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61 Cards in this Set
- Front
- Back
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What 3 forces move urine down the ureters? |
- persistalsis - gravity - hydrostatic pressure |
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Describe how urine is prevented from travelling back up into the ureters |
-ureter enter the urinary bladder into oblique oppenings. - Pressureproduced when the bladder is full presses against the openings,acting as a primitive valve. - Defects related to this valve areassociated with an increase in microbial infections in the kidneys. |
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Describe the layers of the ureters |
-mucosa made of transitional (variable) epithelium (deep). Hasassociated lamina propria with large amounts of collage, elasticfibres and lymphatic tissue. - muscularis made of inner longitudinal and outer circularlayer of smooth muscle. The distal third has an additionallongitudinal layer. The main function of the muscularis isperistalsis. - adventitia is made of connective tissue and containsblood vessels, lymphatic vessels and nerves for the mucosa andmuscularis. It also is attached to the surrounding connective tissueand holds the ureters in place. |
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What is the volume of the bladder? Why is the bladder smaller in females? What is the trigone? |
- 700-800 ml - uterus -the floor of the urinary bladder contains a triangular region calledthe trigone (with the point facing forward). The two posterior pointssignify the two ureteral openings. The single, anterior point, is theopening to the urethra (the internal urethral orifice) |
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Describe the layers of the bladder |
- mucosa with transitional epithelium and lamina propria. Also hasrugae (folds) which allow distension of the bladder. - musculariscalled the detrusor muscle. Has three layers: longitudinal, circularand longitudinal. The muscularis forms two sphincters at the urethra:a superior internal urethral sphincter (smooth muscle) and a inferiorexternal urethral sphincter (skeletal muscle). - superficialadventitia. Surrounded by the serosa – layer of visceralperitoneum. |
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What is the lenght of the urethra in males and females? What are the 3 regions of the male urethra? |
- 20cm vs 4cm - prostatic urethra, membranous urethra and spongy urethra |
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What are the 3 main structures associated with the prostatic urethra? |
(1)ducts that transport secretions from the prostate (2) seminalvesicles (holdsthe liquid that mixes with sperm to form semen) (3) vas deferens (duct which carries sperm). |
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Describe the innervation of the bladder |
-bladder smooth muscle lack gap junctions, suggesting the absence ofelectrogenic coupling – therefore likely acting as a multiunit with1:1 ratio between nerve endings and smooth muscle cells -spincters receive sympathetic and parasympathetic innervation, aswell as somatic innervation -sympathetic nerves arise from T10-L2, and reach thebladder and internal sphincter via the hypogastric nerve -parasympathetic nerves arise from S2-S4 and reach the bladder via thepelvic splanchnic nerve -somatic motor neurons arise from S2-S4 and control the voluntaryskeletal muscle in the external sphincter via the pudendal nerve |
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Describe the micturition reflex (essay answer) |
-bladder tone is determined by the relationship between volume and itsinternal pressure (intravesical) -volume increase up to 300ml have almost no influence on pressure. Atvolumes above 400ml, however, passive pressure begins to increasesteeply -the pontine micturition centre in the brain is responsible forinhibiting the micturition reflex, regulating both the detrusormuscle and the urinary sphincters. -during the storage phase, stretch receptors in the bladder sendafferent (sensory) signals to the pontine micturition centre viapelvic splanchnic nerves – urges begin volume of ~150ml -the sense of fullness is reached at 400-500ml, though efferent(motor) reflexes inhibit parasympathetic neurons in the sacral spinalcord (S2-S4), preventing them from stimulating the detrusor muscle -voiding begins with voluntary relaxation of the external urinarysphincter, then followed by the internal urinary sphincter -when a small amount of urine reaches the proximal urethra, afferentneurons signal to the cortex that voiding is imminent -at this point, inhibition parasympathetic neurons by the pontinemicturition centre is removed, causing the detrusor muscle tocontract -intitial contractions trigger more sensory impulses from stretchreceptors, further promoting voiding and inhibiting the externalurinary sphincter -voluntary urination also involves contraction of abdominal muscles,further raising bladder pressure and emptying |
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List 3 causes of bladder obstruction |
-BPH -bladder calculi -bladder tumours -pelvic tumours (cervix, prostate, uterus, rectum) -urethral stricture (scar tissue) |
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Describe how bladder obstruction can lead to renal insufficiency (essay answer) |
UPDATED: - obstruction>>increase in intraluminal urethral pressure>>decline in GFR - compensatory increase in GFR occurs (temporary). - Continued obstruction causes peristalsis to be overcome, causing hydrostatic pressure to be exerted in the direction of the nephrons>> dilation of the calyces and renal pelvis>>nephron damage - if obstruction persists, renal blood flow and GFR fall>>ischaemia, infections, inflammation, fibrosis, nephron loss>>renal failure END -obstruction – at any level – causes an increase intraluminalurethral pressure -GFR persists for a period due compensatory mechanisms, and recyclingof the filtrate through the lymphatic and venous system. Continuedfiltration without excretion, however, causes the calyces and renalpelvis to dilate -peristalsis can be overcome with prolonged obstruction, causing thebackflow of urine and for hydrostatic pressure to be exerted in thedirection of the nephrons -hydrostatic pressure increases pressure throughout the nephron:pelvis, collecting tubule proximal tubules and Bowman's space,causing GFR to fall. -if the obstruction persists, renal blood flow decreases, resulting inischamia and incremental nephron loss – obstructive uropathyleading to obstructive nephropathy -recovery of GFR depends on; the duration of and level of obstruction,preobstruction blood flow, and co-existing illnesses of infection. -obstruction also triggers a interstitial inflammatory reaction,causing interstitial fibrosis |
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What is the normal range for urea in the blood? Why is urea abundant in urine? What happens to the levels of urea in the blood and kidne function falls? |
- 2.5-7.8mmol/L -nitrogenous waste product of proteins and amino acids - increases |
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What is the normal reference range for blood potassium? What percentage of potassium is reabsorbed in the kidney? At what GFR is hyoerkalaemia most likely to occur? |
- 3.5-5.2 mmol/L -90% is reabsorbed in the PCT and loop of Henle - <10-15ml/min |
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From where is cretinine produced? What is it mosy commonly measured with? |
- breakdown of muscle metabolism - total protein (ratio) |
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Describe the variations in the amount of urea and creatinine between acute and chronic renal disease |
- AKI: urea is elevated more than creatinine - CKI: creatinine is elevated more than creatinine |
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What are the normal values for bicarbonate? What levels are considered pathogenic? |
- normalvalues: 22-28mmol/L - pathogenic: <10 or >40mmol/L |
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What happens to the levels of creatinine, urea, potassium and GFR during renal disease |
- all increase except for GFR which goes down |
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Give 3 reasons why H+ needs to be maintained at the appropriate level |
- maintain cellular function - maintain 3-dimensional shape of proteins - maintain blood pH |
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What are the 3 main mechanisms for regulating H+? Briefly describe what happens in each |
- buffers systems: bind H+ making it uncreactive though do not remove it from the body - C02 exhalation: removes carbonic acid from the blood whcih raises the pH - renal excretion of H+: slower but the only way of eliminating H+ directly |
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What are the 3 main buffer systems used in the body? |
- protein buffer systems - carbonic acid-bicarbonate buffer system - phosphate buffer system |
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Describe how protein buffer systems work (4) |
- functional component is amino acids - carboxyl (COOH) and amino groups (NH2) - able to buffer acids and bases - COOH donates H+ - lowering the pH - NH2 accept H+ - raising the pH |
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Describe how the carbonic acid-bicarbonate system works (3) |
- functional componets are bicarbonate (HCO3-) and carbonic acid (H2CO3) - when there is excess H+, HCO3- accepts H+ produding neutral H2CO3 - when the too little H+, H2CO3 dissociates, producing H+ and HCO3- |
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Describe how the phosphate buffer system works (3) |
- functional components are dihydrogen phosphate ions (H2PO4-) and monohydrogen phosphate ions (HPO42-) - H2PO4- is able to solutons less alkaline by accepting 0H-, producing H20 and HPO42- - when solutions are too acidic, HPO42- is able to accept H+, producing H2PO4- |
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Describe how the inhalation/exhalation of CO2 affects H+ concentration Using an equation, explain how this happens |
- deeper breathing reduces H+ and vice versa |
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Where are changes in blood H+ detected (3) |
- medulla oblongata - aortic bodies - carotid bodies |
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What is the physiological response following the stimulation of the respiratory centre in the medulla oblongata? |
- diaphragm and otherrespiratory to contract more quickly and forcefully, decreasing bloodC02. |
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What is a non-volatile acid? Give an example of one |
- acidproduced in the body from sources other than carbon dioxide, and isnot excreted by the lungs. - sulphuric acid |
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Describe the 5 ways in which H+ is regulated by the function of the kidneys (essay answer) |
(1)in the PCT, H+ is secreted in exchange for Na+ via Na/H antiporters (2)intercalated cells in the collecting duct have H+ pumps (ATPases) inthe apical membrane – can make urine 3 pH units (x1000) more acidicthan blood (3)another type of intercalated cell also has proton pumps (H+ ATPases),though in its basolateral membrane, as well as Cl-/HCO3- antiportersin its basolateral membrane. The overall effect is the excretion ofH+ when pH is too low, and the excretion of HCO3- when pH is toohigh. (4)blood pH can also be increased in the kidney by reabsorbing HCO3-. Inintercalated cells, the dissociation of H2C03 allows HCO3- to crossthe basolateral membrane through Cl-/HCO3- antiporters, and thendiffuse into peritubular capillaries. (5)other H+ buffers found in the tubular fluid include monohydrogenphosphate (HPO42-) and NH3 (ammonia). H+ combines with HPO42- to formH2PO42- (dihydrogen phosphate) and NH3 to form NH4 (ammonium). Theseions are unable to be reabsorbed and are therefore excreted. |
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What are the blood values for; normal blood pH acidosis alkalosis |
-arterial blood pH is 7.35-7.45 -acidosis is pH <7.35 (more acidic) -alkalosis is pH >7.45 (more alkaline) |
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What are the consequences of acidosis? What are the consequences of alkalosis? |
-acidosis casues depression of synaptic transmission, resulting indepression of the CNS – causing disorientation, comatose, thendeath -alkalosis causes overexcitability of the CNS and peripheral nerves.This causes neurons to synapse repetitively in the absence of normalstimuli, resulting in nervousness, muscle spasms, convulsions, thendeath. |
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How does the body compensate for alkalosis/acidosis? |
- if due to metabolic causes, hypo or hyper ventilation - if due to respiratory causes, renal compensation (H+/HCO3-) |
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Describe the speed of action of respiratory and renal compensation |
-Respiratory compensation occurs within minutes and can reach maximumwithin hours - renal compensation begins in minutes, though can takedays to reach maximum. |
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What is the arterial pCO2 pressure in respiratory acidosis? Name three conditions which might result in respiratory acidosis |
- >45mmHg - emphysema,pulmonary oedema, injury to the respiratory centre of the medullaoblongata, airway obstruction, and disorder of muscles involved inbreathing |
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What is the arterial pCO2 pressure in respiratory alkalosis? Name three conditions which might result in respiratory alkalosis |
- <5mmHg - oxygendeficiency due to pulmonary disease, altitude, stroke, or severeanxiety. |
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What is the blood HCO3- level of metabolic acidosis? Name three situations which might lead to metabolic acidosis? |
- systemicarterial blood HCO3- <22mEq/L - (1)loss of HCO3- (e.g. severe dehydration, renal dysfunction); (2)accumulation of an acid other than carbonic acid, such as in ketosis;(3) failure of the kidneys to excrete H+ |
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What is the blood HCO3- level of metabolic alkalosis? Name three situations which might lead to metabolic alkalosis? |
-systemicarterial blood HCO3- >26mEq/L. - the most frequent cause of metabolic alkalosis is likely vomiting,where there is substantial loss of HCl. Other causes include; gastricsuctioning, diuretics, endocrine disorders, excessive intake ofantacids, and severe dehydration |
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Describe the 5 stages of kidney disease including GFR for each stage |
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List 5 potential treatments for someone admitted with AKD |
-fluid balance treatment: kidney failure may be linked to either toomuch or too little fluid. As such, treatment may involve IV fluids,or diuretics -regulation of blood potassium: too much potassium in the blood canlead to muscle weakness, arrhythmias and death. In such cases,calcium, glucose, or sodium polystyrene may be prescribed. -medications to restore calcium -dialysis: removal of toxins from blood and potentially excesspotassium -if glomerulonephritis, cyclophosphamide will be given (autoimmune) |
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List 5 lifestyle changes for somone with CKD |
- stopsmoking - eat healthy diet - restrict salt - exercise - moderate alcohol - lose weigh - avoid NSAIDs |
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Name 3 medications which might be used to lower blood pressure in patients with hypertension |
- ACEinhibitors - angiotensin II receptor blockers. - Diuretics will alsooften be prescribed in conjunction with a low salt diet. |
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What medication might be prescribed to lower cholesterol? Why is lowering cholesterol important in people with CKD? |
- statins - CKD has an increased risk of MI and stroke |
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What medication would you give to treat anemia in CKD and why? |
- erythropoietin. Ferroussulphate is also given for iron deficiency -erythropoietin is produced in the liver and therefore reduced in CKD |
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What 3 drugs might be prescribed in CKD for those with poor bone health? |
- calcium, vitamin D and phosphate binders |
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Why do people with CKD have poor bone health? |
- Phosphateis elevated in CKD and, with calcium, Is needed normally formaintaining bone health. However, too much phosphate can upset thebalance and lead to thinning of bones
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What is cleared by the kidneys faster; the drug or its metabolites? What type of are likely to be able to pass through the slit membrane? |
- metabolites - MW <20,000 and not bound to albumin |
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Other than size, name 2 factors which influence the passage of drugs into the glomerulus |
- GFR and rate of plasma binding |
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How are drugs able to enter the tubules through the PCT (3)? |
- secretion using 2 energy-dependent symporters - Organic Anion Transporter and Organic Cation Transporter - low specificity means the are able to transport drugs - can occur even when bound albumin |
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What % of blood passes throug the glomerulus/peritubular capillaries? |
- 20/80% |
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Describe how transport differs in the OAT and OCT |
- OAT transports against a gradient - OCT transports down a gradient |
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How does diffusion across the renal tubules differ between lipid-soluble and and polar drugs? |
- lipid-suluble drugs are excreted poorly - polar drugs tend to remain the lumen becoming increasingly concentrated |
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Name 3 drugs which are excreted largely unchanged in the urine? |
- furosemide, gentamicin, digoxin and methotrexate |
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Describe how acidity/alkalinity affects the excretion rate? What is this called? Why is this imoportant clinically? |
-basic drugs are more rapidly excreted in acidic urine, and viceversa. Called ion-trapping. - can be used to slow or enhance the elimination of a drug e.g. in an overdose |
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Describe the difference between phase 1 and phase 2 reactions |
- phase 1: involveeither the addition of hydroxyl groups or the removal of blockinggroups from hydroxyl, carboxyl, or amino groups - PhaseII reactions that use conjugation with sulfate, glycine, orglucuronic acid to increase drug polarity. The conjugates areionized, and the charged molecules cannot back-diffuse out of thekidney lumen. |
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Define renal clearence |
- “volumeof plasma containing the amount of a substance removed by the kidneysover a given time" |
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Name 5 groups of people which would be susceptible to nephrotoxic drugs |
- older age - CKD and AKD - congestive heart failure - liver failure - neonates |
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Describe how NSAIDs are associated with renal damage (essay answer) |
-in general , NSAIDs are relatively safe, though their widespread usemakes them a common cause of renal damage -inhibition of prostaglandins is responsible for the majority of thenegative effects -major normal function of prostaglandins in the kidney isvasodilation, needed for adequate renal perfusion -the negative effects of NSAIDs or renal function is magnified inthose who are hypovalaemic or on ACE inhibitors -NSAIDs are also involved - in conjunction with inhibition of prostaglandins- in inhibiting the RAA system – resultingin hyperkalaemia and acidosis -also involved in sodium-retention leading to hypertension and oedema |
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Describe how ACE inhibitors are associated with renal damage (essay answer) |
-widely used for hypertension and congestive heart failure (as in PBL) -angiotensin II contricts both the afferent and efferent arterioles,though its effect is more pronounced on the efferent arteriole -its net effects is increased intraglomerular pressure -subsequently, this interferes with autoregulation of GFR. This isnormally well-tolerated, though can precipitate acute renal failurein certain patients: bilateral renal artery stenosis in singlekidney, volume depletion, and combined use of NSAIDs, cyclosporineand tacrolimus -combined use of NSAIDs and ACE inhibitors or angiotensin II receptorblockers has a cumulative effect on renal damage and should beavoided – especially in those with CKD |
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Name 4 types of antibacterial agent associated with renal damage |
- aminoglycosides - trimethroprim - vancomycin - penicilin |
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Name 2 chemotherapeutic agents associated with renal damage Name a immnosupressive agent associated with renal damage |
- displatin and ifosfamide - cyclosporine |
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How do radio-contrast agents cause nephrotoxicity? How is this minimised? |
- happens with iodinated media. Happens due to vasoconstriction,causing medullary hypoxia and acute tubular necrosis, followed byosmotic nephrosis. - hydration strategy |
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Whcih drug used to treat bi-polar disorder is also associated with renal damage? What medication used to treat acid reflux is alsoassociated with renal damage? |
- lithium - PPIs |
