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Renal 1.1
UWORLD Renal Review
| Question | Answer |
|---|---|
| Hyperphosphatemia in chronic kidney disease | CKD leads to decreased GFR, which causes a decreased 1, 25 -Vit D , leading to decreased serum Calcium, and to Phosphate retention, elevating serum phosphate levels |
| Low serum Ca and High serum phosphorus causes --> | Secondary Hyperparathyroidism |
| What type of Hyperparathyroidism is seen in CKD? | Secondary Hyperparathyroidism |
| Elevated levels of PTH and Calcium in blood, are seen in: | Primary Hyperparathyroidism |
| Vitamin D Toxicity exhibits: | High blood calcium with low PTH in blood levels |
| Vitamin D deficiency has _________ of serum Calcium and _______ serum PTH. | Low Calcium and Low PTH |
| What is the serum difference in PTH/Calcium profile between kidney failure and Primary Hyperparathyroidism? | Kidney Failure has High levels of PTH and low Calcium, while 1-Hyperparathyroidism has high levels of Calcium and PTH. |
| The levels of PTH and Calcium in CKD, resemble the closest to those seen in: | Secondary Hyperparathyroidism |
| What is the relation in serum levels between PTH and Ca2+ seen in Primary Hypoparathyroidism? | Low levels of Calcium and PTH |
| Patient with a PTH-derived malignancy, produces ____________ of PTH and _________ of Calcium in blood serum. | Low PTH; High Calcium |
| Vitamin D deficiency share similar levels of Calcium and PTH as: | Primary Hypoparathyroidism |
| Which category of people are most seen with Renal Artery Stenosis with unilateral kidney atrophy? | Elderly and women of childbearing age. |
| Pathogenesis of Renal Artery stenosis seen in the elderly? | Atherosclerosis changes in the arterial intima |
| Fibromuscular dysplasia in women of childbearing age, predisposes them to increase risk of developing what renal-related condition? | Renal Artery Stenosis with unilateral kidney atrophy |
| What are associations and clinical manifestations of Renal Artery Stenosis? | Associated with hypertension and an ABDOMINAL BRUIT. |
| What is the effect of compensation seen in Renal artery stenosis? | Enlargement of the healthy kidney |
| Immunosuppressant, SIROLIMUS, binds to which protein ? | FK506 in the cytoplasm |
| The binding of Sirolimus and FK506 | Inhibits the mTOR |
| What are the effects of mTOR inhibition? | Blockade of IL-2 signal Transduction preventing cell cycle progression |
| Calcineurin inhibits: | 1. Cyclosporine 2. Tacrolimus |
| What drugs inhibit the de Novo Purine nucleotide synthesis? | Mycophenolate and Leflunomide |
| Which substances have same filtration and excretion rate/content? | Inulin and Mannitol |
| Glucose, Na+ and Urea have gratear ____________________, than _______________. | FILTERED >>>> excretion |
| EXCRETION >>>>> filtered | PAH and Creatine |
| Inulin clearance is equal to __________ | GFR |
| 100% of _____________ is excreted and 0% of _________ is reabsorbed. | Inulin; Inulin |
| A GFR equal to 100 mL/min, equals to ____________ of inulin clearance. | 100 mL/min of Inulin clearance |
| PAH clearance estimates ___________________ | Renal Plasma Flow (RPF) |
| Inulin clearance estimates _________________ | GFR |
| RPF = | C-PAH (clearance of PAH) |
| RPF = C-PAH = | (Urinary-PAH x Volume) / Plasma -PAH |
| What is the the essential difference between calculating Inulin clearance and PAH clearance? | The use of ether Urinary PAH or Inulin and/or Plasma PAH or Inulin. |
| Loss of Pelvic floor support and Incompetence or urethral Sphincter, describes the pathogenesis of? | Stress Incontinence |
| Patient complains of involuntary loss of urine, while coughing or sneezing | Stress incontinence |
| The increase in ___________________ in patients with stress incontinence leads to the _________________ loss of urine. | Abdominal pressure; Involuntary |
| What are the causes of Stress incontinence: | 1. decreased urethral tone 2. Urethral hypermobility |
| Leakage with cough, lifting and sneezing | Stress incontinence |
| Detrusor hyperactivity, leads to development of: | Urge incontinence |
| Sudden, overwhelming urge to urinate | Urge incontinence |
| What are the 2 main causes of OVERFLOW incontinence? | 1. Impaired detrusor contractility 2. Bladder outlet obstruction |
| The impaired function of the detrusor muscle is associated with development of __________________ incontinence, while its overactivity develop ___________ incontinence. | Overflow; Urge |
| Patient complains of not voiding completely, and indicates often involuntary urine dribbling. | Overflow incontinence |
| MCC of nephrotic syndrome in children | Minimal Change Disease (MCD) |
| Massive proteinuria (selective for Albumin), reduced plasma oncotic pressure, hypoalbuminemia, edema, and increased risk of thrombotic event in child? | Minimal Change Disease (MCD) |
| What are basic characteristics of Nephrotic Syndrome? | 1. Increased glomerular permeability 2. MASSIVE proteinuria 3. Hypoalbuminemia 4. Increased liver protein synthesis leading to HYPERLIPIDEMIA (increased thrombotic events) 5. Increased aldosterone and ADH secretion --> Edema --> Increased oncotic pressure |
| RBC casts are seen in | Nephritic syndrome |
| Features of Nephritic Syndrome | RBC casts/Hematuria, HTN, Oliguria, decreased GFR, minimal proteinuria |
| Features of Nephrotic Syndrome | Massive proteinuria, hypoalbuminemia, Edema, hyperlipidemia, and lipiduria |
| Which conditions are considered PURELY Nephrotic syndromes? | 1. Focal Segmental Glomerulosclerosis 2. Membranous Nephropathy 3. Minimal Change Disease 4. Amyloidosis 5. Diabetic Glomerulonephropathy |
| 1. PSGN 2. RPGN 3. Berger Disease (IgA nephropathy) 4. Alport Syndrome | Nephritic Syndromes (only) |
| Which 2 conditions are considered Nephritic and Nephrotic simultaneously? | 1. Diffuse Proliferative GN 2. Membranoproliferative GN |
| What is the most common cause of asymptomatic primary glomerulonephritis? | IgA nephropathy (Berger Disease) |
| Berger disease is a _______________, and Buerger disease is a _______________________. | IgA nephropathy (Nephritic syndrome); Small/Medium artery vasculitis seen in smokers |
| IgG4 antibodies to the phospholipase A2 | Membranous Nephropathy |
| What 2 different antibodies are seen in Membranous Nephropathy? | 1. IgG4 antibodies against Phospholipase A2 2. PLA2R antibodies |
| What are the clinical manifestations of Aspirin toxicity? | Tinnitus, fever and tachypnea. Initially seen with Respiratory Alkalosis, followed by mixed Respiratory Alkalosis and anion-gap Metabolic Acidosis. |
| What are the acidotic-alkalotic balances seen in Aspirin toxicity? | First RESPIRATORY ALKALOSIS followed by METABOLIC ACIDOSIS (anion-gap) |
| IgA immune complexes deposited in glomerular membrane | Berger Disease |
| Presents with recurrent, self-limited, painless hematuria, seen 5 days after Upper Respiratory infection. | Berger Disease |
| How is the time between Berger Disease and PSGN infection differs? | Berger Disease precipitating is 5 days after URI, and PSGN preceding URI is seen 2-3 weeks after. |
| Streptococcal pharyngitis | PSGN |
| Antibodies against Streptococcal antigens that deposit on GMB | PSGN |
| Electron microscopy views Subepithelial humps | PSGN |
| What is seen on IF in PSGN? | C3 granular staining along GMB |
| Antibodies against Type 4 Collagen develops what disease? | RPGN (Goodpasture Disease) |
| IF: Linear staining (IgG) along GMB | RPGN (Goodpasture Disease) |
| RPNG | LM seen in Glomerular crescents; IF -> Fibrinogen crescents |
| LM: hypercellular hypercellularity | Berger Disease |
| Defective Type 4 collagen in GMB | Alport Syndrome |
| EM: lamellated appearance of GMB | Alport Syndrome |
| AT II works on the ___________________ arteriole and it causes __________________. | Efferent arteriole; Vasoconstriction |
| What type of drug works on the efferent arteriole? what does it cause? | ACE inhibitors and ARBs and cause Vasodilation, leading to a fall in GFR. |
| The afferent arteriole vasodilation is caused by? Vasoconstriction? | Vasodilate with Prostaglandins and ANP Vasoconstric by the use of NSAIDS |
| Which arteriole forms the glomerulus? | Afferent arteriole |
| What is the glomerulus? | A knot formed by the afferent arteriole inside the Bowman's capsule |
| Which arteriole carries grater amount of water? | Afferent arteriole |
| The renal arteries branching forms the _____________ arteriole. | Afferent |
| Which vascular structure "brings in" O2 rich blood into kidney? | Afferent arteriole |
| Which lumen is narrower, the afferent or efferent arteriole lumen? | Efferent is twice as narrow |
| The EFFERENT arteriole divides to form the __________________ which envelopes the renal ________________. | Vasa recta; tubule |
| High resistance outflow pathway is seen in the ______________ arteriole. | Efferent |
| Fraction of plasma flowing through the glomeruli that is filtered across the glomerular capillaries to the Bowman's space | Filtration Fraction (FF) |
| Glomerular Filtration rate divided by Renal Plasma Flow | Filtration Fraction (FF) |
| RBF (renal blood flow) x (1-hematocrit) | RPF |
| RBF is equal to ________________. | Clearance of PAH |
| Volume that is occupied by RBC, and it is UNABLE to cross the glomerular capillaries. | Renal Blood Flow (RBF) |
| So if GFR is the same as ___________________, and RPF is the same as __________________, then the filtration fraction may be defined as? | Inulin clearance; PAH clearance; Ratio of Inulin clearance to PAH clearance |
| What is a normal FF? | 20% or approximately 180 L/day |
| What is a role of FF? at which part of the nephron most importantly? | Estimation of Tubular Reabsorptive Efficiency, at the proximal tubule. |
| As FF increases, the | plasma protein concentration increases |
| RPF is defined as: | Volume of plasma that is ABLE to pass through the glomerular capillaries. |
| What is the primary substance controlling the GFR? | Angiotensin II |
| What conditions cause increased AT II? | Condition of volume depletion (dehydration, hemorrhage) |
| Angiotensin II has a preference to Vasoconstric the __________ arteriole. | Efferent |
| Constriction of Ureter causes: | No change in RPF but decrease in GFR and FF |
| Constriction of the ________________ arteriole causes a increase in FF, as it ____________ GFR and ____________ RPF. | Efferent; Increase; Decrease |
| Constriction of the afferent arterioles, causes what changes in FF? | It produces a reduction in GFR and RPF, thus no change in FF. |
| Common causes of Metabolic Alkalosis? | 1. Loop diuretics 2. Vomiting 3. Antacid use 4. Hyperaldosteronism |
| Histeria, hypoxemia, salicylates (early), tumor, and pulmonary embolism, are? | Common causes of Respiratory Alkalosis |
| Respiratory acidosis is most commonly caused by: | 1. Airway obstruction, 2. Acute and Chronic lung disease 3. Opioids, sedatives, 4. Weakening respiratory muscles |
| Patient with rapidly progressive ascending paresthesias after consuming contaminated food followed by severe periods of bloody diarrhea. Overtime, patient will develop what acid-base imbalance? | Respiratory Acidosis caused by advancing Guillain Barre syndrome. |
| What is the pH range in arterial blood? | 7.35 - 7.45 |
| HCO3 levels range between _________-_________ mEq/L. | 20-28 mEq/L |
| The PCO2 levels are marked normal between __________ and _______ mm Hg. | 36 and 44 mmHg |
| The imbalance is considered Respiratory alkalosis if? | PCO2 levels fall below 36 mm Hg and pH is greater than 7.45 |
| What is the normal range of the anion-gap? | 8-12 mEq/L |
| What is the formula to obtain the anion gap? | = Na - (Cl+HCO3) |
| What causes metabolic acidosis with anion gap of 14? | MUDPILES: Methanol, Uremia, DKA, Prolyethenly glycol, Iron and INH, Lactic acidosis, Ethylene glycol, Salicylates (late) |
| HARDASS: | Mnemonic for non-anion gap causes of metabolic acidosis |
| What some causes of Non-anion gap metabolic acidosis: | Hyperalimentation, Addison's disease, Renal tubular acidosis (RTA), Diarrhea, Acetazolamide, Spironolactone, Saline solution |
| Male patient in chronic treatment for edema and low potassium level, develops enlarged breast tissue. This patient is may also develop what kind of Acid-Base imbalance? | Non-anion gap Metabolic Acidosis |
| Example of patient that is more likely to develop metabolic acidosis with a normal anion gap? | Patient stabilized blood pressure with saline fluids over a 5 day hospitalization stay after sustaining severe hemorrhage following a car accident. |
| Patient in HYPERVENTILATION will most likely develop: | Respiratory Alkalosis |
| Why do Hyperventilation develop Respiratory Acidosis? | Increase or rapid loss of CO2 |
| What is the pathogenesis of Thrombotic Microangiopathy? | Platelet activation and diffuse microthrombosis in arterioles and capillaries. |
| Common clinical presentation of Thrombotic Microangiopathy? | Hemolytic anemia with schistocytes, thrombocytopenia, and organ injury. |
| Where does Aldosterone acts most specifically? | On Intercalated cell of the renal collection tubules |
| What is the actions stimulated by Aldosterone? | Reabsorption of Sodium and water, along with the loss ot K+ and Hydrogen ions. |
| What are some Aldosterone antagonists? | Spironolactone and Eplerenone. |
| Ureteropelvic Junction obstruction leads to: | Unilateral Fetal Hydronephrosis. |
| Vesicoureteral junction obstruction is a common cause of? | Vesicoureteral reflux |
| Efferent vasoconstriction is accomplished by administration of _____________ and ___________, leading to the maintenance of ________. | ACE inhibitors; ARBs; GFR |
| What other electrolyte is important to check in a patient with Metabolic Alkalosis to further investigate the Dx? | Urine Chloride |
| Decreased Urine Cl- in a patient with Metabolic acidosis, may indicate? | Vomiting, nasogastric aspiration, or past use of diuretics. |
| Batter Syndrome and Glitterman Syndrome are seen in a patient with __________________ and __________ urine _______, but a state of ___________________. | Metabolic Alkalosis; Low urine Cl; Hypovolemia |
| High urine Cl-, elevated pH, and HCO3 > 24, are seen in a patient with hypervolemia. Possible causes? | Excess mineralocorticoid therapy, Primary Hyperaldosteronism, Cushing disease, or Ectopic ACTH |
| What organism causes Hemolytic Uremic Syndrome (HUS)? | Shiga-like toxin, by E. coli and Shigella. |
| HUS' symptom triad | 1. Microangiopathic hemolytic anemia 2. Thrombocytopenia 3. Acute kidney injury |
| How is kidney injury seen in HUS seen? | Elevated Creatinine (Cr) |
| Diuretics that effectively increase Ca2+ reabsorption for the nephron. | Thiazide diuretics |
| Thiazide diuretics is seen with the development of _______________ secondary to _____________________, and thus highly contraindicated in patients with some type of __________________. | Nephrolithiasis; Hypercalciuria; Hypercalcemia |
| MoA of Thiazide diuretics | Keep Calcium in the Tubular lumen by DEACTIVATING the Na/Ca2+ co-transport. |
| Goodpasture syndrome is a type of _______________________, seen with ___________ deposits of IgG and C3 deposition. | Hypersensitivity 2; Linear |
| + ANCA RNPG | Pauci-immune RPGN |
| Treatment of CN intoxication: | Sodium NITRATE |
| Treatment options of CN toxicity: | 1. Sodium NITRATE 2. Sodium THIOSULFATE 3. HYDROXYCOBALAMIN |
| Elevated level in blood of _________, __________, and _____________ promote crystallization , thus calculi promotion. | Calcium, Oxalate, adn Uric acid |
| Elevated levels of _______________________ prevents kidney stone formation. | Citrate |
| Biopsy demonstrates hyaline arteriosclerosis and nodular glomerulosclerosis | Diabetic Nephropathy |
| What are the EM findings in Diabetic Nephropathy named or called? | Kimmelstiel-Wilson nodules. |
| The ____________________ are seen with glomerular basement membrane (GBM) ___________________ and increased ______________ matrix deposition. | Kimmelstiel-Wilson nodules; Thickening; Mesangial |
| What cells are involved in Type 1 Hypersensitivity? | Basophils and Mast cells |
| PSGN, SLE and serum sickness are: | Type 3 Hypersensitivity reactions |
| What renal Nephritic syndrome is considered a Type 2 Hypersensitivity reaction? | Goodpasture Syndrome |
| What is the humoral activity seen in Type 2 Hypersensitivity reactions? | Increased IgG and IgM production levels and Complement activation. |
| Which cells are seen involved in Cytotoxic Hypersensitivity? | NK cell, Eosinophils, Neutrophils, and Macrophages |
| Onset of Transplant rejection reactions: Hyperacute, Acute, and Chronic? | Hyperacute ---> Minutes to Hours Acute --> Less than 6 months Chronic ---> More than 6 months to years |
| What is the Etiology of Hyperacute organ transplant rejection? | PREFORMED antibodies against graft in recipient blood. SIMPLY: Antibodies of the recipient attack the tissue antigens of the donated tissue. |
| Hyperacute graft rejection presents commonly still during __________, by appearance of _______________________ of graft vessels. It is considered a type ______ hypersensitivity. | Surgery; Thrombosis and Occlusion; Type 2 Hypersensitivity |
| Hyperacute, Acute and Chronic organ rejection are known also as _____________________. | "Host vs Graft" |
| In the writing sequence of organ rejection, the one written first is the one _________________. | Attaking. Ex. "Graft vs Host Disease" ; the GRAFT is attacking the Host's tissue. In "Host vs Graft" the Host (recipient) attacks the donated tissue. |
| What is etiology (pathogenesis) of Acute organ rejection? | The HOST creates a T-cell immune response against the foreign (donor) MHC. |
| How is Acute organ rejection vessel histology presented? | Leukocyte (macrophages and lymphocyte) infiltration of graft vessels (donor vessels) |
| Intimal thickening and fibrosis of graft vessels as well as graft atrophy, in patient with a organ transplant over a year ago. Dx? | Chronic organ rejection |
| Which is the most common type of "Host vs Graft Disease"? | Acute organ rejection |
| Acute organ rejection is a Type _____ Hypersensitivity reaction. | Type 4 |
| Chronic organ rejection is considered a Type _____ and _____ Hypersensitivity reaction. | Type 3 and Type 4 |
| What is the mechanism of pathology seen in "Graft vs Host Disease" (GVHD)? | DONOR T cells proliferate and attack recipient's tissue. |
| What type of transplant yields the highest chance of developing GVHD? | Bone Marrow |
| What is the clinical presentation of GVHD? | Diarrhea, Rash and Jaundice |
| GVHD is considered which type of Hypersensitivity reaction? | Type 4 Hypersensitivity reaction |
| Smooth muscle proliferation and vessel occlusion is seen in? | Chronic Organ rejection |
| Endotheliitis is seen in | Acute Organ rejection |
| What is the humoral response presentation of Acute organ rejection? | C4d deposition, neutrophilic infiltrate, and Necrotizing vasculitis |
| Lymphocytic interstitial infiltrate and endotheliitis, is seen as the? | Cellular response of Acute Organ/Graft rejection |
| Extraperitoneal organ | Bladder |
| During a suprapubic cystostomy, the cannula will pierce the ____________, but NOT enter the ___________________. | Abdominal wall; Peritoneum |
| Causes of secondary Hyperaldosteronism? | Renovascular disease, Malignant HTN, and Renin-secreting tumors. |
| Increased levels of serum Aldosterone and Renin, point to: | Secondary Hyperaldosteronism |
| Patient with renin-secreting tumor-induced Hyperaldosteronism, presents with: | Hypertension, Hypokalemia, and muscle weakness. |
| What 2 syndromes may cause Secondary Hyperaldosteronism? How is blood pressure different in such causes? | Secondary Hyperaldosteronism is usually presented with HTN, unless is caused by: 1. Batter's Syndrome 2. Gitelman's syndrome This cause NORMOTENSIVE Secondary Hyperaldosteronism |
| Renin, this enzyme, stimulates the release of __________________, thus causing an increase in ___________________. | Aldosterone; Blood Pressure |
| Ureter anatomical position with respect to the Internal iliac and Uterine arteries. | Ureter passes ANTERIORLY to Internal Iliac artery Ureter passes POSTERIORLY to the Uterine artery. |
| What urinary system structure passes anterior to the Internal Iliac artery? | URETER |
| Urinary conductive tube-like structure that passes POSTERIOR to the Uterine arteries, bilaterally? | URETER |
| MC area of nephron affected by Acute Tubular Necrosis (ATN) | Straight Proximal Tubules and the Thick Ascending limb of the Loop of Henle located at the Outer medulla. |
| Muddy Brown casts. Dx? | Acute Tubular Necrosis (ATN) |
| Pathognomic cast seen in ATN? | Muddy Brown Cast |
| ATN shows an increased _________ and ________ but a _______________ _____:_______ ratio. | Cr and BUN levels; NORMAL BUN:Cr ratio. |
| What are the MCC of ATN? | Decreased Renal Perfusion due to severe: 1. Hypoxemia, 2. Shock, 3. Surgery |
| What characteristic is shared by the areas MC affected by ATN? | High ATP-consuming activity |
| The three phases of ATN: | 1. Inciting event 2. Maintenance phase 3. Recovery phase |
| Which ATN phase is considered oliguric, and increases the risk of? | Maintenance phase; lasts 1-3 weeks and increases the risk of developing Hyperkalemia, Metabolic acidosis, and uremia |
| Which is the polyuric phase in ATN? | Recovery phase |
| The recovery phase in ATN is seen with: | Fall of BUN and Cr levels, and increase risk of developing hypokalemia, and increased risk of mineral and electrolyte wasting |
| What are the main to kinds of causes of ATN? | 1. Ischemic (due to decreased renal blood flow) 2. Nephrotoxic (mostly due to drugs/toxic substances) |
| Which areas of nephron anatomy are particularly at higher risk of been affected by Ischemic ATN? | PCT and Ascending Limp of Loop of Henle |
| What area is particularly affected by Nephrotoxic ATN? | Proximal tubule |
| Substances often causing Nephrotoxic ATN? | Aminoglycosides, Radiocontrast agents, lead, cisplatin, ethylene glycol. |
| Myoglobinuria and Hematuria are often causes of: | Nephrotoxic ATN |
| ATN causes which type of Acute Kidney injury? | Intrinsic Renal Failure |
| Urine osmolarity < 350 and Serum BUN:Cr < 15 | Intrinsic Renal Failure |
| BUN:Cr ration in blood > 20 | Prerenal azotemia |
| What is the common level of Urine osmolarity seen in Prerenal Azotemia? | Greater than 500 |
| Which level is the only one consistently observed without variation in Postrenal azotemia? | Urine osmolarity < 350 |
| Order of Tubular fluid/ plasma infiltrate along the distance of Proximal Tubule (Greatest --> lowest concentration) | PAH > Cr> Inulin >>>HCO3 > > Glucose |
| If the [Tubular Fluid]/[Plasma] is equal to 1? <1?>1? | = 1 --> solute and water are REABSORBED at same time. =>1 (greater than 1) --> represents solute secretion and/or solute is reabsorbed less quickly than water =<1 (less than 1) --> solute is reabsorbed quicker than water |
| ARPKD is seen in ______________, while ADPKD is mostly seen in __________________. | Children; Adults |
| What is the clinical presentation of ARPKD? Findings in ultrasound? | Renal insufficiency (oligohydramnios), Nephromegaly, and HTN. The U/S depicts bilateral, enlarged echogenic kidneys. |
| ARPKD patients are often associated with what other condition? | Potter Sequence (flattened face, limb deformities, and Pulmonary hypoplasia) |
| Patient presents with facial features resembling a crushed, flat face, femur, ulnar and radial deformities, and Hx of steroid use as premature baby. Dx? | Potter sequence. (steroids probably given to develop the lungs) |
| Why is ADPKD seen in adults and not in children? | The cysts produced by the Autosomal Dominant version of the disease, are very small, and thus not seen until later in life as they become symptomatic. |
| How do ADPKD cysts become symptomatic? | Compress the renal parenchyma. |
| What chromosomes have the gene involved in ADPKD? | Chromosomes 4 and 16 (PKD-1, and PKD-2, respectively) |
| Which part of the Ureter is irrigated by the Renal Artery? | Proximal part (top area) |
| Variable anastomotic blood supply, provides irrigation to most of the ________ portion of the ureter. | Middle |
| Which artery provides blood supply to the Distal ureter? | Superior Vesical Artery |
| Ureter blood supply: | Renal artery (proximal/top part), Anastomotic (middle section), and Superior Vesical Artery (DIstal/lower/bottom area). |
| Another (larger) artery that supplies the distal section of the ureter, besides the Superior Vesical artery? | Internal Iliac artery |
| Tumor Lysis Syndrome | Occurs in HIGH cell turnover tumor is treated with chemotherapy |
| In Tumor Lysis syndrome, the destruction of cells leads to: | 1. Release of intracellular K+, phosphorus and uric acid. |
| The increased level of uric acid seen in conditions such as Tumor Lysis syndrome, it leads to: | Acidic environment at the Distal Tubules and the collecting tubules, which may be prevented with Allopurinol. |
| What drug is commonly used to ALKALINIZE urine, in conditions such as Tumor Lysis Syndrome? | Allopurinol |
| Tumor Lysis Syndrome is most commonly seen in: | Lymphomas and Leukemias |
| What is the reason of acute kidney injury in Tumor lysis syndrome? | Increase breakdown of nucleic acids, leads to an state of Hyperuricemia, which cause the kidney injury. |
| What are the important blood levels in Tumor lysis syndrome? | Hyperkalemia, Hyperphosphatemia, and HYPOcalcemia |
| What drugs are used to prevent and treat the hyperuricemia seen in Tumor lysis syndrome? | 1. ALLOPURINOL 2. Rubicase 3. Aggressive hydration |
| What factors regulate FF, GFR and RPF? | The AFFERENT or EFFERENT vasoconstriction or vasodilation. |
| What two changes constitute a decrease in GFR? | 1. Constriction of Afferent arteriole and, 2. Dilation of Efferent arteriole |
| Constriction of Efferent arteriole and Dilation of Afferent arteriole cause | Increased GFR, and overall increase in FF. |
| What are the main effects of Theophylline intoxication? | 1. SEIZURES which are treated with Benzodiazepines and Barbiturates 2. Tachyarrhthmias treated with B-blockers |
| Why are benzodiazepines used in a patient that is suffering a Theophylline intoxication? | Theophylline OD provokes SEIZURES which are treated with benzodiazepines such as Clonazepam. |
| Classification of Theophylline | Phosphodiesterase inhibitor |
| Theophylline action in treatment of lung disease/asthma | Causes bronchodilation by increasing cAMP levels |
| Theophylline is similar to ___________________, as it interacts with CYP450 with ___________________ and ______________, in the same way. | Warfarin; Inducers and Inhibitors |
| Theophylline blocks the actions of ____________________. | Adenosine |
| Adenosine actions are blocked or inhibited by ______________, | Phosphodiesterase inhibitor, Theophylline. |
| Possible drug to treat Theophylline-induced arrhythmias? | Propranolol |
| Which sex is more susceptible to developing Pyelonephritis? Why? | Women; Urethra is closer to the rectum, and the urethra is also shorter than male's. |
| What lifestyle choices increase the risk of developing urethritis and cystitis? | Sexual activity |
| Clinical features of Urethritis or cystitis? | Dysuria, frequency, PYURIA, and bacteriuria. |
| What key feature distinguishes cystitis? | Suprapubic tenderness. |
| A person with cystitis may develop Pyelonephritis due to: | The pathogens ascend up to the ureters to penetrate the kidney. |
| What is the clinical presentation of Pyelonephritis? | Flank/abdominal pain, and COSTOVERTEBRAL angle tenderness. |
| WBC casts | PYELONEPHRITIS |
| Precipitate found in the nephron tubules, that precipitate with Tamm-Horsfall protein? | WBC casts (seen in Pyelonephritis) |
| Interstitial nephritis, Papillary necrosis of the medullary vasa recta. These are seen in what condition? | Analgesic Nephropathy |
| Common Osmotic diuretic | Mannitol |
| Mechanism of action of mannitol | Increased osmolality. It leads to extraction of water from the interstitial space into vascular space, leading to diuresis |
| Mannitol common uses? | 1. Treat ICP |
| What is Mannitol most severe side effect? | Pulmonary edema |
| In what patients does Renal osteodystrophy commonly presents? | CKD secondary to Hyperparathyroidism, leadinto to Hyperphosphatemia and Hypocalcemia |
| In which conditions is Mannitol contraindicated? | Patients with anuria or HF |
| Mannitol may be used to reduce ICP and _______________________ | Intraocular pressure |
| Mannitol may cause, as side effect, hypo- and/or hyper______________. | Natremia. (Na+ levels) |
| Failure of Vitamin _____ _______________________ is seen in patients with renal osteodystrophy. | Vitamin D Hydroxylation |
| What condition is seen with subperiosteal thinning of the bones? | Renal Osteodystrophy |
| The increased glomerular membrane permeability seen in MCD, causes __________________________, seen in EM. | Effacement of the PODOCYTES |
| Which properties of the GMB are lost as cause of effacement podocytes in MCD? | Anionic properties |
| What is the ultimate result of Podocyte effacement in MCD? | GMB losses anion properties, leading to the loss of SELECTIVE Albumin |
| Which is the only nephrotic syndrome that is selective of protein loss> | Minimal Change Disease (MCD) |
| With MCH as the exception, all Nephrotic syndromes are ________________________, in respect of protein loss. | Non-Selective |
| 12 yo male complains of swollen legs, red-brown urine, and nearly 21 ago he was treated for Strep infection with penicillin. Dx? | Post-Strep GN (PSGN) |
| BPH is a common cause of which type of urinary involuntary loss? | Overflow incontinence |
| Why are BPH patients often found with higher rates of UTIs? | The higher resistance to urine outflow,lead to residual urine, serving as medium for bacterial growth. |
| Yellow-brown, diamond shape crystals, that are radiolucent on plain X-ray. | Uric acid kidney stones |
| Which conditions favor the precipitation of uric acid kidney stones? | Low urinary pH, Low urine volume, and high uric acid concentration, in the setting of chronic diarrhea |
| Hexagonal kidney stone | Cysteine |
| Mg-NH3-PO3 nephrolithiasis | Enveloped-shaped crystal |
| Which kidney stones required acidic environment? | Calcium-oxalate stones, Uric Acid stone, and Cysteine Stones |
| What is the general clinical manifestation of kidney stones on a patient? | 1. Unilateral flank tenderness 2. Colicky pain radiating to groin 3. Hematuria |
| Which kidney stones require an alkalotic environment to precipitate? | Calcium-Phosphate stones and Ammonium-Nitrate-Phosphate stones. |
| All kidney stones are _________________________, except for ______ which is _____________________, in X-ray view. | RadioPAQUE; Cysteine is RadioLUCENT in x-ray view. |
| Which kidneys stones are wedge-shaped prism? | Calcium-Phosphate |
| Coffin-like shaped kidney stone? | Mg-NH3-PO3 stone |
| Ethylene glycol (antifreeze) ingestion, Vitamin C abuse, hypocitraturia, Crohn's disease | Common disorder that present Calcium-Phosphate kidney stones |
| What is the treatment of Calcium kidney stones? | Thiazides, citrate, and low sodium diet |
| The organisms involved in Mg-NH3-PO3 stone formation, cause the __________________ of urine. | ALKALIZATION |
| Hydrolyze urea to ammonia | Action seen in Urease positive organisms causing the Alkalization of urine in Struvite formation |
| What 3 common urease + organisms cause Mg-NH3-PO3 kidney stones? | Proteus mirabilis, Staph saprophyticus, and Klebsiella. |
| What conditions predispose uric acid kidney stone formation? | Strongly associated to hyperuricemia (Gout) and to leukemias with high cell turnover |
| Treatment of Uric acid nephrolithiasis | Alkalization of urine and ALLOPURINOL |
| Defective Cysteine-transporter in PCT cells leads to ______________, leading to greater chances of developing ______________ kidney stones. | Cystinuria; Cysteine |
| Sodium cyanide nitroprusside + test | Cysteine kidney stones |
| The hereditary condition leading to cysteine kidney stones, due to defective Cysteine-transporter in PCT , also lead to poor absorption of which amino acids? | COLA (Cysteine, Ornithine, Lysine, Arginine) |
| Which is the most common type of renal cell cancer? | Clear cell carcinoma |
| Where is the most common site to find clear cell carcinoma? | Epithelial cells of the Proximal renal tubules. |
| Clear cell carcinoma is derived from _________________ cells. | Epithelial cells of the Proximal renal tubules. |
| Gross-examination of affected tissue shows a sphere-like mass made of GOLDEN-YELLOW cells, with high-lipid content, and areas of necrosis and hemorrhage. | Clear Cell renal carcinoma |
| MC sites of metastasis of renal cell carcinoma | Lungs and Bone due to hematogenous spread |
| Renal cell carcinoma is associated with which AD condition? | von Hippel Lindau Syndrome, due to chromosome 3 mutation |
| Which gene and on what chromosome is mutated n VHL? | VHL gene on chromosome 3 |
| Which paraneoplastic syndromes are associated with RCC? | PEAR : PTHrP, Ectopic EPO, and ACTH, and Renin |
| PEAR | Mnemonic of paraneoplastic syndromes associated with RCC |
| PTHrP, Ectopic EPO, ACTH, and Renin paraneoplastic syndromes | PEAR; associated with RCC |
| What is the most common Primary renal malignancy? | Renal cell carcinoma (RCC) |
| Resistant to chemotherapy and radiation | Renal cell carcinoma (RCC) |
| Malignancy commonly seen with flank pain, painless hematuria, SECONDARY POLYCYTHEMIA, and palpable abdominal mass? | Renal cell carcinoma (RCC) |
| Filtration rate equation | Filtration rate of Sub X = (Inulin clearance * (Plasma [X]) |
| Filtration rate of X minus Tubular reabsorption of Sub X | Net Excretion of Sub X |
| What renal condition is associated with the use of antibiotics such as B-lactams, sulfonamides, adn rifampin, and others such as PPIs, NSAIDS, and diuretics? | Acute Interstitial Nephritis |
| Patient recently started with a 3rd generation cephalosporin, visits doctor's office due to new rash and fever. Dx? | Acute Interstitial Nephritis |
| Another name or denomination for Acute Interstitial nephritis? | Tubulointerstitial Nephritis |
| What is a common sign of Tubulointerstitial nephritis? | PYURIA with administration of new drug |
| WBC casts + Pyuria + Hematuria + New Drug | Acute Interstitial Nephritis |
| What is likely to be found in urine examination of a patient with acute Interstitial nephritis? | Eosinophilia and urinary eosinophils |
| Osmotic diuretic | Mannitol |
| Acetazolamide | Carbonic anhydrase inhibitor |
| Alkalinizes urine (diuretic) | Acetazolamide |
| Treatment of Altitude sickness | Acetazolamide |
| Furosemide, Butamide and Torsemide | Sulfonamide Loop diuretics |
| Non-sulfonamide Loop diuretic? | Ethacrynic acid |
| Side effects of Loop diuretics | Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), metabolic Alkalosis, Nephritis (interstitial), Gout |
| Which type of Loop diuretic is more ototoxic? | Non-sulfonamide Loop diuretic |
| Loop diuretics increase the loss of what ion? | Calcium |
| Which are the most common Thiazide diuretics? | Hydrochlorothiazide, chlorthalidone, and metolazone |
| Side effects seen in HCTZ? | HypoKalemic Metabolic Alkalosis, Hyponatremia + Hyper: Glycemia, Lipidemia, Uricemia, Calcemia |
| HyperGLUC? | Mnemonic used to indicate the elevated levels of glycine, Lipids, Uric acid, and Calcium seen in Thiazide diuretics side effects |
| Which labs are decreased in Thiazide side effects? | Hypokalemia and Hyponatremia |
| The Thiazides ___________________ calcium ______________. | Decreased Ca excretion |
| Gout like effects are often seen in which type of diuretics? | Thiazides and Loop diuretics |
| Which K-sparing diuretics are competitive antagonists of Aldosterone? | Spironolactone and Eplerenone |
| Which K-sparing diuretics block the Na+ channels? | Triamterene and amiloride |
| Spironolactone is an ________________________________________. | Competitive Aldosterone Antagonist |
| K+-sparing diuretics work more at the _______________________ ___________________ tubule. | CORTICAL COLLECTING tubule |
| Hyperaldosteronism, HF, K-depletion, hepatic ascites, and antiandrogenic | Clinical uses of K+ sparing diuretics |
| Which Potassium sparing diuretic is specifically used in management of Nephrogenic DI? | Amiloride |
| NaCl in urine increases with? | In the use of diuretics |
| Which type of diuretics increase Urinary K+ the most? | Loop and Thiazide |
| Which diuretics cause Acidemia? | Carbonic anhydrase inhibitors and K-Sparing diuretics |
| Which pair of diuretics cause Alkalemia? | Loop and Thiazide |
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rakomi
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