Lecture 37 March 2nd-renal

1DDX: LECTURE 37 – MARCH 2ND, 2007 CONDITIONS OF THE RENAL SYSTEM CONGENITAL ABNORMALITIES • “polycystic” anything is a congenital abnormality. Blind tubules form and fill with fluid, forming cysts. • Autosomal dominant PKD: enlarged kidneys, they keep growing. Cysts will appear in other organs too. •

Tubes can be obstructed in a number of ways: can clog it, can pinch it, can put stuff in the tube that will block it over time.

HYDRONEPHROSIS • Distal obstruction: will be backup pressure. Kidney has no capsule (unlike prostate, spleen). Pressure from blood, net oncotic pressure. Can enlarge to 4x regular size. • Kidney formed of pyramidal structures. Increase in pressure, the tissue of the KI is pushed to the sides, the kidney is mostly water. Pressure atrophy of tissue. This is usually a chronic condition that develops over time. If the tissue is damaged, it can regenerate to a certain degree. ACUTE OBSTRUCTION • CVA=costo-vertebral angle • Pathognomonic: KI pain doesn’t change with stretching, temperature changes (ddx from muscular pain) • Uretal colic: Passing stone: colic-y pain. Not constant. CHRONIC OBSTRUCTION • (covered in hydronephrosis). • Can also have asymptomatic obstruction. Over time, their kidney function is compromised. • Oligurea: little urination • Polyurea: they are urinating a lot but not getting rid of wastes. Filtrate is not concentrated. • Megaureter: plugged ureter will enlarge. Usually occurs in chronic state. Body will deposit calcium in ureter to prevent it from rupturing. • In chronic condition, don’t have pain because the body has adapted to it. Have pain in acute. Not perceived in the same way by the body. UROLITHIASIS • Pain can be confused with cramping from diarrhea. • Not quite sure what causes KI stones. Has something to do with calcium? Not due to high calcium intake. Uric acid stones can be linked to gout, purine-containing foods. Stone-forming salts in urine. • There are normally compounds in urine that prevent formation of salts. • Dehydration may be a factor increasing supersaturation. • Pre-formed nuclei. Areas of inflammation may cause deposit of salts. Inflammation may disappear, but nucleus remains. • Hypertension seems to play a role too. • Pain will depend on where the stone lodges. • Staghorn calculi (see picture below) : can be huge: 2/3 the size of kidney! Forms with point, following the shape of the interior of kidney.

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Stones will keep growing: they are nuclei themselves. Magnesium will help calcium-based stones. Things that cause breakdown: prolonged fasting, starvation DDX LECTURE 37, MARCH 2ND, 2007 – PAGE 1

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Things don’t happen in isolation: stone blockage can cause pyelonephritis (“-itis” in the kidney pelvis) Good to have a microscope in office to identify crystals in urine to be able to identify what type of crystals you are dealing with. Can assess whether they are there still after treatment.

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“Urinary tract infection”: This is a blanket term, covering all of the urinary system. Better to be specific: urethritis, cystitis, pyelonephritis.

URETHRITIS • Normally no hematurea in urethritis • Nephritis is like pneumonia: the end of the progression of infection. • Usually gram (–) anaerobic bacteria. Can survive in urine, no oxygen. CYSTITIS • Inflammation of the bladder. Not necessarily an infection. • Normally only have nocturia with inflammation that occurs near trigone. This area senses when you need to urinate. If there is inflammation here, will always feel like you have to urinate. • In men, repeated bouts of cystitis are often the result of an anatomical problem. Can develop over time. • In older women, there will be a bit of urine that stays behind after micturation. The more urine stays behind, the more likely there is for an infection to follow. Emptying half-way encourages infections. • Part of etiology is hygiene: keeping the urethra unclean, wiping the wrong way (P to A), infrequent bathing. More of concern in women. • Usually Sudden Onset! Wake up with it. Don’t need all of DDX features, but if you have some of them, suspect it. PYELONEPHRITIS • Cystoscope: inserted through urethra to take picture of bladder. Slides showing pictures. Normal looks like fundus of eye. In acute, can’t see vessels, looks red. Chronic cystitis, see vessels. • See effect of elimination diet: almost returned chronic case of cystitis to normal on cystoscopy. • Lung produces surfactant to prevent collapse of alveoli. Kidney doesn’t produce surfactant: will get washed away with urine. KI secretes proteinaceous mucous instead which are passed in the urine. Indication of what is happening in the KIDNEY. Hallmark of pyelonephritis is WBC casts, included in the proteinaceous mucous. PYONEPHROSIS (“pus forming”) • Osis vs. It is = Otis implies that it is not quite inflammatory. • A retro-infection. A hydronephrosis gone bad: now includes an infection. • Lots of pus in one area of the body: what symptoms do you expect? Fever, pallor, patient will look sick, high WBC in blood, tachypnea, inability to exert self. (Skip next page: blood born urinary infection to renal tuberculosis) NEPHRITIC SYNDROME, NEPHROTIC SYNDROME • Neither are pathologies, they are descriptions. • Nephritic: applied if you have oliguria (<500mL urine per day) anuric <25mL urine per day, or none. Azotemia: high ammonia (uric acid) in blood. • Nephrotic: losing protein therefore develop oncotic edema, losing protein faster than the liver can make it. • Acute post-streptococcal-glomerulonephritis: cross-reaction of immune system: destruction of KI following infection.

CLINICAL ASSESSMENT Not tested on this (I don’t think…) Know mixed picture. (for test? Unclear) Is it primary or secondary? Amyloidosis: can’t excrete protein. Rest of material is not testable. (renal failure onwards) DDX LECTURE 37, MARCH 2ND, 2007 – PAGE 2