Renal pre-exam 2

jdlevenson's version from 2015-05-07 02:53

Lecture 26

Question Answer
Starting at 115/75, CVD risk goes up by () with each increment of 20/10Doubles.
Hypertension causes kidney disease viaMalignant HTN and Chronic Hypertensive Nephrosclerosis.
If your less than 60, BP should be<140/ 90
If your more than 60, BP should be<150/90
If CKD, BP should be<140/90.
ANP actionIncreased cGMP + Reduction in Sympathetic Tone -> Vasodilation, Decrease Renin -> Natiuresis and Diruesis Decreased Blood Volume -> Decrease Blood Volume and Pressure. Arterial, venous and coronary vasodilation.
Glomerulonephritis causes HTN by...Resistance to ANP. More HTN. Increase in Na/K ATPase.
Flash pulmonary edemaBilateral RAS and ACE-I.
Signs of RASFlash pulmonary edema with ACEi/ARB; Increase in creatinine by >30% on initiation of ACEi or ARB; Asymmetric Kidney sizes; newly difficult to control BP in a patient formerly well controlled.
RAS DxRenin and aldosterone. U/S, MRA, CT.
Angiotensin II to AT1 receptors leads to blood vessel contraction andAdrenal cortex aldosterone secretion via increasing desmolase activity (rate limiting step of steroid synthesis) and aldosterone synthase.
Fibromuscular dysplasia associationString of beads
Fibromuscular dysplasia diagnosisString of beads; increased renin and aldosterone (from turbulent blood flow); u/s, MRA, ct angiogram.
Why string of beadsAlternating aneurysmal dilatation -> hypertrophy constriction/ stenosis -> aneurysmal...Etc. Defect in artery – intima, media or adventitia. Most common in media. Lack internal elastic lamina in the aneurysms.
Which type of Scleroderma may have renal crisisDiffuse cutaneous systemic sclerosis (Vs CREST). Collagen is all over the place – mask facies, sclerodactyl, etc. And even at arteries around kidney as well making for pinpoint openings.
CREST syndrome, CREST stands forCREST involvement: Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. More benign clinical course.
Sclerodermal renal crisis diagnosisIncreased renin and angiotensin. Renal biopsy too. Abrupt moderate to severe htn with quick and rapid AKI.
Sclerodermal renal crisis treatmentACEi or ARB.
Liddle’s syndrome isOveractive ENaC. Limited to kidney itself (transplant kidney and it will go away).
Liddle’s geneticsAutosomal dominant.
Liddle’s triad of symptomsEarly age HTN, Hypokalemia and Metabolic Alkalosis.
Liddle’s dxLow renin and aldosterone.
Liddle’s treatmentAmiloride (or triamterene).
More CKD, lower GFR, means...Higher BP.
Malignant HTN presentation in eyeFlame hemorrhages; papilledema, cotton wool spots, hard exudates and bulging of disc.
With moderate BP elevation, how does kidney respondVasoconstriction. Wants to prevent increase in pressure from being transmitted to smaller more distal vessels. Smaller vessels also have tensile strength. But in severe cases, autoregulation reaches a limit.
Malignant HTN leads to what kind of necrosisFibrinoid.
Chronic HTN leads to nephrosclerosis withOnion skinning. Decreasing blood flow.

Lecture 27

Question Answer
For intravascular volume, giveIsotonic -> Normal saline or plasmalyte.
When don’t you give plasmalyteRenal failure since it has potassium and potassium is already high.
For free water (hypernatremia case)Give hypotonic fluid such as D5W or ½ normal saline.
85% of CKD patients haveHTN.
High sodium leads to renal damage viaDirect effects and increasing BP.
DASH diet is useful for () because ()Good for patients without severe CKD since its low sodium and high K. Fruits, veggies, low fat and non fat dairy.
Potassium excretion90% kidneys, 10% GI.
Why does high potassium potentially cause arrhythmiasHigher extracellular K/ blood K will lead to resting potential at less negative (-90 -> -60) and thus more susceptible to arrhythmias.
Hyperkalemia management1. Loop diuretics and thiazides (though HCTZ not effective if GFR <30), 2. Kayexalate, 3. Underlying acidosis with bicarbonate supplements.
Acidemia causes what change in K+ levelsLower as more goes intracellularly.
Beyond Ca levels, what else triggers PTH?High phosphate levels also triggers PTH since PTH will inhibit Phosphate absorption/ promote excretion via inhibiting Na/P cotransporter.
Renal osteodystrophy signs in bodySubperiosteal bone resorption and acro-osteolysis (bones becoming tips). Also vascular calcification as well as CaP joint deposition.
Mortality increases when P goes over...>6 mg/dL.
High protein leads to increased BUN andAcidosis as expressed in low bicarb as well as glomerular hyperfiltration.
Hyperfiltration is associated withDiabetic nephropathy and FSGS (remnant kidney and obesity).

Lecture 28 and FA:

Question Answer
Honeymoon cystitisSex -> UTI/ acute bacterial cystitis.
Sexually active young women and UTIMost common is E. Coli but Staph Saprophyticus is common too. (And proteus, klebsiella, enterococcus fecalis).
Nosocomial pathogens causing UTICitrobacter, Serratia, Pseudomonas, Candida as well as E. Coli.
Sterile pyuria and negative urine cultures suggestNeisseria Gonorrhea or Chlamydia.
4 key bugsE. Coli, Staph saprophyticus, Klebsiella, Proteus.
Risk factors for UTI in youngFemale sex, sexual intercourse, indwelling catheter, history of UTI (-> more adhesion receptors on genitourinary mucosa; also may lack fucosyl transferase activity), DM, impaired bladder emptying, parity.
Risk factors for UTI in olderAD, PD, CVA and men – BPH, stricture and women – loss of estrogen, incomplete emptying of bladder, urethroceles, bladder diveritcula.
Why does foreskin have propensity for colonizationPropensity for colonization with P-fimbriated bacteria.
How does prostate protect from UTI?Zinc in prostatic secretion prevents ascending infections.
Uncomplicated UTIInfection in a patient with structurally and functionally normal urinary tract. Most isolated or recurrent cystitis and pyelonephritis and usually short course of antibiotics.
Complicated UTIInfection in a patient with structural or functional impairments that would reduce efficacy of anti-microbial therapy.
Asymtpomatic BacteriuriaNot treated unless obstruction or DM or pregnancy.
Acute pyelonephritis symptoms Dysuria, increased frequency, fever, chills, flank pain. Costovertebral angle tenderness.
Pyelonephritis on CTStriated parenchymal enhancement. Affects cortex with relative sparing of glomeruli and vessels. May form perinephric abscess- bad!
Acute vs Chronic pyelonephritisAcute- renal parenchyma. Chronic – recurrent, leading to diffuse interstitial inflammation and usually result of vesicoureteral reflux or chronically obstructing kidney stones.
Thyroidization of kidneyTubules containing eosinophilic casts resembling thyroid from chronic pyelonephritis.
Perinephric Abscess, signs and symptoms?Pyuria, proteinuria, bacteremia,...Requires percutaneous or open drainage.
STI usually causes infection whereUrethra.
Diagnosis of UTI via cultureLow colonies for symptomatic patient with pyuria.
For pregnancy, after E. Coli, thinkKlebsiella or Proteus.
For catheter, after E. Coli thinkPseudomonas.
UTI pregnancy treatmentAmoxicillin, cephalexin (1st gen), nitrofurantoin, sulfonamides. Worried about E. Coli but also Klebsiella and Proteus.
Bactrim good except againstPseudmonas and Enterococcus.
UTI, which antibiotic to useBactrim + aminoglycosides (no pseudomonas and enterococcus) -> Nitrofurantoin (no pseudomonas or proteus) -> cephalosporins and aminopenicillins.
If UTI and penicillin allergyAztreonam.
Complicated UTI, use?Fluoroquinolones (they can treat pseudomonas but contraindicated in children, pregnancy and people on antacids).