
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Definition
| • Protein and blood in urine instead of uremia, they will have azotemia |
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Term
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Definition
| • Large amounts of large amounts of nitrogenous substances in the blood: uremia |
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Term
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Definition
• Pathway to renal failure
• Slow, tedious, ongoing loss of glomerular (could take years)
• Kidney nephrons atrophy, tubular part thickens
• Kidney will weigh 50 g; normal 350g
• Lose > 75% GF = renal failure |
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Term
| 10. Explain the relationship between hypertension of chronic renal failure |
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Definition
• One way to maintain GFR is by maintaining BP
• Glomeruli is a capillary, but pressure it is subjected to is higher than any other capillary.
• Blood enters through: afferent approx. 60 mmHg (right up there with diastolic pressure), if overall pressure drops, means that incoming blood will not be coming in with enough pressure to circulate blood through kidneys every 20 minutes
• Indicates renal failure
• How to reduce the BP in glomerulus when the BP is high:
• Compensate: Vasoconstrict afferent; vasodilate efferent
• Pressure in the middle has been decreased - large coming in, small going out – will work to a degree, but if pressure continues to rise – not much can be done – will eventually blow it out – nonrepairable
• When afferent dilates – small group of cells called maculus densa cells (JG)– they are pushed against and stimulated to release renin – renin causes the angiotensin I, and enzyme in lungs converts angio I to angiotensin II – vasoconstricts all blood vessles – raises BP; renin also causes the adrenal glands to increase their production of aldosterone – aldosterone means retain sodium, retain sodium also retain H2o, increased BL volume and increased BP |
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Term
| Explain malignant hypertension |
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Definition
| • Dangerous, marked by unusually sudden rise in blood pressure to very high levels, often accompanied by headache, blurred vision and seizures |
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Term
| 12. Give the most likely cause of renal artery stenosis |
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Definition
• Atherosclerosis: laying down of plaque in renal arteries specifically,
• About 10% of high BP is a result of this |
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Term
| 13. Explain renal tubular acidosis in terms of H+ and HCO3 |
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Definition
• Characterized by a defect in H ion or HCO3 ion excretion; despite the fact that GFR is normal
• Typically if GFR function goes down, have problem with H or HCO3, with this disorder GFR is normal |
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Term
| 14. Identify the differences and the pathology of Distal RTA and Proximal RTA |
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Definition
• Type I Renal Tubule Acidosis (Placid RTA, Distal RTA)
• Problem with Distal Convoluted tube: inability to maximally acidify urine
• Unable to excrete the metabolic load of acid in the vascular system
• Can’t excrete H+ they go into blood stream, decreased pH (academia) - acidosis
• More common in children, in adults, more common in females
• Type II RTA – Proximal Renal Tubule Acidosis RTA
• Problem with Proximal Renal tube: have Alkaline urine
• Problem in ability to reabsorb HCO3 (excrete them all out) back into vascular system – to buffer H+ ions (H+ elevated – no balance on them)
• Causes decrease in pH which leads to acidosis |
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Term
| 15. Explain how chronic renal failure may lead to secondary gout |
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Definition
• Increase in vascular system uric acid, normally excrete it out through urine, but in
• Secondary gout: renal system is compromised ability to excrete is compromised that build up goes to the joints of big toe (people who are heading into renal failure)
• Uric acid crystallizes (also uric acid kidney stones) appears to have thousands of little razor blades and pee that out – it shreds the surrounding tissues – extremely painful
• Chronic lead intoxication can lead to secondary gout as well, lead impedes kidneys ability to excrete uric acid – see child with elevated levels…think lead poisoning |
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Term
| 16. Explain toxic nephropathy |
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Definition
• Kidneys very vulnerable to toxic substances and they concentrate chemicals and drugs
• Kidneys filter entire blood volume in 20 minutes, so anything in blood will go into kidneys
• Analgesic abuse: 1- 2% of all end stage renal disease patients
• Aspirin most common (typical AM dose (6-8 tablets/day) for arthritis, over period of 6-7 years)
• Distal tubule affected; women b/c women more likely to abuse analgesics
• Classic: female, chronic back pain or HA, 14 different meds from 7 different physicians and mixes and matches medications – at some point runs risk of damaging DCT
• Aspirin used to be made in combination with– a deadly combination – now use a metabolite of phenactin - acetominophin – which causes liver damage/failure |
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Term
| 17. Explain the effects of lead on the kidney |
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Definition
• Nephritis is the pathology of damaged renal tubules
• Interfering with H, HCO3, absorption and excretion; also the counter current mechanism; K, Na absorption and excretion |
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Term
| 18. Explain uremic syndrome in terms of GFR |
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Definition
| • Only 5 – 10% of GFR remaining (has lost 90 – 95%) |
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Term
| 19. Explain how renal failure leads to metabolic acidosis |
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Definition
• Leads to metabolic acidosis
• Decreased ability to excrete H+
• H+ reabsorbed into vascular system and decreased pH, this causes a shift:
• Increase in plasma K+ levels, forces K+ out of cell into vascular system causes:
• Dysrhythmia
• Can be fatal when reach 7-8 mEq/L |
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Term
| 20. Explain the effects of sodium imbalance in uremic syndrome |
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Definition
• Kidneys lose ability to excrete Na (normally kidneys have good ability to handle Na)
• Lose 90% of GFR also lose 90% of ability to handle Na – unable to excrete
• Decrease Na output – Retain Na, H2O follows causes increase in blood volume and that caused increase in BP
• Real increase in blood volume – heart becomes taxed in terms of moving increase volume around – individual is
• Edematous, high BP and CHF
• Respiratory changes:
• Kussmauls respiration = long exhale; short inhale (almost like a sigh)
• Lungs think reason for acidosis is CO2, but the reason for acidosis is an increase in H+ and
• Lungs trying to compensate, but can’t –
• Become hypoxic and dyspnea
• O2 levels down not taking deep breaths |
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Term
| 21. Explain the Hematologic problems associated with uremic syndrome |
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Definition
• Anemia: Normocytic, normochromic = morphology okay
• Means problem with production or loss b/c nothing morphologically wrong, problem is production because they have lost kidney and the ability to produce erytropoietin
• Decreased erythropoietin Decreased RBC
• Erythropoietin is one of stimulus to produce RBC
• Will produce RBC just not as many and not as long life-span
• RBC’s produced with out influence of erythropoietin have ½ the life-span of those produced with erythropoietin
• Environment is very acidic: Ureia, Na, K shortens life of RBC even more |
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Term
| 22. Explain the skin discoloration associated with uremic syndrome |
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Definition
• Waxy, pastyfeel and site
• Pale yellow, looks like they have been embalmed |
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Term
| 23. Explain the reasons for CNS disturbances (pathologies) in uremic syndrome |
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Definition
• Parallels development of azotemia or uremia
• Ex: lethargy, restless, convultions, comatose, insominia
• BUN (blood, urea, nitrogen): measurement of nitrogenous agents
• One way to look at how well the kidneys are filtering nitrogenous agents
• The higher the level the more severe the neurological affects
• Increase BUN because of:
• Increase protein diet
• Dehydrated
• Overhydrated
• BUN is hydration dependent and diet influenced
• Creatinine clearence = muscle metabolism
• Not hydration or diet dependent or influenced
• More accurate way to monitor loss of renal function
• Creatinine clearence
• Blood, 12 hr urine, blood
• 98% is excreted in urine
• S/b equal amounts in blood and urine – if not – big time renal function |
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Term
| 24. Explain the reasons of skeletal disorders in uremic syndrome |
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Definition
• Osteodystrophies: group of pathologies that fall under skeletal disorders stemming from kidney malfunction
• Osteomalacia: soft bones
• Similair to osteoporosis
• Unable to activate Vitamin D and absorb Ca, overtime bones become weak and soft and break easily
• Chronic renal patients important to pay attention to bone densities
• Children = rickets
• Bone densities are critical, must supplement
• Normally, sun exposure produces inactive form of vitamin D, simple process in kidneys allows activation – so that calcium can be absorbed into bones for strong bones |
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Term
| 25. Explain the causes of Acute Renal Failure (ARF) in terms of prerenal, post renal and renal causes |
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Definition
• Pre Renal: happens before getting to kidneys (the kidneys are not the problem)
• MI, septic shock, burn, pulmonary embolism (traumatic event)
• Decrease in urine output, kidneys are fine, but b/c of decreased blood volume, pressure or whatever else is going on
• Post Renal: kidneys filter okay but; clot or obstruction in rest of urinary system (urethras or ureters)
• Volume decreases – anything less than entire volume in 20 minutes = renal failure
• Renal: problem with kidneys
• Antibiotic should not have given,
• X-ray dye or person injested
• Antifreeze (ethylene glycol – taste sweet) – urine glows under black light
• Antifreeze has “glow” about it |
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Term
| Define Transverse Fracture |
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Definition
| : fracture that proceeds directly across the bone |
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Term
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Definition
| fracture at an angle; difficult to control; breaks through the skin |
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Term
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Definition
| result of putting torsion on a limb or bone and breaking it in a spiral fashion |
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Term
| Define Impaction Fracture |
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Definition
| AKA compression. Two bones compress another one |
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Term
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Definition
| high activity level. Pounding from running. Typically not visible right away, will complain of achy pain. Heal: stop activity |
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Term
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Definition
| separation of a fragment of bone at the sight of tendon or ligament insertion. Is a chip at the sight |
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Term
| 27. Explain the four R’s of fractures (basic concepts of fractures) |
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Definition
• Recognition: ask how did it happen, what were you doing
• Reduction: manipulation of the bone back to original location
• Closed fractures: typically heal without surgery
• Oblique’s: require surgery and pins in order to heal;
• Retention: holding in place – cast above and below nearest joint to immobilize. Also use traction – use different devices to keep in place
• Rehabilitation: if there is still malunion |
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Term
| 28. Explain the difference between dislocation and subluxation |
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Definition
• Dislocation: no connection between articular and mating cartilage
• Ex: shoulder is classic – holding up arm with other arm so it stays in socket. If they can’t tense deltoid they also pulled out axillary nerve and ripped, if you abduct and adduct fingers if no they also ripped out ulnar nerve – must have surgery and airplane cast – 6 weeks
• Subluxation: deviation from the normal relationship between articular (joint) and mating cartilage
• Ex: slight dislocation of the shoulder |
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Term
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Definition
: infected bone. Very difficult to get rid of. Bacteria growing in bones can lead to permanent damage
• Most common bacteria: staph and strep |
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Term
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Definition
• Excessive curvature and sometimes lateral curvature of spine
• Impaired ability to rotate spine
• Spine normally curved to absorb shock, provide flexibility
• Idiopathic, common in females, if there is also rotation involved female may have to wear brace until puberty |
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Term
| 31. Explain Risser’s sign |
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Definition
| typically stops rotation of spine with scoliosis. Piece of bone on either side at the base of the spine that appears at puberty and prevents rotation |
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Term
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Definition
: proliferation of immature cell and mature plasma cells in bone marrow
• Softens bone tissue, secondary to the disease
• Tends to occur: age 60; (younger: abnormal – poor prognosis), people of color, no cure; males more common; palpable lesions
• Clinical consequences:
o Bone destruction and replacement of normal bone marrow elements – leading to anemia, thrombocytopenia, and leucopenia, altered immune function with increased risk of infections, hemostatic abnormalities with bleeding manifestations, and cryoglobulinemia and hyperviscosity related to the abnormal protein M component |
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Term
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Definition
tumors; young adults; females; almost always benign, occur at end of long bones; reoccurable.
• Present very similar t osteogenic sarcoma |
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Term
| Explain Osteogenic Sarcoma |
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Definition
: malignant neoplasm of the bone; occurs at the end of long bones; specially around the knees; very common young people; no gender preference; strong genetic correlation – abnormal gene chromosome 13 – having gene predisposes; amputation, chemo, radiation; slow metasises b/c primary cancer
• Only way to distinguish the two is to biopsy |
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Term
| 32. Explain the pathology of osteoarthritis |
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Definition
• Disorder of the moveable joints
• Most common form of arthritis
• Women about 10:1; could be hormonal
• Increases with age – around 70; with repeative motion - earlier
• Loose the water content of synovial fluid in cartridge and joints are stiff – hurts most in AM, correlated with repetitive use (typing)
• Joints really swollen – big nodules called Heberden’s nodes – fingers look deformed
• Supportive treatment only; no cure |
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Term
| 33. Explain the pathology of rheumatoid arthritis |
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Definition
• Chronic affects bone, but also multiple systems
• Females 2:1; increases with age
• Unknown etiology; could be autoimmune
• Develop excessive amount of hydrolytic enzymes. Have them normally, but with RA goes up tremendously.
o Break down: proteins, connective tissue, collagen (which are the components of synovial fluid) loose cushioning effect of SF
• Develop Pannus (latin for cloth) tissue – lay down burlap: rough, grainy tissue in the joints
• Joint inflamed and irritated; pain AM
• Fluid from joint of WBC about 15,000 – 20,000 in fluid alone
• Proteinelectrophroesis large amount of IgG in SJF
o Looking at these two along with other things are part of dx criteria
• Over time, the excessive amounts of enzymes will affect other organs and tissues (heart, lung, eye) – multi system disease |
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Term
| 34. Explain the pathology of SLE discussing arthritis, butterfly rash, Raynaud’s syndrome and antinuclear antibody |
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Definition
• Women, autoimmune, butterfly rash
o 40% rash
o 40% Raynauds syndrome – fingers get cold
o 95% of time can demonstrate the antinuclear Ab (have Ab to the protein in the nucleus of the lymphocyte)
o Connection with Lupus and arthritis
o Symmetry in joint pain:– red flag they have arthritis and Lupus (both wrists, elbows etc) |
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Term
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Definition
• Connective tissue disease
• Women 3:1
• Fibrous nodules develop under skin in joints
• Skin becomes taut = no wrinkles
• Rayaud’s common
• Etiology: unknown; autoimmune suspected
• Environmental correlations: exposure to vinyl chloride used to make plastic |
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Term
| 36. Explain the basic pathology of gout |
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Definition
• Described by Hippocrates (primary gout)
• Nine variations (metabolic disorders)
• Secondary: decreased ability to excrete uric acid (kidneys diseased)
• Primary: increased uric acid production (kidneys okay)
o 95% males = primary gout
o Joint of big toe = inability to put pressure on it
o Responds to gravity – settles in joints that are subjected to most gravity
o Crystals have very sharp, razor blade characteristics in the joints of toe – with movement – cuts into surrounding joint tissues
o Alcohol makes it worse – avoid alcohol (beer & wine)
Preservative urades a precursor to uric acid
Alcohol raised lactic acid level in blood, lactate interferes with the excretion of uric acid by kidneys – run risk of developing uric acid kidney stones
o Packaged deli meats, prepackaged meats
Endocrine metabolic |
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Term
| 37. Explain the reasons for giantism and Acromegaly |
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Definition
• Excess production of growth hormone by anterior pituitary gland
o Giantism: children - grow longitudinally to a point, until maxed out,
o Acromegaly: adult - pituitary is still producing growth hormone grow wider, or after people have reached their maximum longitudinal growth
o Drwarfism: anterior pituitary glands failure to produce growth horomone
o Anterior pituitary gland also produces
TSH- Thyroid Stimulating Hormone
FSH- Follicle Stimulating Hormone
• Males – sperm production
• Females – estrogen out of ovary
LH – Leutinizing Horomone
• Female –big serge mid-cycle – causes ovulation egg out of ovary
• Males – testosterone production
Prolactin
• Breastfeeding, mamillary gland manipulation |
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Term
| 38. Explain the differences between Graves disease and toxic nodular goiter |
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Definition
• Hyperthyroidism = Thyrotoxicosis
o Two types
Graves
• Females, fatigue, heat intolerance, increased sweating, appetite, muscle weakness, with prolonged untreatment: exothalmus (bulging eyes) b/c of influx of lymphocytes into orbital area
• Autoimmune
Toxic Nodular Goiter
• Big basketball lump on neck – b/c of failure to seek medical treatment
• Same symptoms of Graves, not as common
Overactive thyroid: increased metabolism, no weight problem |
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Term
| 39. Explain the differences between primary and secondary hypothyroidism |
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Definition
• Hypothyroidism = inactive, or under active thyroid gland
o Two types
Primary thyroid gland is hypo function; problem with thyroid gland itself
Secondary = pituitary problem
o Symptoms: cold intolerance, decreased sweating, slow, sluggish, overweight,
o Estimate 10% of female population has hypo functioning thyroid
o Familial – symptoms appear about same age; incidence not as high in males with first degree female
• Reason for primary and secondary is b/c of feedback mechanism –
o Determine primary or secondary problem
Primary: (thyroid gland problem) TSH normal, T3 and T4 down; replace with thyroid hormone
Secondary: (pituitary problem) TSH levels are down, T3 and T4 levels are down b/c the stimulus is not enough to make them kick out |
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Term
| 40. Explain the differences between papillary, follicular and medullary thyroid carcinoma |
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Definition
• Thyroid neoplasm’s present as discrete enlargements – risk of malignant growth:
o 50% < 14 yrs
o 10% older
o Growth in neck and have had head or neck radiation – growth malignant = greatly increases malignancy risk
• Three types of thyroid cancer: most common to least common -
o Papillary carcinoma: 80% of cases in children and adults
o Follicular carcinoma: 20% of cases
Both are slow growing, don’t metastasize quickly if addressed with,
Treatment: remove thyroid, little radiation
o Medullary: start in middle of gland, highly secreting portion of gland – worse place to get carcinoma.
Slow growing, high metastatis rate b/c cancer cells are being sent out with thyroid hormone |
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Term
| 41. Explain the role of parathyroid hormone in hypercalcemia |
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Definition
• Hypercalcemia: serum calcium > 10.5
o Most likely cause: excess secretion by parathyroid hormone b/c of a benign adenoma in the gland – which is responsible for not being able to excrete Ca
o Inverse relationship between Ca and serum P (phosphorus)
Increase Ca; decrease P (drinking lots of soda causes too) |
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Term
| 42. Define the clinical signs of hypocalcemia |
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Definition
• Hypocalcemia: serum calcium <9.0
• No parathyroid gland;
• Idiopathichypoparathyroidism: hypofunctioning of unknown reason
o Seizures, irritability, confusion, tetinay, eventually Bone softening |
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Term
| 43. Explain the role of ACTH in Cushings syndrome |
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Definition
• Adrenal cortex produces 4 hormones
o Cortisol, aldosterone, androgens, estrogens
Males get estrogen levels also get androgens from testicles
Females get androgen levels also get estrogen from ovaries
• Cushings syndrome: increased levels of cortisol: two ways
o ACTH dependent Cushings
Excessive cortisol causes stored proteins to be broken down into components: amino acids –
Excess cortisol promotes release of fatty acids from adipose tissue, then stimulate the liver to form glucose from non-carbohydrate source (gluconeogenesis)
• High blood sugar = hyperglycemia; looks diabetic, but not. Forming glucose from amino acids and fatty acids. When glucose goes up more difficult to excrete Na, as blood glucose rises, retain Na, H2O, increases blood volume, BP and looks puffy
• Cushings: typically overproduce lots of hormones, typically androgens
o Females also excessively overproduce androgens and have masculirizing characteristics: deep voice, hairy
o ACTH independent Cushings
o Adrenal corticotropin hormone (from hypothalamus) |
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Term
| 44. Define the clinical consequences of aldosteronism |
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Definition
• Result of excess aldosterone
• Related to fluid and electrolyte imbalance
• Primary and secondary – end result is the same
• Secondary: kidneys not being properly profused – RAAS kicks in
o Increase aldosterone – enhances reabsorption of Na (not excreting), Na is postive charge, excrete K+ and H+ ions
o Hold on to Na, H2O, increase blood volume and BP
o Excrete K+ and H+, blood becomes more alkaline
o These patients would have: increased BP and alkalosis
• Primary problem with adrenal gland |
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Term
| 45. Explain Hirsutism in terms of androgen excess |
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Definition
• Females
• Hirsutism (Latin = shaggy) – male hair growth pattern; deep voice; breast tissue atrophy; increased muscle development
• In males, to up the amount – get really hairy |
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Term
| 46. Define Addison’s disease and explain the effects of cortisol, aldosterone and androgen deficiency in this disease |
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Definition
• Addisions: hyposecretion; decreased cortisol, more common in males
o Involves most of adrenal hormones
Lack cortisol, androgen, aldosterone
o Decreased amounts of cortisol, causes an increase in cells sensitivity to insulin = more glucose = decreases blood sugar = hypoglycemia
o Real problem for IDDM, even more sensitive to insulin – difficult to regulate
o Excrete Na, H2O, decrease blood volume, decreased BP
• Decreased androgens: decreased amounts of body hair (male and female) |
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Term
| 47. Explain the difference between insulin dependent diabetes and non-insulin dependent diabetes |
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Definition
• Diabetes Mellitus (Latin for honey); intolerance to carbs; increased blood sugar
• IDDM: genetic, but gene doesn’t cause diabetes; gene has to be activated (viral etc)
o Once activated: produces Ab against Beta cells (insulin producing cells) ability to produce insulin is compromised
o Rule of thumb: reasonable diet, until lost greater than 90% of Beta cells, will be okay, after that don’t have enough insulin production must be subsidized with insulin injections
• NIDDM: have Beta cells, they are functioning, often times hyperfunctioning
o Problem is cells susceptibility to insulin
o Familial, correlated with overweight (80% of people); 80% of time lose weight, diabetes goes away
Could be fat plugging up insulin receptor sites on cells |
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Term
| 48. Explain the criteria for diagnosis of non PG diabetes |
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Definition
• Dx: fsting blood sugar: > 126 more than 1 occasion and/or GTT (glucose tolerance test) fast after midnight, 7 am blood sugar, give horrible drink, 30 min later do another blood sugar, 30 min later another blood sugar, 1 hr later another blood sugar, then 2 hours another blood sugar
• > 180 after 2 hour interval and one other time (1/2 hour, 1 hour etc)
• For more accurate check: run out over 4, 5, 6, 7 hours (fasting entire time)
• Looking for 2 peaks and 2 valleys = accurate GTT
• Impaired GT = early diabetic
• Ex: 2 hr 170, 30 min 170 doesn’t quite meet criteria, but close |
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Term
| 49. Explain why ketoacidosis is a complication of diabetes |
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Definition
• Most complications are with IDDM; can be seen in NIDDM, but takes longer
• Ketoacidosis: (keytones by product of fat metabolism) being put into vascular system
• Body takes some of them and turns them into Na salts, excrete out in urine along with H2O, become thirsty = dehydrating (is blood sugar high enough that developing)
• Excreting Na; holding onto K and going up; pH going down. Becoming acidotic
• Trying to blow off CO2 (Kussmals sign) |
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Term
| 50. Explain the vascular complications of diabetes |
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Definition
• Some cells don’t need insulin receptors
o Retina, peripheral nerves, vascular tissue
• Elevated blood sugar level – these cells have unlimited source of glucose they are getting fat and sluggish, clogging up capillaries
• Problems in these areas: glaucoma, gangrene, vascular problems
• Can happen in both IDDM and NIDDM –
• Control diabetes decrease probability of these things happening, still possible |
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