Genitourinary and Renal Flashcards
Signs of nephrotic syndrome:
Anasarca (extreme edema)
Bilateral Lower ext. edema
Microscopic hematuria
Sign’s of impending strangulation of bowel:
In the setting of SBO or LBO:
Acidosis
Fever
Leukocytosis
Tachycardia
Diagnostic Workup of SBO:
Abdominal Plain Films
CT
Indications for Emergent Surgery for SBO:
Hemodynamic instability
Peritonitis
Signs of Impending Strangulation
No response to conservative tx (NPO, analgesia, fluids, NG tube)
Clinical differences between pyogenic and amebic liver abscesses:
History: Pyogenic liver abscesses are typical in patients with recent GI surgery, appendicitis, or other GI infection. Amebic is associated with travel to endemic areas and recent bloody diarrhea (from colonic infiltration by entameoba histolytica).
Presentation: Pyogenic abscesses have a much more severe presentation–the patients look and are very ill.
Differentiating between colonic angiodysplasia and diverticulosis:
Colonic angiodysplasia is associated with aortic stenosis and end stage renal disease. Aortic stenosis causes disruption of the vWF multimers and increases bleeding–allowing the angiodysplastic vessels in the colon to be discovered.
In ESRD there is uremic dysfunction of platelets causing increased bleeding and discovery of bleeding colonic dysplastic vessels.
Diverticulosis is evident on colonoscopy–whereas angiodyplasia is not–unless the patient is bleeding.
Electrolyte complications of Renal Failure:
Hyperkalemia - reduced excretion, increased release from dying cells and increased ICF –> ECF transfer due to associated metabolic acidosis of renal failure
Hyponatremia - occurs if water intake is greater than body losses.
Hyperphosphatemia
Metabolic Acidosis
Hyperphosphatemia
Hypocalcemia - due to loss of ability to activate vitamin D and decreased sensitivity to PTH
Indications for dialysis in renal failure:
GFR ≤15
Symptomatic Uremia
Intractable Acidemia
Intractable Hyperkalemia
Intractable volume overload
Definition of Chronic Kidney Disease:
GFR < 60
or
Kidney damage for over 3 months
Uremic Platelet Dysfunction:
Platelets do no degranulate, and therefore fully activate, in an uremic environment
Seen in renal failure.
Can induce unveiling of colonic angiodysplasia.
Calciphylaxis
Necrotic skin lesions caused by vascular calcium deposits secondary to Ca-Po4 precipitates resulting from hyperphosphatemia, which commonly results from renal failure.
Common US findings in CKD:
Smaller kidneys–however–normal sized kidneys do not rule out CKD
Main electrolyte complication of ACE inhibitors. Explain.
Hyperkalemia
Reduction in AngII reduces aldosterone production –> decreased action of Na/K pump in distal tubules, etc.
Mneumonic for Absolute Indications for Dialysis:
AEIOU
A - Acidosis (intractable)
E - Electrolytes (severe persistent hyperkalemia, hyperphosphatemia)
I - Intoxications
O - Overload (volume)
U - Uremia (severe uremic symptoms)
Symptoms of Uremia:
Nausea + vomiting
Lethargy / Deterioration in mental status / seizures / encephalopathy
Pericarditis
Complications of nephrotic syndrome:
Edema - from hypoalbuminemia
Hyperlipidemia - liver produces more along with albumin
Hypercoagulable state - loss of anti-coagulant proteins in urine
Increased Infection - Loss of Ig in Urine
Diagnoses t consider with gross hematuria:
Bladder or kidney cancer (until proven otherwise)
Stones also high on list but less concerning
In general, you should think of post-renal diseases with gross hematuria
4 Possible Presentations of glomerular disease:
Isolated proteinuria
Isolated Hematuria
Nephritic Syndrome - (1) Hematuria; (2) HTN; (3) Azotemia
Nephrotic Syndrome - (1) Proteinuria; (2) Edema; (3) Hypoalbuminemia; (4) Hyperlipidemia
Alport’s Syndrome
Define:
Presentation:
Treatment:
Hereditary nephritis with X-linked or AD inheritance with variable penetrance
Presentation: hematuria, pyuria, proteinuria, high frequency hearing loss without deafness, and progressive renal failure
Treatment: no effective treatment
Classic Triad of Goodpastures:
Proliferative, cresentic glomerulonephritis
Pulmonary Hemorrhage
IgG anti-glomerular basement membrane antibody
Distuinguishing between ATN and AIN:
Can be impossible to do without a renal biopsy
Most common causes of AIN:
Allergies to meds
Collagen Vascular Diseases
Autoimmune Disorders
Infections in kids
Clinical feature most associated with AIN:
Eosinophils in the urine
Short description of each RTA type and the distuinguishing clinical features:
Type 1 (Distal) RTA - Issue with the H+/K+ antiporter in the distal tubules. There is an issue excreting H+ and therefore new bicarbonate cannot be regenerated since the synthetic milleu within the cells is too acidic. As a response, the kidneys excrete all electrolytes, except for H+ and Cl-. Therefore the patients will develop a hyperchloemic, non-anion gap acidosis. There is formation of kidney stones due to massive increase in Ca and PO4 within the tubules and ureters. Treat patients with NaHCO3 and Phosphate.
Type 2 (Proximal) RTA - issue is in reabsorption of HCO3-. There will be no kidney stones now, because HCO3- is taking up all of the “anion space.” Patients will still lose cations like K+ and Na+. Na restriction will help these patients, because there will be increased reuptake of Na, which will indirectly increase uptake of HCO3. Can distinguish by the fact that there will be the same electrolyte issues as in type 1, but without stone formation. Additionally, urinary excretion of Ig light chains is a common feature–therefore multiple myeloma should always be on the differential.
Type 4 RTA - issue is hypoaldosteronism, or reduced reaction to aldosterone due to interstitial renal disease (diabetic nephropathy, or AIN). There will be decreased Na reabsorption and therefore increased K and H reabsoprtion. Therefore the distinguishing feature here is hyperkalemia.
Simple Renal Cysts
Describe + Clinical Course
Extremely common
Increased incidence with age
Asymptomatic and found incidentally
Diagnosed by US
No treatment needed
Renal Artery Stenosis pathophysuilogy and clinical features:
Stenosis usually caused by atherosclerosis or fibromuscular dysplasia (thickening of the walls of arteries–usually in women).
Renal artery stenosis results in restricted blood flow through the glomerulus and therefore the kidney senses a decreased in blood pressure.
This induces RAAS –> HTN
Renal vein thrombosis pathophys and clincal course:
Can be seen in a host of different clinical settings including: preganant women, women using OCPs, dehydrated infants, AAA, LAD, nephrotic syndome, venus invasion by RCC, and trauma.
Patients present with HTN, renal failure, hematuria, proteinuria, flank pain.
Diagnosis is either a doppler test or IVP
Treatment is anticoagulation.
Kidney Stones:
Types and appearance:
Size of stones that will and will not spontaneosly pass:
Rate of Recurrence:
- Calcium Stones - Bipyramidal, biconcave, envelop-shaped / Radiodense (most common)
- Uric Acid Stones - Flat sqaure plates / radiolucent (gout, chemotherapy, acidiuc urine)
- Struvite Stones - Rectangular prisms / Radiodense (urease producing bacteria)
- Cystine Stones - hexagon shaped crystals which are generally poorly visualized (genetic predisposition to cystinuria)
>1cm stones will not spontaneously pass.
50% recurrence rate
Diagnostic modalities for kidney stones:
Labs: Urinalysisl culture; 24-hr urine; serum chemistry
Imaging: Plain films; CT; IVP; US
Most common treatments for kidney stones:
Analgesia
IV fluids
Antibiotics if there is UTI
Extracorpeal Shock Wave Lithotripsy
Early, later, and late signs of prostate cancer:
Early - asymptomatic since cancer begins in the periphery (might be “lucky” if the doc performs a DRE then)
Later - Some obstructive symptoms (has likely already metastasized)
Late - Bone pain from metastasis
Most common sites of prostate cancer metastasis:
Vertebral bodies
Pelvis
Long bones of legs
How to treat prostate cancer:
Localized to Prostate - radical prostactectomy or nothing if old
Locally Invasive - Radiation + anti-androgen medications
Metastatic Disease - reduction of testosterone levels
