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Renal 2
Clinical Medicine: Renal Part 2
| Term | Definition |
|---|---|
| Diabetic nephropathy: Definition | A microvascular complication of diabetes marked by albuminuria and a deteriorating course from normal renal function to ESRD. |
| Leading cause of ESRD (end stage renal disease) in US? How much of the ESRD percentage has it? | Diabetic nephropathy; accounts for 1/3 of patients w/ ESRD. |
| T/F: 30% of individuals progress to macroalbuminuria from microalbuminuria over the next 10 years in Type 1 diabetics | False, 50% of individuals will |
| T/F: steady decline in GFR once macroalbuminuria is present and 50% will reach ESRD within 10 years in Type 1 diabetics | True |
| 4 differences from Type 2 diabetic nephropathy from type 1 | 1) microalbuminuria or macroalbuminuria may be present when DM2 Dx...reflecting long asymptomatic period. 2) HTN more commonly accompanies these. 3) Microalbuminuria less predictive. 4) Albuminuria may be 2ndary to factors unrelated to DM2 (HTN, CHF) |
| 8 risk factors for diabetic nephropathy | 1) Age 2) Race 3) Ethnicity 4) Hx of microalbuminuria 5) HTN 6) Poor glycemic control 7) Smoking 8) FHx of nephropathy |
| Microalbuminuria: Definition | manifestation of diffuse endothelial cell injury (marker for HTN progress, CVD, CKD). |
| 3 things we can understand from microalbuminuria | 1) Glomerular damage 2) endothelial damage system wide 3) increased risk for CV events |
| Extremely important physical exam to do when suspecting diabetic nephropathy? | Fundoscopy. Diabetes that is advanced enough to effect the vasculature of the kidney almost always has affected the vasculature of the retina. Look for retina plaques. |
| What type of arteriosclerosis is almost pathognmonic for diabetes | Efferent; Efferent arteriolosclerosis is rarely, if ever, encountered in individuals who do not have diabetes. |
| 5 steps of pathogenesis in hyperglycemia in diabetic nephropathy | 1) induce mesangial expansion and injury 2) increased activity of growth factors 3) activation of cytokines 4) Formation of reactive oxygen species (ROS) 5) accumulation of advanced glycosylation endproducts in tissues |
| What test would identify this process in diabetes: Sugars + Proteins -> alter configuration (crosslinked) of protein (advanced glycosylation endproducts or A.G.E.) -> loss of elasticity | A1c |
| A.G.E.s (Advanced Glycosylation Endproducts) contribute to some of the following diseases: (9) | 1) HF, 2) atheroscleorisis, 3) systolic HTN, 4) diabetic nephropathy, 5) ED, 6) non-obstructive uropathy, 7) diabetic retinopathy, 8) diabetic neuropathy, 9) ESRD |
| 3 initial screening tools for diabetic nephropathy | 1) spot urine albumin: creatinine ratio 2) 24 hour urine collection for albumin 3) Dipstick: semi-quantitative (checking for microalbumin) |
| Hard Dx and inferred Dx for diabetic nephropathy | Hard: renal Bx if diabetic w/bland urine or rampant onset. Inferred: Hx of DM for 7-10 years, diabetic retinopathy, macroscopic proteinuria |
| Diabetic Nephropathy: Management (4) | 1) Glycemic control 2) HTN control (JNC VIII recommended <140/90 mmHg) 3) ACEI or ARB 4) Lipid management |
| DCCT: Outcome | Intensive glycemic control therapy vs conventional therapy reduced microalbuminuria and albuminuria by 39 and 54% respectively. Early control gave lasting and significant benefit even after 9 years that was never matched again by conventional therapy. |
| RENAAL: Primary/Secondary endpoints, Results | primary: endpoints of time to first baseline 2x of creatinine, ESRD, Death. 2ndary: CV events, progression of renal disease, changers in proteinuria; Results: ARB had significant results in lowering all but death |
| Polycystic Kidney Disease: 2 genetic possibilities | 1) ARPKD: autosomal recessive polycysitic kidney disease (rare) 2) ADPKD: autosomal dominant polycystic kidney disease (more common) |
| What extra-renal problem occurs in 80% of autosomal dominant polycystic kidney disease? | Liver cysts |
| Polycystic Kidney Disease: Hx, Sx, Imaging, Criteria for Dx | Hx: (+) FH; Sx: frequently ASx, HTN, flank pain, gross hematuria; Imaging: Ultrasound Dx; Dx: 1) at least 2 unilateral or bilateral cysts in <30yo. 2) at least 2 cysts in each kidney if 30-59. 3) at least 4 cysts in each kidney in >60 |
| Polycystic Kidney Disease: Management and Causes of death (2 and 3 respectively) | Tx: 1) ACEI 2) screen for occult cerebral aneurysm (MRA recommended routinely for: pts w/FH of CVA, new onset/SEVEr HA; CoD: 1) Heart disease 2) Infx 3) Neurologic event; NEVER renal cancer |
| Tx when progressed to ESRD (2) | 1) Transplantation 2) Hemodialysis |
| Acute pyelonephritis: 2 causes (which more common); commonly comorbid in (3); Sx | Causes: 1) Ascending infx due to vesicoureteral reflux into renal pelvis (more common) 2) Hematogenous seeding due to septicemia; Comorbid: 1) immunocompromise 2) incompetent ureteral valves 3) diabetes. Sx: Flank pain, fever, dysuria, pyria, bacteriuria |
| Tubulointerstitial Disease: Definition, Primary, Secondary | Inflammation or fibrosis of renal interstitum and atrophy of tubular compartment. 2ndary: consequences of disease that target glomeruli or vasculature (can overlap chronicially). Primary: disorders primarily affect tubules & interstitium sparing glomeruli |
| Acute Tubulointerstitial Disease: Association, Example, Definition, What are in the blood? | Most often associated w/ acute kidney injury. Ex: interstitial nephritis. Inflammatory infiltrates lead to edema, tubular cell injury and compromised flow, or by obstruction by renal debris. Eosinophils in blood or urine, usually after sulfas. |
| Chronic Tubulointerstitial Disease: Features (2) | Indolent features; Tubular dysfns including: polyuria (increased urine, ex: nephorgenic diabetes inspidus), defective proximal tubular reabsorption (ex: Fanconi Syndrome) |
| Chronic Tubulointerstitial Disease: Manifestation (4) | 1) non-anion gap metabolic acidosis/hyperkalemia 2) progressive azotemia (rising BUN/Creatinine) 3) modest proteinuria 4) renal U/S may reveal changes |
| Chronic Tubulointerstital Disease: Pathology, Bx?, How to get Dx (4) | interstitial fibrosis w/ patchy mononuclear cell infiltration and widesperad tubular atrophy, luminal dilation, thickening of basement membranes. Bx rarely provides specific Dx. Dx: Hx, drug/toxin exposure, Sx, imaging. |
| Chronic Tubulointerstital Disease: Etiology (4) | 1) Vesiculouretal reflux 2) Sickle Cell 3) Medications/Toxins: analgesic nephropathy, lead, heavy metals 4) Metabolic: hypercalcemia, hyperuricemia |
| Chronic Reflux Nephropathy: 2 forms, important cause of: | Chronic tubulointerstitial inflammation w/ renal scarring; important cause of ESRD; 2 forms: reflux-associated (more common) and obstructive. Eventually causes dilated, blunted, deformed calyx. |
| Chronic Reflux Nephropathy: Microscopic changes (2), Clinical changes (4) | Micro: 1) Tubules and interstitium show atrophy and hypertrophy 2) thyroidization (looks more like thyroid gland on Bx than kidney. Clincial: Recurrent Infxs, tubular dysfn, HTN, CRF |
| Sickle Cell Nephropathy: Pathogenesis, Sequelae, Sx, Tx | occlusion of vasa recta in renal medulla. Sequelae: hyposthenuria, hematuria, papillary necrosis. CKD present in 12-20%. Sx: proteinuria present in 20-30% (nephrotic range asso. w/ renal failure). Tx: ACEI reduce proteinuria. SCD-> INTERSTITIAL DZ |
| Analgesic Nephropathy: Definition, Characteristics, Sx | results from long-term use of phenacetin (banned now), aspirin, caffeine. C: renal insufficiency, papillary necrosis. Sx: small, scarred kidneys w/papillary calcifications, polyuria, non-anion gap metabolic acidosis from tubular damage, hematuria, colic. |
| Multiple Myeloma: Definition, Etiology/Prognosis, Sx | Plasmacytoma: tumor composed of mature and immature plasma cells. Older pts and grave prognosis.. Sx: Lytic bone lesions, circulating monoclonal immunoglobulins, pathological fractures. Tubulointerstitum is common target. Renal insufficiency in 1/2 pts |
| Multiple Myeloma: Factors contributing to renal damage (4) | 1) Bence Jones proteinuria and cast nephropathy 2) Amyloidosis 3) Light-chain deposition disease ( 4) Hypercalcemia/hyperuricemia (increased Sed rate) |
| Thrombotic Microangiopathy: Definition, Sx, Syndrome includes: | microangiopathic hemolytic anemia and thrombocytopenia in absence of another cause. Sx: fever, neuro abnormalities, renal insufficiency, bland U/A, not nephritic, low platelet count "chewed up RBCs". Includes: TTP, Hemolytic uremic syndrome. |
| Hemolytic-uremic syndrome: Triad of clinical manifestations; Pathogenesis in pediatric patients | 1) microangiopathic hemolytic anemia 2) thrombocytopenia 3) acute nephropathy 90% of peds cases due to E.coli |
| Thrombotic Thrombocytopenic Purpura (TTP): Pentad of manifestations; Etiology: | 1) microangiopathic hemolytic anemia 2) thrombocytopenia 3) acute nephropathy 4) neurologic involvement 5) fever; systemic complaints: E: Idiopathic: autoantibodies against ADAMTS-13 molcule and accumulation of ultra-large von-Willebrand factors. |
| Microangiopathic Anemia: Peripheral Blood Smear (5) | 1) red cell fragmentation 2) platelet number reduced 3) thrombocytopenia 4) schistocytes 5) reticulocytes |
| Neurologic Sx that can occur patients w/ thrombotic microangiopathy (5) | 1) confusion 2) severe HA 3) focal objective abnormalities (TIAs), 4) grand mal seizures 5) coma |
| Cardiac involvement w/ thrombotic microangiopathy (5) | 1) diffuse platelet thrombi and hemorrhage in cardiac tissues 2) arrhythmias, 3) sudden cardiac death, 4) MI, 5) shock HF |
| TTP: Causes and Tx | Top 4: Idiopathic, drug associated, autoimmune, infection. Tx: immediate admin of plasma exchange (Platelet transfusions CONTRA) |
| Tumor Lysis Syndrome: Metabolic abnormalities, Sx | MA: hyperkalemia, hyperphosphatemia, HYPOcalcemia, hyperuricemia, uric acid/calcium phosphate crystals -> AKI. Sx: N/V/D, anorexia, lethargy, hematuria, HF, dysrhythmias etc. |
| Tumor Lysis Syndrome: Higher risks (5), Clinical features predisposing (4) | HR: high tumor cell proliferation rate, chemosensitivity of malginancy, large tumor burden (lymphomas), LDH pretreatment 2x normal limit, organ infiltration/marrow involvement. CF: preTx hyperuricemia, preexisting nephropathy, oliguria, dehydration |
| T/F: There are certain illnesses that can be diagnosed off of a blood pressure alone | False: HTN only indicates vascular ill health. Indicates a "gateway to investigate vascular system for a cause" |
| T/F: JNC 8 only used outcome studies. No surrogate marker studies. | True! (It's the way to go anyway) |
| T/F: Being 120/80 on 3 anti-hypertensives is almost equivalent to being 120/80 with no other complications and living a healthy lifestyle. | False, sadly no. These are NOT the same. |
| JNC 8: general population 60 yo or older to initiate pharmacologic Tx for BP? What grade? | <150/90; Grade A |
| JNC 8: general population YOUNGER than 60 yo to initiate pharmacologic Tx for BP. Grade? (there are 2 here) | Diastolic <90; Grade A and Systolic <140; Grade E |
| JNC 8: CKD population 18 yo or older to initiate pharmacologic Tx for BP. | <140/90 |
| JNC 8: Diabetes population 18 yo or order to initiate pharmacologic Tx for BP. What Tx (for non-black)? (4) | <140/90; 1) Thiazide diuretic 2) CCB 3) ACEI 4) ARB |
| JNC 8: black population INCLUDING those w/diabetes Tx (no CKD) (2) | 1) Thiazide diuretic 2) CCB |
| JNC 8: Tx for 18 yo+ w/ CKD. Who else does this apply to? | 1) ACEI or ARB; This applies to EVERYONE regardless of race, or diabetes status. Trumps all! |
| What did the ONTARGET study show? | No benefit to combining an ACEI and an ARB, and there are more adverse effects. |
| What were a couple of main things not included in JNC 8? (2 main ones) | 1) No definition of prehypertension or hypertension 2) Compelling indications: CHF, previous CVA, high CAD risk, post-MI (we are to defer to respective appropriate guidelines) 3) |
| What did the ALLHAT study show? | Multiple anti-hypertensive agents are needed to achieve target BP in high risk patients. |
| What does systolic BP have to be to autoregulate? 3 ways modulation of afferent and efferent arteriole tone can autoregulate GFR. | 80-180; 1) Myogenic reflex in afferent arteriole (acute renal perfusion evokes constriction or dilation) 2) Tubuloglomerular feedback (increased solute delivery leads to afferent constriction) 3) angiotensin II mediated vasoconstriction of arteriole |
| Normal Renal Physiology: Increase in BP; Decrease in BP; Is this a local or systemic mechanism? | Increase: afferent constricts preventing increase in blood flow and GFR, efferent dilates. Decrease: afferent dilates increasing blood flow and GFR and efferent constricts to help build pressure in glomerulus. LOCAL MECHANISM |
| What are some intrarenal autoregulation vasodilators? Vasoconstrictors? | Dilators: prostaglandins, kinins, Nitrous oxide, atrial natriuretic peptide. Constrictors: Renin, Angiotensin II, endothelin, anti-diuretic hormone |
| What is the final common pathway regardless of source of initial injury (glomerular or tubulointerstitial) of kidney disease. | Progressive renal disease; Critical amount of primary nephron loss produces maladaptive deterioration of remaining nephrons due to hyperfiltration of initially non-damaged nephrons leading to damage here. |
| Pathogenesis of Progressive Renal Disease (6 steps) | persistent glomerular injury -> protein leak into tubular fluid -> local HTN in capillary tufts -> increasing local production of angiotensin II -> cytokine bath (macrophages and T lymphocytes) -> accumulation of interstitial mononuclear cells (nephritis) |
| What is the most general problem about angiotensin II in chronic renal disease? | It is a vicious cycle |
| Pathophysiology of HTN and Renal Parenchymal Disease (3) | 1) Cardiac output normal or elevated 2) Expanded extra-cellular volume, impairing Na secretion. 3) Elevated systemic vascular resistance, increasing adrenergic tone, activating RAAS system among others |
| Hypertensive nephrosclerosis | Caused by sustained HTN, Hyaline arteriolarsclerosis occurs where small arteries/arterioles become thickened and scarred. Eventually insufficiency and failure if HTN becomes moderate |
| Malignant nephrosclerosis: what is it? what does it cause? (7) | Rapid progressive BP elevations accelerated nephrosclerosis. Affects heart, brain, kidneys (causes hypertensive emergencies). Causes papilledema, encephalopathy, CV abnormalities, renal failure, hemolysis, fibrinoid necrosis, smooth muscle proliferation |
| Malignant nephrosclerosis: Pathogenesis | most start with chronic HTN, rate of rise more important than absolute rise; degree of target organ damage rather than BP determines how fast BP should be lowered. If not catastrophic, lower w/in hours not minutes |
| Initial therapeutic reduction goal for hypertensive encephalopathy | No more than 25% BP reduction w/in minutes to 2 hours |
| T/F: Hypertension and proteinuria are both dependant variables that predict long term decline in renal function? T/F: Renal disease is both a cause and a consequence of HTN | False, both independent variables; True, reducing BP lowers CV and renal risk. |
| Proteinuria associated with risks of what two disease? | 1) Progressive kidney disease 2) Cardiovascular disease |
| What did the REIN CORE study show? | ACEI reduced proteinuria and ESRD rates (renoprotective; barely touched BP |
| T/F: Worse renal function had greatest improvement with ACEI | True! |
| What did the MICRO-HOPE trial show in patients w/ DM? | Those taking 10 mg of ramipril had SIGNIFICANT reductions of stroke, MI, CV mortality, nephropathy |
| What did the RENAAL trial show in patients w/ DM? | Same thing as MICRO-HOPE study...all reductions in ESRD, creatinine doubling rates, death from ESRD. |
| What did AASK study show? | Significant reduction in poor outcomes with ramipril in African Americans |
| ESRD in ALLHAT studies with diabetes? | Minimal difference in the way AAs with diabetes were treated between ACEI and CCBs when looking for renal protection. CCBs preferred. |
| Renal artery stenosis can lead to a reduction in perfusion pressure that: (3). What do those 3 events lead to? | 1) activates RAAS system 2) reduces Na excretion 3) activates SNS adrenergic pathways. These 3 events lead to angiotensin dependence in early stages, loss of circadian BP rhythms (will stay elevated at night), accelerated target organ injury (3) |
| Renal Artery Stenosis: Etiology, Clinical Findings, Work up | Et: Atherosclerotic ischemic renal disease (80-90%) or Fibromuscular dysplasia (10-15%). CF: Refractory/new onset HTN, flash pulmonary edema, acute kidney fn reduction w/ ACEI, abdominal bruit, unequal sizes of kidneys. WU: U/A -> U/S |
| Patients with ischemic renal disease who reach ESRD do poorly: (hint: regarding mortality) | have the highest mortality rate among all etiologies of ESRD |
| Ischemic Renal Disease: Pathophysiology (3) | Reversible adaptive changes: structural renal atrophy diminished cortical blood flow, reduction in GFR to decrease O2 demand; hypertorphy of contralateral kidney; hyperinflation occurs in functional nephrons of non-effective kidneys |
| What 3 disease does ischemic renal disease include? | 1) HTN 2) CKD 3) Renal Artery Stenosis |
| T/F: Renal angiography is the gold standard and should be performed on every patient. | False, while angiography is the gold standard, Doppler ultrasonography is highly sensitive and specific and is a more efficient. |
| Ischemic Renal Disease: Management | Controversial, Medical management vs angioplasty +/- stenting vs surgery. Angioplasty may be curative in fibromuscular dysplasia. No seperation or benefit of stenting vs medical Tx in studies. |
| Renal Artery Stenosis: Tx (6) | 1) RAAS blockade w/ caution (ACEI/ARBs) 2) BP control 3) Statin therapy 4) Aspirin 5) Cessation of smoking 6) Factors that favor revascularization (a) progressive decline in GFR b) failure to achieve BP control c) deterioration of GFR w/ACEI d) CHF |
| Renal Vein Thrombosis: Clinical Features; Imaging, Tx | insidious onset and produces no Sx referable to kidney (acute presentation may be ASx), pulmonary embolus main clue. Imaging: CT Angiography most sensitive, but U/S used for screening. Tx: anti-coag initially w/ heparin then warfarin. |
| 2 categories of metabolic acidosis and their sub-categories and topics | 1) High anion gap a) lactic acidosis b) diabetic ketoacidosis c) alcoholic ketoacidosis d) CKD e) toxins; 2) Normal anion gap: a) diarrhea b) renal tubular acidosis |
| What should systemic arterial pH be maintained at? | 7.35-7.45 |
| What system regulates pCO2? HCO3? | Respiratory, Renal |
| T/F: Kidneys must excrete acid in amount equivalent to production of nonvolatile acids | True |
| Nonvolatile: Definition | acid in body from sources other than CO2 and therefore NOT excreted by lungs |
| What is matched by the reabsorption of HCO3 (bicarbonate)? | secretion of H+ (hydrogen) ions |
| What happens when there is a loss of bicarbonate in the urine? | Lead to acidosis |
| T/F: secretion of H+ ion in the proximal tubule is dependent on the ATP-driven proton pump. | True, H+ secretion in the proximal tubule is driven by an antiport in exchange for Na+ active transport by Na+. |
| What are the two variables of pH? | 1) Bicarbonate 2) arterial pCO2 |
| What is the primary abnormality in respiratory function in respiratory acidosis? Alkalosis? | Acidosis: hypoventilation Alkalosis: hyperventilation |
| What is the compensatory response to metabolic acidosis? Does respiratory or metabolic compensation happen faster? | Compensatory response for metabolic acidosis is respiratory hyperventilation. Respiratory compensation mechanisms provide a faster response to pH (a few hours vs a few days) |
| What are Kussmaul respirations? | Deep and labored breathing -> increased tidal volume in response to acidosis. |
| Name a common mixed acid base disorder and what is occurring within it? | Salicylate intoxication a possibility. A lower than expected pCO2 is seen in response in someone with metabolic acidosis suggesting respiratory alkalosis on top of the metabolic acidosis. Suggests over-compensation of hyperventilation. |
| What is an anion? | negatively charged electrolyte |
| How is an anion gap calculated and what is the normal? The lower the HCO3, the _______ the anion gap? How does a normal anion gap occur? | AG= Na-(Cl+HCO3); normal= 10-12 mmol/L; Lower HCO3, greater the anion gap; Normal anion gap occurs as the fall in HCO3 is offset by an increase Cl. Either way, Bicarb drops which is causing the metabolic acidosis in the first place. |
| What are the 4 main categories of Increased Anion Gap Acidosis? | 1) Lactic acidosis 2) Ketoacidosis 3) Renal failure 4) Toxins |
| Lactic Acidosis: 2 Types, Which is more severe? What is included in each? | Type A: poor tissue perfusion (causes increase production of lactic acid); circulatory insufficiency, severe anemia, sepsis all causes. Most severe. Type B: aerobic disorders: malignancies, thiamine deficiency due to alcoholism, hepatic failure, metformin |
| Diabetic Ketoacidosis: What is it? Sx, Dx | Increased fatty acid metabolism and accumulation of ketoacids. Presence of Type 1 insulin insufficiency. Sx: hyperglycemia, volume depletion, Dx: Hx and (+) urine ketone test (acetoacetate) |
| Alcoholic Ketoacidosis: What is it, Dx, Sx | abrupt cessation of alcohol consumption combined with poor nutrition. (-) urine ketone test b/c only tests for acetoacetate but (+) serum Beta-hydroxybutyrate. Sx: hypophosphatemia, hypomagnesemia, hypokalemia, volume depleted |
| Toxins Name two other than the mixed | Salicylate intoxication: mixed respiratory alkalosis and high AG metabolic acidosis and lactic acid levels. Alcohols: ethylene glycol (oxalate crystals in urine) and menthanol (optic/CNS damage). High AG acidosis and osmolar gap |
| Stage 4/5 renal failure leading to high AG metabolic acidosis | progresses from hyperchloremic acidosis of moderate renal insufficiency. Distinct from RTA (renal tubular acidosis). Reduced rate of NH4 production/excretion. Acid buffered by bone salts ->significant loss of bone mass due to reduction of calcium. |
| Normal Anion Gap Acidosis: Extrarenal possiblity? | 1) GI loss: small bowel/pancreatic secretions contain large amounts of bicarb, so massive diarrhea and volume loss -> acidosis. Hyperchloremia: secretion of bicarb in exchange for Cl by counter-transport. |
| Normal Anion Gap Acidosis: Intrarenal acidosis | RTA (renal tubular acidosis): Hyperchloremic acidosis with a normal anion gap, near normal GFR in the absence of diarrhea |
| Methanol toxicity: | severe optic nerve damage and CNS damage |
| What cause a negative urinary anion gap? When do you use a urinary anion gap? What kidney ability is reflected in urinary anion gap? Why would it be low or high? | A high urine Cl; Use once serum anion gap comes back normal. NH4+ excretion. Would be low due to renal tubular acidosis (RTA); would be high due to diarrhea. |
| What would cause a negative urinary anion gap? Positive urinary anion gap? | Negative: GI with diarrhea. NH4Cl renal excretion (increased urinary Cl). Positive: Distal renal tubular acidosis where there is an inability to excrete H+ as NH4Cl (decreased urinary Cl) |
| RTA Type 1: What occurs and Sx | selective deficiency in H+ secretion in in collecting tubule. Despite acidosis, urine cannot be acidified (pH>5.5). Urinary anion gap POSITIVE. Causes HYPOkalemia. Can cause nephrocalcinosis and nephrolithiasis due hypercalciuria. |
| A few highlighted things that cause RTA Type 1 | Idiopathic, familial, autoimmune (SLE, Sjogren's), hereditary hypercalciuria, Amphotericin B, chronic hepatitis. |
| RTA Type 2: What occurs and Sx | selective deficiency in proximal tubules ability to reabsorb filtered bicarb. Distal delivery of bicarb declines as plasma bicarb decreases (Urinary anion gap POSITIVE). Cause HYPOkalemia. |
| Causes of Type 2 RTA | Idiopathic, familial, FANCONI'S SYNDROME (which is a generalized proximal tubule dysfn (doesn't matter how or why). In blood: hypophosphatemia, hypouricosuria. Can be acquired by MM, Acetazolamide, heavy metal poisonings, amyloidosis. |
| Of the 3 types of renal tubular acidosis, which is the most common in clinical practice? | Type 4 RTA |
| RTA Type 4: What occurs and Sx | Caused by an aldosterone deficiency (like Addisons) or distal tubule resistance to aldosterone. Impaired Na/K/H+ cation exchange. Decrease H and K secretion (plasma buildup) along with Na wasting (so HYPERkalemia and pH <5.5). |
| Causes of Type 4 RTA: 3 general categories | 1) Decrease renin due to diabetic nephropathy, NSAIDs, interstitial nephritis. 2) Normal renin but reduced aldosterone due to ACEI/ARBs, heparin. 3) Reduced response to aldosterone due to: K+ sparing drugs (Sprinolactone, septra) or sickle cell, SLE etc. |
| 5 Tx of Type 4 RTA | 1) dietary restriction of Na 2) avoid K+ retaining drugs 3) K+ restricted diet 4) Furosemide 5) oral alkali supplementation |
| Mainstay treatment of RTA | Bicarbonate therapy |
| Respiratory Acidosis: Problem, Etiology, Acute, Chronic | increase pCO2 and decrease pH. E: HypoTn due to pulm disease, resp. muscle disease, and abn vent control due to meds. Acute: immediate increase in HCO3 (1mmol/L for 10mmHg) Chronic: additional HCO3 increase (4mmol/L for 10mmHg) |
| What can occur with a rapid increase in PaCO2? Chronically? | Acutely: anxiety, dyspnea, confusion, psychosis, hallucinations -> -> coma. Chronically: sleep disturbances, loss of memory, daytime somnolence etc. |
| T/F: Hypoxia is driving respiratory center and removal of stimulus may aggravate hypoventilation. | True. In other words, don't give lots of O2 quickly...Too quick a correction will cut off respiratory center completely. |
| Metabolic Alkalosis | Elevated arterial pH, increase serum HCO3 and increase PCO2 due to compensatory alveolar hypoventilation. Hypochloremia and hypokalemia often accompany. Etiology: Some will respond to saline, other won't. |
| Metabolic Alkalosis: Saline responsive | Extracellular volume contraction due to vomiting, NG suction. Normotensive, postural HypoTN. With gastric acid losses come: HCl loss initiates and Cl loss maintains alkalosis. Tx: Correct IV volume. |
| Chloride depletion alkalosis: | Most common (90% of clinical cases). Cl and HCO3 are mostly only anions present in ECF: decrease in one leads to increase in the other. Causes: gastric acid loss, eneteric Cl loss (villous adenoma), diuretic use. Tx: volume with Cl required to correct thi |
| Metabolic Alkalosis: Saline unresponsive | Hypokalemic, normovolemic. Causes: Chronic K depletion, NH4 production and absorption are enhanced -> HCO3 reabsorption stimulated. Tx: Repair of K deficiency corrects alkalosis. Hyperaldosteronism: increased distal Na reabsorption, increases H and K loss |
| Respiratory Alkalosis: Etiological Factors | EF: Hyperventilation leading to hypocapnia and electrolyte shifts, compensation mechanism for metabolic acidosis, impaired gas exchange including vent/perf imbalance due to PE or pulm edema, anxiety, fever, hypoxemia increasing RR. |
| Respiratory Alkalosis: Clinical Findings | Blood pH increased, measured PaCO2 decreased (less H leaving due to compensatory hypoventilation), Sx: N/V, paresthesias due to hypophosphatemia, carpal-pedal spasms due to hypocalcemia. |
| Chronic vs Acute Respiratory Acidosis causes | C: neuromuscular diseases (myasthenia gravis etc.), kyphoscloliosis, COPD. A: Depression of central respiratory center (encephalitis/trauma) or drugs; airway obstruction related to acute exacerbations of asthma/pnumonia. |
| Chronic vs Acute Respiratory Alkalosis causes | C: Pregnancy, hyperthyroidism, hepatic failure, PE; A: Pain, anxiety, fever, stroke, meningitis, trauma, severe anemia, salicylate toxicity, pneumonia, pulmonary edema, PE, aspiration, CHF, sepsis |
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crward88
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