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Kidney Lect 14
Pathology of Vascular and Tubulointersitial Diseases
| Question | Answer |
|---|---|
| The tubules get their blood supply through the ... | peritubular capillary plexus and vasa recta, these blood vessels arise from the efferent arteriole as it leaves the glomeruli Any disease affecting glomerular capillaries will cause tubular ischemia and tubular necrosis or cell death. |
| Renal vascular diseases most commonly part of ... | systemic disease; some isolated to kidney vasculature, but these are less frequent |
| What vascular diseases affect vessel lumen? | thrombosis, emboli |
| What vascular diseases affect vessel wall? | vasculitis, hypertension |
| What vascular diseases affect tubular epithelial cells? | drugs, toxins |
| What vascular diseases affect interstitium? | inflammation, infection |
| What is the most common cause of renal failure in older adults? How is diagnosed? | Hypertension; persistent diastolic BP>95 mmHg |
| What are the two types of hypertension (in terms of prognosis)? What sets them apart? | Benign (chronic, long standing; 'silent killer'); malignant (male>female, <40 yoa, African Americans>whites; presents with severe headache, retinopathy, acute and chronic renal failure; diastolic BP usually > 115 mmHg) |
| What is the difference between primary and secondary hypertension? | primary: usually idiopathic in 95% of cases. secondary: can be attributed to renal, endocrine, or vascular causes |
| What are some renal causes of secondary hypertension? | acute glomerulonephritis, chronic glomerulonephritis, renal artery Stenos is, vasculitis…etc |
| Endocrine causes of secondary hypertension | mostly due to adrenocortical hyperfunction..etc. |
| Vascular diseases that lead to secondary hypertension | mostly due to atherosclerosis, renal vascular stenosis…etc. |
| Benign Nephrosclerosis pathology | affects medium and small size arteries, sparing the capillaries. Microscopically we see arteriolar hyaline sclerosis, thickening and arterial Fibroelastic intimal hyperplasia |
| Malignant Nephrosclerosis pathology | affects all the blood vessels of the kidneys including the glomerular capillaries. Microscopically, we see arteriolar fibrinoid necrosis, glomerular capillary necrosis, crescent and arteriolar hyperplasia with “onion skinning” |
| Vasculitis | inflammation of the blood vessel walls. It is usually systemic, affecting most blood vessels of the body, including the blood vessels of the kidneys. It is seen mostly in autoimmune diseases and is usually caused by circulating antibodies. |
| Different types of vasculitis can be diagnosed ... | Morphologically: visualizing the abnormal blood vessels. Serologically: detecting the appropriate antibodies in the patient’s serum. |
| Polyangiitis: pathology in kidney | arcuate and intralobular arteries necrosed; neutrophils attack the walls of the arteries, and infiltrate the arterial walls on the biopsy; blood vessel injury-->healing with aneurysm formation + microinfarcts-->sclerosis-->fibrosis |
| How can you distinguish serologically between polyangitis and Wegner's granulomatosis? | Polyangitis: Serologic testing includes the detection of antineutrophilic cytoplasm antibodies P-ANCA in the patient’s serum (perinuclear pattern). W.G: detection of C-ANCA in the patient’s serum (cytoplasmic pattern) |
| Wegener's granulomatosis pathology in the kidney | presents as a granulomatous inflammation of the blood vessels and destruction of Bowman’s capsule. The inflammatory cells invading the blood vessels are mostly histiocytes, with occasional giant cells. Giant cells are seen around renal artery. |
| What are the following diseases associated with serologically: Microscopic polyarteritis, Idiopathic crescentic, necrotising glomerulonephritis, Other small-vessel vasculitides, Drug reactions, eg. propylthiouracil (rare) | MPO-Positive P-ANCA |
| What are the following diseases associated with serologically: Wegener’s granulomatosis Other small-vessel vasculitides Ulcerative colitis (uncommon) Drug reactions, eg. propylthiouracil (rare) | Pr-3 Positive C-ANCA |
| Thrombotic diseases that affect the kidney | DIC Thrombotic Thrombocytopenic Purpura (TTP) Hemolytic Uremic Symdrome (HUS) |
| Clinically, thrombotic diseases present with ... (3) | thrombocytopenia, anemia and neurological symptom (stroke) |
| Hemolytic uremic syndrome is associated with what etiologies? | E. Coli poisoning, metastatic Breast Cancer, Drugs, Oral contraceptives |
| Therapy of thrombotic diseases | mostly supportive, symptomatic and includes plasmapheresis |
| Pathologically, thrombotic diseases show... | arteriolar and capillary microthrombi with endothelial cell injury and ischemia and collapse of the glomeruli causing secondary tubular changes |
| What are the main causes of renal infarcts? How are they discovered? | They are mainly caused by dislodging of the mural thrombi of left heart. Other causes include Vegetative endocarditis and aortic aneurysms; typically they are silent and are discovered in autopsy |
| Pathologically, how renal infarcts present? | Pathologically, renal infarcts are seen grossly as wedge-shaped abnormalities, usually multiple and bilateral |
| How can you distinguish a recent infarct from an old one? | Recent infarcts are yellow-white and ringed by hyperemia, while old infarcts are seen as fibrous scars and loss of cortical architecture |
| Cluster of abnormalities that, early on, affects the renal tubules and the interstitium; Spares the glomeruli and the blood vessels | Tubulo-interstitial diseases |
| TIDs can be divided into what (6) categories? | ischemic, infections, toxins, neoplasms, and immunologic reaction |
| Acute tubular necrosis (ATN) | destruction of tubular epithelial cells. It usually affects the proximal convoluted tubules; major cause of renal failure; **reversible with full recovery of renal function; can be ischemic or nephrotoxic |
| Ischemic ATN | preceded by hypotensive episode and is usually focal with large skip areas |
| Nephrotoxic ATN | due to ingestion, injection or inhalation of toxins |
| What is the pathophysiology of ATN? | 1) Necrotic epithelium occlude lumen of tubue-->rise in tubular pressure + decreased filtration. 2)Pressure rise vented by tubular backleak 3) tubulo-glomerular feedback-->afferent arteriolar vasconsrict-->decrease filtration further |
| Tubulointerstitial nephritis due to drugs | Inflammatory cells can accumulate within the renal parenchyma-->interstitial inflammation and tubular damage. Acute reaction is usually due to an ALLERGIC REACTION (eosinophil, though others immune cells may be there too) |
| Chronic damage in tubulointerstiial nephritis due to drugs is proportionately and directly related to ... | the amount and duration of the exposure to the drug. |
| Acute Drug-induced Interstitial Nephritis: cause and time until presentation | due to hypersensitivity to medication; extended list includes sulfonamides, synthetic penicillins, diuretics, NSAIDs, Zantac; clinically occur 2-40 days after exposure to drugs |
| What are the presenting symptoms of acute drug-induced interstitial nephritis? | patient presents with fever, peripheral blood eosinophilia, hematuria and proteinuria. Itchy skin rash is present in 25% of all patients and serum Ig E levels high in all cases. |
| What are the pathological findings of acute drug-induced interstitial nephritis? | kidney shows interstitial edema with eosinophilic and neutrophilic inflammatory infiltrate. Less commonly seen are mononuclear inflammatory cells. Certain drugs like Methicillin and Thiazides cause a granulomatous infiltrate with Giant cells |
| What are the serological/histological findings of acute drug-induced interstitial nephritis? | Immunofluorescent studies reveal linear Ig G and Complements along tubular basement membrane. |
| Chronic Interstitial Nephritis: definition and causes | Clinicopathologic term used for advanced stages of tubulointerstitial diseases. Renal damage can be due to drugs (Chronic analgesic nephritis) or chronic infections (Pyelonephritis). |
| Chronic Analgesic Nephritis: definition and causes | usually presents after prolonged intake of analgesics like Aspirin, caffeine, Acetaminophen, Codeine, Phenacetin, etc; due to large doses; women more affected; due to combination of covalent binding and oxidative damage caused by drug involvement |
| What clinical signs and symptoms are seen in patients with chronic analgesic nephritis? | Clinically, chronic analgesic nephritis presents as inability to concentrate urine and renal distal tubular acidosis. Pyuria or pus in the urine, mostly sterile, is seen in 100% of patients. |
| What serious late complication should be considered in patients with chronic analgesic nephritis? | serious late complication to consider is transitional cell carcinoma or the renal pelvis and ureters. |
| What radiographic and gross findings are seen in chronic analgesic nephritis? | Absent renal papillae due to papillary necrosis; normal size kidneys with raised and depressed areas (atrophy over necrotic papillae); interstitial fibrosis and dilated calyces due to lost papillae; |
| What microscopic findings are seen in patients with chronic analgesic nephritis? | microscopically, cortical tubulointersitital nephritis, necrosis, and calcification with sloughing of papillae |
| Pyelonephritis or inflammation of renal parenchyma: differences between acute and chronic etiologies | Acute Pyelonephritis is due to acute episodes of bacterial infection Chronic Pyelonephritis due to repeated episodes of acute pyelonephritis |
| UTI: epidemiology | affects females 15-40 years of age with female to male ratio 8:1 |
| UTI: infrecting organisms reach kidney by which routes? | 1. Ascending route (more common) 2. Blood borne (more dangerous) |
| UTI: most common infecting organisms | usually patients own flora; most common organisms cultured from urinary tract infections are gram negative bacilli with E. Coli the most common organism, followed by Proteus, Klebsiella, Enterobacter, Mycobacteria (T.B) |
| Predisposing factors for UTI | diabetes pregnancy, urinary tract obstruction as seen in benign prostatic hyperplasia (BPH), or tumors. Other causes include vesico- ureteric reflux, immunosuppression and iatrogenic causes |
| Microscopically, acute pyelonephritis shows mostly ___. | acute inflammatory cells (neutrophils) in the interstitium. This is later followed by tubular damage. Small microabsesses in interstitium-->perinephric abscesses (very painful) |
| Chronic Pyelonephritis | due to recurrent bacterial infections as seen in vesicoureteral Reflux and/or obstructions. |
| Pathologically, Chronic Pyelonephritis shows what type of pattern? | irregular broad scars in a “geographic pattern”; |
| What are the microscopic findings found in chronic pyelonephritis? | Microscopically, calyces and renal pelvis are thickened and fibrosed; dense lymphocytic infiltrate and interstitial fibrosis are usually present, together with periglomerular fibrosis, focal segmental sclerosis and tubular atrophy |
| Nephrocalcinosis (calcium in the kidney) | due to calcium deposition in the kidney leading to stone formation; |
| What are the possible causes of nephrocalcinosis? | causes include hyperparathyroidism causing hypercalcemia, Multiple Myeloma, Vitamin D intoxication, excess milk intake or bone metastasis of solid tumors, causing bone resorption and calcium deposition in the kidneys. |
| How does nephrocalcinosis present clinically? | Clinically, nephrocalcinosis presents as slowly progressive renal insufficiency and calcium stones are detected radiographically; pyelonephritis may be present |
| What microscopic findings are seen in nephrocalcinosis? | Ca++ deposits within tubular epithelial cells; Calcium is also seen in the basement membranes of tubules. The renal cortex shows atrophy, with scar formation |
| Renal stones: epidemiology, pathophysiology, composition | men > women; stone size varies from gravel size to large stones; stones dilate renal pelvis and calyceal system; most common composition is calcium oxalate, phosphate, urates, or mixed |
| Infection with urea-splitting bacteria leads to ... | alkaline urine and large calculi |
| When are uric acid stones typically seen? | in 25% of patients with Gout; usually small (<2cm) and radioluscent |
| cystine stones | Cystine stones are seen exclusive in children with hereditary cystinuria and are very uncommon |
| Mixed uric acid and calcium stones | Very common; present with severe cholicky pain; may be present as stones are passing from kidneys through ureters and into urinary bladder |
| Vasculitis is due to... | circulating auto-immune antibodies |
| Thrombodic diseases (DIC) cause damage by... | clogging up the lumen |
| Renal infarcts are due to.. | occluded vessels, are very common, and heal with scar formation |
| ____ can be due to ischemia or toxins and is usually reversible | ATN |
| ____ will lead to transitional cell carcinoma (late complication) | chronic drug-induced interstitial nephritis |
| can be acute and chronic; affects F>M; may be caused by instrumentation that introduces bacteria (usually host's); obstruction causes bacteria to multpiply; | pyelonephritis |
| If you see eosinophelia... | think hypersensitiviy (allergic reaction) or parasite |
| If you see neutrophils... | think acute bacterial infection |
| If you see lymphocytes... | think chronic bacterial infection or viral infection |
| If you see giant cells... | think fungal infection and foreign body reaction |
| IF you see histiocytes... | think necrosis and clean up crew |
Created by:
karkis77
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