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530 Cards in this Set
- Front
- Back
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Etiology of Feline Lymphoma |
-Viruses: |
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Feline Lymphosarcoma subtypes
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-Large cell |
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Demographics of Feline Lymphosarcoma
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-Young cats: FeLV positive |
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Clinical signs of Lymphoma in Cats
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-Depends on anatomic location |
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Physical Exam of cat with Lymphosarcoma
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-Depends on anatomic location and cell type
-GI large cell: abdominal mass -GI small cell: intestinal thickening, enlarged lymph nodes (diffuse abnormalities) -Mediastinal: decreased lung sounds, poor chest compliance -Nasal: decreased air flow, facial deformity, nasal discharge, epistaxis |
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Diagnosis of Feline Lymphoma
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-Requires assessment of cells or tissue from suspected lesion
-Large cell: fine needle aspirate and cytology is often sufficient --biopsy is recommended if cytology is not conclusive --cells are so large and distinctive cytology is often adequate -Small cell: biopsy is required for definitive diagnosis --neoplastic cells look a lot like normal lymphocytes --combination of cytology, PARR, and clinical findings may be acceptable |
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Large cell Lymphoma Cytology
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-Will see a large number of lymphoblasts
-Can see mitotic figures |
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Small Cell Lymphoma
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-Diffuse thickening
-Extensive infiltration of small lymphocytes -Small lymphocytes can look a lot like normal lymphocytes -Muscularis layer is most commonly affected |
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PARR test for Lymphoma
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-Test to determine if a population fo cells is monoclonal or polyclonal |
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Diagnostics for Cat with Lymphoma
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-CBC/Chem
-Urinalysis -Abdominal ultrasound -Check T4 -Fine Needle Aspirate and cytology |
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Lymphosarcoma Staging |
-Few cats have multicentric disease
-Lots of variety in anatomic location -Classified according to anatomic location instead of number stage --Intestinal --mediastinal --Multicentric --Extranodal (nasal, renal, CNS) --Bone marrow/blood --Mixed, combination of locations -Most cats are substage B when diagnosed -Staging tests are completed as part of workup, fill in necessary additional tests as needed |
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Staging tests for Feline Lymphoma
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-Bloodwork
--CBC, Chem, Urinalysis --FeLV, FIV test --Serum cobalamine test -Chest radiographs -Abdonimal ultrasound -Bone marrow test is nor performed unless indicated by CBC results |
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Prognosis for Feline Lymphoma
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-Cell type is most important prognostic factor
--Small cell lymphoma has longer remission and longer survival times than large cell -FeLV status -Anatomic location -Substage -Body weight -Response to treatment |
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FeLV and Lymphoma
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-FeLV positive cats with lymphoma have shorter remission periods and shorter survival times
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Anatomic location of Feline Lymphoma
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-Affects prognosis
-Nasal location has longest survival time -Renal, CNS, locations have shorter survival times -Mediastinal location is shorter, confounds FeLV status |
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Substage as a prognostic factor for Feline Lymphoma
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-Most cats are substage B
-Substage A is longer remission times and longer survival |
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Body weight and Feline Lymphoma
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-Lower baseline body weight results in shorter survival
-Body weight is positively correlated with remission status -Weight loss during the first month of treatment is associated with shorter survival |
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Feline Lymphosarcoma treatment
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-Goal is to achieve remission with good quality of life
-Large cell vs. small cell have different treatments -Anatomic location --systemic treatment --localized therapy for some locations |
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Large Cell Lymphoma Treatment
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-Combination chemotherapy is the standard of care
-COP -CHOP -Prednisone/prednisolone alone may be palliative |
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COP
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-Cyclophosphamide
-Vincristine/vinblastine -Prednisonoe/Prednisolone |
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CHOP
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-Cyclophosphamide
-Vincristine/vinblastine -Prednisone/Prednisolone -Doxorubicin |
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Lymphoma treatment Toxicity
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-Side effects due to chemotherapy
-Poor appetite, weight loss, vomiting, diarrhea -Challenging to distinguish lymphoma and chemo toxicity -Myelosuppression leading to neutropenia --consider long-acting antibiotic injection in cats --Cats have low risk of neutropenia sepsis |
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Feline Large Cell Lymphoma expected outcome
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-50% response rate
-Overall median survival is 6-8 months -Cats that do not respond have median survival time of 2-3 months -Cats that do respond have median survival time of up to 20 months |
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Feline Small Cell Lymphoma Treatment
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-Indolent clinical course
--cells are not dividing as quickly, less aggressive disease -Treatment is not as aggressive as large cell -Combination of prednisolone and chlorambucil -May take a longer time to respond -Treat for 12 months then discontinue chlorambucin and wean prednisone |
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Small Cell Lymphoma toxicity
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-Minimal toxicity
-May develop idiosyncratic liver toxicity --monitor liver values -Mild myelosuppression |
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Small cell lymphoma expected outcome
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-Clinical response rate is 90%
-Higher expected survival, 20-24 months |
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How to assess response of cats to Lymphoma treatment
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-Clinical signs: improvement of lymphoma-related signs
-Physical exam: --weight gain, reduced size of the mass, reduced intestinal thickness -Restaging: blood work and imaging repeated |
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Rescue Chemotherapy
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-Treat with protocol that is not 1st line treatment
-Lomustine and doxorubicin -Low response rate to doxorubicin, lomustine has higher response rate -Cyclophosphamide can be used for small-cell lymphoma |
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Localized therapy for Feline Lymphosarcoma
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-Considered for cats with solitary lesions
--nasal, mediastinal -Surgery: solitary lesion that is amenable to surgery --intestinal perforation or obstruction -Radiation therapy --solitary lesion that is not amenable to surgery --solitary lesion that is not responding to systemic therapy |
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Supportive care for Feline Lymphosarcoma
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-Most cats are ill at the time of diagnosis |
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Feline Lymphoma Quality of Life concerns
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-Anti-emetic therapy (ondansetron, dolasetron, maropitant) |
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Mast Cells
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-Bone marrow derived cells
-Involved in inflammation |
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Mast Cell tumors
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-Round cell tumor
-Contain intracytoplasmic granules --can be helpful for diagnosis --can contain heparin, histamine, vasoactive amines that cause clinical signs -Stain with toluidine blue, diff-quick, and wright-geimsa stains -Common in dogs, most common skin tumor in the dog --some breed predispositions --possible association with skin allergies -Not common in cats |
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Presenting complaint for Mast Cell Tumors
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-Skin or subcutaneous mass
-Owner report that the mass swells and shrinks, sometimes bleeds -Systemic signs are indicative of GI ulceration --due to increased gastric acid production, stimulated by histamine |
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Mast Cell Physical Exam
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-Can be found as incidental findings on routine exam
-Essential to record size, location, and description of masses that are palpated --can compare changes over time -May find regional lymphadenopathy, cranial organomegaly, melena, weight loss |
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Diagnosis of Mast Cell Tumors
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-Cannot diagnose based on history and physical exam
-Need to obtain cells/tissue -Fine Needle Aspirate and cytology -Incisional biopsy and histopathology -Excisional biopsy and histopathology |
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Fine needle Aspirate Procedure
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-Insert needle alone or with syringe attached
-Move around in different directions -Attach syringe, express needle contents onto a slide -Smear slide, let dry and stain -Observe cells |
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Mast Cell prognostic Factors
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-Grade
-Stage -Location -Growth rate -Size -Breed -Local recurrence -Age of animal -Markers of cellular proliferation -c-kit mutation |
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Mast Cell Tumor grade
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-Most consistent prognostic factor
-Determined by histopathology, not cytology -Patniak grading system is older system -Subjective measurement! Lots of variability |
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Patniak grading system for Tumors
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1: well-differentiated, confined to dermis, metastasis and local recurrence are rare after complete excision
2: Intermediate differentiation, extends deeper into the dermis, metastasis/recurrence is uncommon after complete excision 3: Poorly differentiated, high chance of metastasis and local recurrence after complete excision |
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New Grading System for Mast Cells
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-Only has 2 grades, eliminates intermediate grade
-Will allow for more accurate prediction of clinical behavior |
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“High Grade” tumors
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-more than 7 mitotic figures in 10 hpf
-More than 3 multi-nucleated cells in 10 hpf -More than 3 bizarre nuclei in 10 hpf -Select fields that are most highly mitotically active or have highest degree of anisokaryosis |
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Canine mast Cell Tumor staging system
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1: one tumor with no metastasis
2: one tumor with lymph node metastasis 3: multiple cutaneous tumors and/or large infiltrative tumor --may or may not have lymph node metastasis 4: Any tumor with distant metastasis -Substage a: no systemic signs -Substage b: systemic signs are present |
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Mast Cell Tumor Stage and Prognosis
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-Stage 4 is associated with grave prognosis
-Dogs with multiple cutaneous tumors without metastasis do not have different prognosis from dogs with 1 tumor, as long as it can be treated -Stage 2 prognosis is controversial --adequate local and regional treatment can result in adequate outcome |
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Mast Cell Tumor Staging Tests
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-CBC/Chem/Urinalysis
-Regional lymph node fine needle aspirate -Abdominal ultrasound -Bone marrow fine needle aspirate --do if clinical picture looks like metastasis -Chest radiographs |
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Lymph Node Cytology for Mast Cell Tumors
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-Mast cells are found in normal canine lymph nodes
--presence of mast cells does not mean there is metastasis -Lymph node is effaced by mast cells -More than 5 aggregates or more than 3 mast cells -Aggregated mast cells with criteria of malignancy |
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Clinical prognostic factors for Mast Cell Tumors
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-Location
--preputial, scrotal, subungual, muzzle, oral, mucocutaneous sites associated with poorer prognosis -Growth rate: --faster growth is poor prognosis -Breed: --boxers and pugs get lower grade tumors --Shar-peis get high-grade aggressive mast cell tumors |
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Cellular Proliferation Measurements for Mast Cell Tumors
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-Tests done on biopsy samples
-Look for markers of cellular proliferation -Higher score indicates high number of cells that are proliferating in the tumor --indicates more aggressive behavior -Mitotic index |
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Mitotic index
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-Evaluated on routine histopathology of canine Mast Cell Tumors
-Number of mitotic figures sennin 10 consecutive hpf -Does not require special stains -Inversely related to survival time -Appears to more consistently predict prognosis |
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KIT
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-Receptor on mast cells that stimulates cellular proliferation and survival
-Needs to be activated by ligand binding -30% of canine Mast cell tumors have mutation in c-KIT gene --results in constitutive activation of the receptor -Mutation is more common in high-grade tumors -Mutation is associated with shorter survival time |
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Mast Cell Tumor Treatment Options
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-Depends on prognostic factors and feasibility of local therapy
-Local therapy with chemotherapy is mainstay of definitive treatment -Definitive vs. palliative treatment |
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Surgery for Mast Cell Tumors
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-Complete surgical excision is most effective
-2-3cm margins around the tumor -1 tissue plane deep -High grade tumors can recur even with complete margins --additional local therapy may be recommended even with complete surgical excision |
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Radiation therapy for mast Cell Tumors
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-Most mast cell tumors are round cell tumors
-Respond well to radiation therapy, very sensitive -Can be used as radiation therapy in the bulky tumor stage |
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Loco-regional treatment for Mast Cell Tumors
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-Surgery or radiation therapy to lymph node in addition to
local therapy to primary tumor -Indicated in patients with stage II disease -Can excise lymph node or radiate it |
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Adjuvant Chemotherapy treatment for Mast Cell Tumors
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-Goal is to delay/prevent metastatic disease
-Recommended for dogs at risk for metastatic disease --grade III tumors or stage II tumors -Prednisone, vinblastine, lomustine, cyclophosphamide are common drug treatments |
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Neoadjuvant Chemotherapy for Mast Cell Tumors
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-Goal is to shrink the primary tumor and make local therapy a better option
-Pre-treatment tumor measurement is essential to gauge response -Complete staging before initiating therapy -Prednisone and Vinblastine are most commonly used |
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Palliative therapy for mast Cell tumors
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-Palladia
-Kinavet -Will still have some toxicity, still affect same normal cells in body as chemotherapy |
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Supportive care options for Mast Cell Tumor
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-H2 blockers or proton pump inhibitors
--decrease GI ulceration -H1 blockers: decrease tumor degranulation -Sucralfate if there is GI ulceration -Antibiotics, pain medications |
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Feline Cutaneous Mast Cell Tumors
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-Siamese cats are predisposed
-Can have just 1 or can have many tumors -Head and neck are the most common sites -No histopathological grading system exists -2 histopathologic types --Mastocytic --Histiocytic |
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Diagnostics for Feline mast Cell Tumors
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-Fine needle aspirate
-Excisional biopsy |
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Mastocytic Feline Mast Cell Tumor
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-Primary cells are mast cells
-Can be compact (benign) -diffuse (malignant potential) |
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Histopcytic Mast Cell Tumors
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-In Cats
-Primary cells are histiocytes -Hard to diagnose with cytology -Can spontaneously regress |
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Staging cats with Mast cell Tumors
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-CBC/Chem/Urinalysis
-Regional lymph nodes -Abdominal ultrasound -Buffy coat test |
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Buffy coat test
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-Done in cats with mast cell tumors
-Sensitive and specific test for diagnosing mast cell tumors in bone marrow in cats -Sensitive but not specific in dogs --can be for many different reasons, not just mast cell disease |
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Prognostic factors for Feline Mast Cell Tumors
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-Local recurrence and metastasis is low
-Surgical margins are not prognostic for local recurrence, do not really matter -Most are considered benign -Metastasis to local lymph nodes and visceral organs has been reported -Chemotherapy and radiation therapy is not as well researched |
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Definitive treatment options for Feline Mast Cell Tumors
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-Surgical excision (wide margins are not necessary)
-Radiation therapy if surgery is not possible due to tumor size or location -Adjuvant chemotherapy is not recommended --unless there is documented metastatic disease |
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Palliative therapy for Feline mast Cell Tumors
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-Chemotherapy has 50% response rate with lomustine treatment
-Radiation therapy -H1 and H2 blockers -Pain medication and antibiotics as needed |
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Feline Visceral mast Cell Tumors
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-Rare in dogs
-50% of feline amst cell tumors -Uncommonly associated with cutaneous mast cell tumors -Spleen and GI are most common locations |
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Spleen and Mast Cell Tumors
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-Often systemic disease is present
--can regress if there is a splenectomy -Prognosis is better for cats than for dogs with splenectomy |
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GI Mast Cell Tumors
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-Poor prognosis even with surgical excision |
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Mammary Tumors in Dogs
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-Most common tumor in the intact female dog
--40-50% -Breed predispositions -Peak incidence in middle aged/older patients -associated with total ovarian hormone exposure --early OHE has protective effect -Increased risk with progestins/estrogen exposure -Increased risk with short heat cycle intervals -Diet/obesity is associated with increased risk |
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Breed predisposition for Mammary tumors
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-Toy and miniature poodles
-English springer spaniels -Brittany spaniels -Cocker spaniels -English setters -Pointers -German shepherds -Maltese -Yorkshire terriers -Dachshunds |
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Comparison between Human and Dog mammary cancer
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-Most common cancer in women in USA
-Peak incidence in middle-aged to older individuals -Risk is influenced by cumulative estrogen exposure --endogenous and exogenous hormones -Diet/obesity is linked to increased risk -50-80% of breast cancers express estrogen receptors -Hormonal therapy is an effective treatment modality in humans --not in dogs |
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Hormones and growth factors playing a role in mammary cancer
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-Estrogen and progesterone are necessary for normal mammary gland development
-Mitogens for breast tissue --allows for growth during puberty -Progestin can induce growth hormone and growth hormone up-regulation in mammary tissue -HER2/Neu protein is over-expressed in mammary tumors --associated with worse prognosis -Opportunities for therapeutic exploitation with hormones |
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Histopathological continuum of Mammary Tumors
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-All mammary tissue is exposed to hormones
--“Field effect” -multiple tumors are common -Tumors can be at different stages in tumor development -Regional differences: caudal glands are more affected in dogs -Areas adjacent to tumors may be associated with pre-malignant lesions --indicates gradual progression from benign to malignant tumors |
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Association between Mammary tumor grade and hormone receptors
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-Low grade tumors are more likely to be hormone receptor tumors
-high-grade tumors are more likely to be independent of hormone stimulation --hormone receptor negative -Inverse relationship between estrogen receptors and nuclear proliferation indices --tumors with higher growth and proliferation rate are undifferentiated, less likely to have estrogen or progesterone receptors -Inverse relationship between hormone receptors and HER2/neu profile |
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Dog hormonal status and mammary tumors
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-Influences what the tumor will look like
-If dog is in anestrus, old, or spayed, will have hormone negative tumors -Younger dogs in diestrus or estrus will have hormone receptors |
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Presentation of dogs with Mammary tumors
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-Older dogs
-intact or had OHE later in life -Usually have more than 1 tumor (70%) -Caudal glands are more affected than other glands -Tumor size varies -Variable duration of tumor growth -Most dogs are systemically healthy -Distant metastasis is rarely seen at initial presentation --depends on tumor size and type |
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Inflammatory Mammary Carcinoma
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-Can look just like mastitis
-Diffuse, swollen, painful, edematous gland -Not discrete tumors that are typically seen |
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Diagnosis and staging of Mammary Carcinoma
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-Assess general health of the animal
-Localize and measure all mammary tumors present -Assess local and regional lymph nodes --if palpable, do fine needle aspirate -CBC/Chem/Urinalysis -Thoracic radiographs -Excisional surgical biopsy |
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Staging system for Mammary tumors
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T: primary tumor
-T1: less than 3cm -T2: 3-5cm -T3: more than 5 cm N: Regional Lymph Node status -N0: no metastasis -N1: metastasis M: Distant Metastasis -M0: no distant metastasis -M1: distant metastasis is detected |
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Histopathology of Mammary Gland Tumors
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-Complicated issue! Constantly changing
-40-50% of tumors are malignant and risk for malignancy increases with size -Tumors can arise from all types of tissue within the mammary gland --epithelial tissue (glands) --myoepithelial tissue --mesenchymal tissue --combination of tissue types -Dogs with multiple tumors can have tumors of different histologies |
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Simple Mammary carcinoma
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-Epithelial tumor, consists of only one tissue type
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Complex mammary carcinoma or adenoma
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-Combination of epithelial and myoepithelial tissues
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Mixed mammary tumor
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-Combination of epithelial and mesenchymal tissues
-If one part is malignant: mixed malignant -If both parts are malignant: carcinosarcoma |
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Mammary tumors of mesenchymal origin
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-Primary mammary sarcoma
-Mammary tissue is the most common site for sarcomas out of the bone |
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Mammary tumors of myoepithelial origin
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-Malignant myoepithelioma
-Extremely rare |
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Mammary tumor Grade
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-Strong correlation between outcome and grade of tumor
--high grade tumors have poor prognosis -Prognosis is determined by the most aggressive histology and largest tumor --often the same tumor |
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Mammary tumor treatment
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-Surgery is most important part of therapy
-Cure benign tumors and small malignant tumors -Goal is to remove all tumors with clean margins -Obtain tissue for histopathology -All tumors must be biopsied, can vary in type -Biopsy and send in draining lymph node if possible |
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Simple vs. Radical Mammary tumor Surgery
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-No difference in dogs with malignant tumors
-Is the goal of surgery to treat current tumor OR treat current and prevent new tumors? |
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Traditional surgical approach for mammary tumors
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-Size of surgery depends on number and size of tumors
--do not need a bigger surgery -New tumors in other glands are common in dogs |
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Prophylactic unilateral mastectomy
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-Beneficial in prolonging disease-free interval
-Decreases risk for new tumors to have impact -Need to advise tumors that new tumors in other glands are common |
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Adjunctive treatments in Canine Mammary tumors
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-Surgery is curative in early stage well-differentiated tumors
-Dogs with high-grade locally advanced tumors need more than local treatment -Hormonal therapy or chemotherapy |
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Prognostic factors for Mammary tumor systemic therapy
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-Tumor size
-Tumor type -Tumor grade -Tumor stage -Presence of distant metastasis |
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Mammary tumor size and prognosis
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-3cm is “magic cut-off”
-Less than 3cm, good prognosis |
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Hormonal Therapy for Mammary Tumors
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-based in human treatments
-Use therapy in all patients that have hormone-positive tumors --significantly improves survival -Goal is to prevent breast cancer cells from getting stimulation from estrogen --Can be done surgically or medically --medical management is less common in dogs |
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Indications for Chemotherapy for Mammary tumors
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-High-risk tumors
--lymph node metastasis, large tumors, anaplastic histopathology -Doxorubicin, cyclophosphamide, 5-fluorouracil, carboplatin -No prospective randomized trials, no way to believe results |
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Summary of Mammary Tumors in Dogs
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-Early OHE is protective
-Both malignant and benign forms exist -Wide histological spectrum and lots of different biological behavior -Surgical approach may vary -Prognostic factors determine the need for systemic therapy -Hormonal therapy and chemotherapy can both be used |
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Mammary tumors in Cats
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-2nd or 3rd most common malignancy in cats
-Siamese cats are over-represented -Older cats -hormonal influences play a big role --Spaying a cat early reduces risk -Regular use of progestins increases risk |
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Physical exam on Cat for Mammary Tumors
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-Older cats
-Fibroepithelial hyperplasia in younger cats --not malignant, progesterone induced -More than one tumor is common -Caudal glands are more commonly affected -Tumor size varies -Regional lymph node may be enlarged -Systemic signs of illness may or may not be present --depends on stage of disease |
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Fibroepithelial Hyperplasia
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-In young cats going through estrus cycles
-Progesterone induced change in mammary glands -Resolves when heat cycles resolve |
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Feline Mammary Tumor work-up and staging
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-Measure and record all tumors
-Evaluate lymoh nodes -CBC/Chem/Urinalysis -Radiographs of chest |
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Staging system for Feline Mammary gland tumors
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-4 stages
-Based on TNM |
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Histology of Feline Mammary Tumors
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-Most tumors are malignant, 95%
-Mostly epithelial tumors: --adenocarcinomas, tubular carcinomas, solid carcinomas -Estrogen receptor sensitivity is less common -Aggressive biological behavior, locally invasive --high incidence of distant metastasis |
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Prognostic factors for Mammary Tumors in Cats
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-Tumor size (bigger is badder)
-Tumor grade -Lymph node status -Distant metastasis |
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Treatment for Feline Mammary Tumors
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-Surgery and Chemotherapy
-Radical unilateral mastectomy, remove axillary superficial lymph nodes on both ends --significantly increases recurrence interval but does not improve overall survival |
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Systemic Therapy for Feline mammary tumors
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-Hormonal therapy is less likely to be effective
--has not actually even been tested -Chemotherapy is indicated due to high incidence of distant metastasis --optimal protocols are not defined -Doxorubicin based protocols are most often used -No good studies about chemotherapy results |
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Summary of Mammary tumors in Cats
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-Early OHE is protective |
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Upper urinary System
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-Kidneys
-Ureters -Renal Artery and Vein -Upper urinary disorders tend to be more severe |
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Lower Urinary System
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-Urinary bladder
-Prostate -Urethral sphincter -Urethra -Penis/vestibule |
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Upper urinary Disorders: Renal
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-Congenital diseases
-Acquired kidney injury (acute or chronic) -Glomerular diseases -Neoplasia -Hematuria |
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Upper Urinary Disorders: Ureters
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-Obstruction (stone, debris, blood)
-Ectopia |
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Lower Urinary Disorders: Bladder
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-UTI
-Cystitis -Neoplasia (Transitional cell carcinoma) |
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Lower Urinary Disorders: Prostate
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-Benign prostatic Hypertrophy
-Prostatitis and abscesses -Neoplasia |
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Lower Urinary Disorder: Urethral Sphincter
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-Incompetence, decreased tone leads to incontinence
-Micturition disorders |
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Lower Urinary Disorders: Urethra
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-Obstruction
--mucus plug, grit, stone, neoplasia, etc. -Hypospadia |
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Clinical signs of Upper Urinary Disorder
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-PU/PD
-Lethargy, vomiting, diarrhea -Metabolic bone disease -Renal colic and pain -Incontinence -Hematuria -Muscle wasting |
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Clinical signs of Lower Urinary Disorder
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-Fewer systemic signs, more issues urinating
-Stranguria -Pollakiuria -Inability to urinate -Incontinence -Tenesmus -Hematuria |
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Questions to Ask about Urinary Issues
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-When did signs begin
-Have signs progressed, improved, or stayed the same -When was the last normal -Exposure to toxins, herbal remedies, drugs before onset of signs -Medications administered for the condition -medications administered for other conditions -Magnitude and duration of response to medication -Diagnostic tests performed --get results of tests for medical record -Describe urination -If incontinence, what age did it start? When does urine leaking happen? -Quantify how much water pet is drinking |
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Functions of the Kidneys
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-Excretion of metabolic waste products (probably most important)
-Electrolyte balance -Acid-base regulation -Water balance and formation of urine -EPO synthesis -Calcitriol synthesis -RAAs activity --renin synthesis, response to angiotensin II and aldosterone -Blood pressure regulation -Drug metabolism and excretion -Gluconeogenesis |
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Disorders of the Renal Vasculature
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-Related to vessel thrombosis, vasodilation, or vasoconstriction
-Impaired blood flow to the kidney or from the kidney -Pre-renal azotemia -Decreased perfusion, kidney is getting less blood and therefore clears less blood of toxins etc. -May result in ischemia and intrinsic renal damage -Mostly due to hypovolemia |
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Glomerulus
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-Tuft of capillaries
-Filters plasma water from the blood -Folds and twists increases surface area -Main function is Filtration -Start of kidney function! |
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Macula Densa
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-Part of distal tubule in nephron
-Splits between the afferent and efferent arterioles -Senses blood to and from the arterioles --constricts or dilates afferent arteriole |
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Mesangial cells
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-Holds loops of capillaries in the bowman’s capsule together
-Constrict and expand to change the surface area |
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Foot processes
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-Epithelial cells that cover capillary loops
-Interlock with each other -Disease will affect filtration |
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Glomerular Basement Membrane
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-Negatively charged
-Prevents RBCs and proteins from getting into urinary filtrate |
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Filtration devices in Glomerulus
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1. Fenestrated endothelium
2. Foot processes of epithelial cells 3. Negative charge of the basement membrane THREE areas of restriction to urine flow -makes up “colander” of the glomerulus |
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Glomerular Filtration Rate
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-Rate at which things are filtered across the glomerulus
-Gold standard measurement of kidney function -Not very easy to measure -Difference between capillary hydrostatic pressure and oncotic pressure -Main determinant is difference in hydrostatic pressure in capillaries --pressure gradient between inside capillaries and outside -Oncotic pressure also factors in (how much protein is in plasma) |
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Plasma Water
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-Water component of blood
-Portion of blood that is filtered through the glomerular basement membrane |
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Proteins in Glomerulus
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-Should not be filtered, should stay in the blood
-Creates oncotic pressure, pulls fluid into blood -GFR is difference between hydrostatic pressure and oncotic pressure due to proteins |
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Glomerular Disease
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-Glomerulonephritis (inflammation)
--can be immune mediated or other -Congenital diseases -Glomerulosclerosis -Minimal change disease |
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Consequences of Glomerular Disease
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-PROTEINURUIA!
--albuminuria -Spaces are dilated, proteins are able to leak through glomerular spaces -Can cause azotemia, but azotemia is not hallmark -Hypoalbuminemia -Hypercoagulability due to filtration of anti-coagulants -Nephron damage and loss |
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Clinical Signs of Glomerular Disease
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-Absent
-Weight loss -Muscle wasting -Uremia and chronic kidney disease |
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Complications of Glomerular Disease
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-Hypertension
-Thromboembolic disease -Tubular dysfunction and nephron loss -Edema, ascites due to low oncotic pressure |
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Nephrotic Syndrome
|
-Proteinuria and loss of albumin leads to hypoalbuminemia
-No albumin in the blood, lack of oncotic pressure -Fluid leaks out of vasculature and into peripheral spaces --causes edema or ascites -Liver releases cholesterol to retain oncotic pressire --hypercholesterolemia -Since cholesterol is not as oncotic, does not do as good of a job as protein in retaining fluid in vasculature |
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4 signs of nephrotic syndrome
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-Proteinuria
-Hypoalbuminemia -Ascites or edema -Hypercholesterolemia -NOT azotemia!! |
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Tubular Dysfunction
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-Each section of the tubule needs to be working properly for the kidney to be working properly
-Numerous causes can contribute to dysfunction -Mild: loss of regional tubule function -Severe: failure and loss of entire nephron --remaining nephrons will hypertrophy |
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Tubular system
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-Proximal tubule
-Loop of Henle: reabsorbs NaCl -Distal Tubule -Collecting Duct: Reabsorbs water and urea -System resorbs and secretes solutes -Acid/base regulation -Water resorption |
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Tubular Loss Parameters
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-Can look at creatinine
-Need 66% loss of nephrons before isosthenuria -Need 75% loss of nephrons before azotemia -Late-changing signs! |
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Azotemia
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-Condition of having metabolic waste products in the blood
-Urea and creatinine in the blood -Need 75% nephron loss or damage to see azotemia -Can be pre-renal, renal, or post-renal causes |
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Uremia
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-Condition of having urine in the blood
-Clinical manifestation of retained uremic toxins -Cannot be uremic unless you are also azotemic -Uremic toxins cause animal to feel sick |
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Symptoms of Uremia
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-Anorexia/nausea
-GI ulceration -Halitosis (Uremic breath) -Oral ulceration and stomatitis -Coagulopathies -Non-regenerative anemia -Platelet dysfunction -Neutrophilia -Lymphopenia |
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Nost-nephron Upper Urinary Disorders
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-Issue with renal pelvis, ureteropelvic junction, or ureter
-Obstruction -Stricture -Idiopathic renal hematuria -Uroabdomen |
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Blockage of one ureter
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-Post-renal complication
-Only one kidney is affected --Will not see Azotemia! |
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Acute Renal Failure
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-Same thing as Acute Kidney Injury
-Retired term |
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Acute Kidney Injury
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-Includes an injury that can be small and not result in “failure”
-Maintenance and recovery phases -Mild decreases in GFR are clinically significant |
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4 Phases of Acute Kidney Injury
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1. Induction
2. Extension 3. Maintenance 4. Recovery |
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Induction phase of Acute Kidney Injury
|
-Injury occurs
-Renal insult causes altered renal function -Do not actually see this happen, clinical signs are usualy absent -Intervention may prevent progression |
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Extension phase of Acute Kidney Injury
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-Additional renal damage occurs
-Altered renal perfusion -Renal hypoxia -Inflammation -Cell Injury -Clinical signs are typically absent |
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Maintenance phase of Acute Kidney Injury
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-Occurs after a critical amount of damage
-Animal is feeling sick -Azotemia (increased BUN and creatinine) -Clinical signs of Uremia -Removing inciting cause will not change course of injury progression |
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Recovery Phase of Acute Kidney Injury
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-Renal tissue undergoes regeneration and repair
-Variable restoration of renal function |
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3 major functions of the Kidney
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1. Maintenance of the Extracellular Volume and environment
2. Secretes hormones --renin, EPO, Active vitamin D 3. Gluconeogenesis |
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Severity of Acute Kidney Injury
|
-Look at Creatinine
--not best marker, does not change until 75% of kidney is damaged -Can grade severity of kidney injury based on creatinine elevation level -Stage I: Progressive non-azoemic increase in serum creatinine more than 0.3mg/dl within 48 hours --does not matter if it is still within normal limits, INCREASE id the key --ignore reference range, look for change over time -Change in creatinine indicates change in GFR |
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Acute vs. Chronic Kidney disease
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-lethargy and vomiting vs. PU/PD, weight loss, decreased appetite
-Normal/regenerative acute hemorrhage vs. normocytic, normochromic, non-regenerative anemia -Symptoms are more severe than azotemia, animal is sick vs. azotemia is more common than severe symptoms -Kidneys are normal/large vs. kidneys are small and irregular -Potassium is normal or high vs. low |
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Pre-renal Acute Kidney Injury
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-Hypoperfusion, kidneys are not receiving proper blood supply
-Kidney is normal, just not getting the blood supply it needs -Biopsy would be totally normal, no damage to kidneys yet --normal renal parenchyma -Decreased GFR --Kidneys cannot filter as much plasma water, are not receiving as much water --filtration decreases -Can develop into renal injury |
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Hypoperfusion and Pre-renal Acute Kidney Injury
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-Can be due to decreased cardiac output
-Heart failure will result in kidneys not getting proper perfusionp -Sepsis or systemic illness will cause renal hypoperfusion -Systemic vasodilation -Renal vasoconstriction |
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Response of kidneys to Hypoperfusion
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-Stimulation of the Renin-Angiotension-Aldosterone System
-Causes retention of salt and water --restores volume deficits -Sympathetic NS is activated, HR increases -More water is in system, kidney gets restored blood flow |
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Renin-Angiotensin-Aldosterone System
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-Constricts the efferent arteriole
-GFR increases -Not a sustainable response or solution, will not fix decreases in perfusion |
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Drugs causing Pre-renal Acute Kidney Injury
|
-NSAIDs
--causes 20% reduction in GFR --inhibits prostaglandin production, prevents dilation of afferent arteriole -ACE inhibitors block RAAs system -Cyclosporine -Radiocontrast |
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Severe Heaptic Diseases causing Acute Kidney Injury
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-Decreased production of prostaglandins
-Blood pooling in liver shunts |
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Pre-renal Acute Kidney Injury Diagnostics
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-Hemoconcentration
--if animal is hypoperfused due to dehydration and hypovolemia -Mild to moderate azotemia -Hyperphosphatemia --Serum phosphorous level is inverse to GFR -Concentrated urine (more than 1,030) with inactive sediment and hyaline casts -Imaging should be normal |
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Treatment for Prerenal Acute Kidney Injury
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-Fluids to restore perfusion
--as long as they are not in heart failure -Improve cardiac output -Discontinue medication that could cause decreased GFR -Treat underlying disease |
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Prerenal Acute Kidney Injury Prognosis
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-Excellent if treated early
-correct the underlying disease -If hypoperfsion is prolonged, will get intrinsic renal ischemia and injury |
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Post-renal Acute Kidney Injury
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-Bladder or urethral obstruction
-Ureteral obstruction -Bilateral ureteral obstruction -Uroabdomen -Kidney is normal, plumbing is busted --urine cannot leave the body -Puts pressure on the kidney |
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Clinical signs of Post-renal Acute Kidney Injury
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-Not PU/PD
-Not azotemic (unless blockage of both ureters) -Not uremic -Lethargic -Maybe straining to urinate if urethral, not so much if higher up -Kidneys will be PAINFUL |
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Pathogenesis of Post-renal Acute Kidney Injury
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-Decreased tubular flow due to backup/obstruction causes initial vasodilation
-Persistent obstruction leads to increased intraluminal pressure -Pressure reversal pushes water backwards --edema within renal parenchyma itself -GFR decreases -Membrane channels are impaired -Back-leak of tubular contents -Pressure reversal |
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Uroabdomen
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-Patient is sick
-Not excreting anything from kidneys, is going into abdomen and being resorbed into blood stream -Post-renal cause of azotemia and acute kidney injury -Will not result in intrinsic renal damage, not affecting kidneys directly |
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Post-renal Acute Kidney Injury diagnostics
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-CBC will be nonspecific
-Azotemia may be absent if one-sided, may be marked if bilateral or urethral -Hyperphosphatemia -Hyperkalemia -Urine concentration will be variable -May see crystals in urine |
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Post-renal Acute Kidney Injury Diagnostics
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-Look for an obstruction
-Abdominal radiographs -Abdominal ultrasound --will see kidney dilation/stretching -Pyelography |
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Treatment for Post-renal Acute Kidney Injury
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-Relieve obstruction
-Treat hyperkalemia if present (can be life-threatening) --calcium gluconate: changes threshold potential of neurons --dextrose and insulin -Catheterize animal if urine leakage is present |
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Post-obstructive renal diuresis
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-MASSIVE urine production after relief of obstruction
-Impaired Na and H2O resorption -Hypokalemia, hypomagnesia -Usually self-limiting condition -Monitor ins and outs to prevent pre-renal issue |
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Post-renal Acute Kidney Injury Prognosis
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-Depends on how long the obstruction has been there
--the longer the obstruction has been there, the less chance for return to complete function -Good chance of recovery for renal function -Chronic renal damage may persist if there was real damage |
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Intrinsic Acute Kidney Injury
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-Damage to the kidney itself
-Diseases involving he large renal vessels -Diseases of the renal microvasculature and glomeruli -Ischemic and nephrotoxic acute tubular necrosis -Acute damage to the tubulointerstitium (infection) -Necrosis is sparse or absent |
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Acute Tubular Necrosis
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-Usually not a lot of necrosis, more apoptosis
-Cells slough into lumen and cause obstruction -Damaged cells result in altered perfusion to kidney --ATP depletion -No ATP, cells are not anchored to basement membrane, cytoskeleton cannot be maintained -Reverse flow of Na, Cl, H2O due to switch of transporters from basolateral to apical side of membrane -Cells slough off into the tubular lumen, results in impaired Na resorption -Precipitation of Tamm-Horsfall Protein and cast formation |
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Pathogenesis of Acute Tubular Necrosis
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-Oxidative injury occurs within tubular cell
-Pro-inflammatory cytokines are produced -ATP deficiency prevents Ca from exiting the cell --Ca accumulates in the cell -Apoptosis -Results in ischemic acute kidney injury or acute tubular injury |
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Etiologies of Intrinsic Acute Kidney Injury
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-Prolonged hypoperfusion and renal ischemia
-Sepsis --renal vasoconstriction, DIC --12% of dogs with sepsis developed acute kidney injury, 86% of those died -Toxins and contrast agents --vasoconstriction and oxidative damage -Myoglobin and Hb in blood --IMHA |
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Nephrotoxic Acute Kidney Injury
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-Contrast agents
-Myoglobin -Hemoglobin -Aminoglycoside antibiotics (gentamicin, amikacin) -Amphotericin B -Calcineurin inhibitors (cyclosporine) -NSAIDs -ACE inhibitors -Cisplatin -Methotrexate -Sucrose containing IVIG -Grapes, raisins, currants (unknown mechanism) -Lily plants -Ethylene Glycol -Melamine (tubular necrosis and obstruction via crystals) -Jerkey treats, sweet potato treats -Cholecalciferol (Vitamin D3, in rat bait) -Leptospirosis -If patient already has kidney disease, do not give nephrotoxic agents! |
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Aminoglycoside Antibiotics and Acute Kidney Injury
|
-Exact mechanism is unknown
-Cumulative toxicity -Appears 5-10 days post treatment -Reversible, but may need dialysis -Monitor closely for casts in urine sediment |
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Lily Toxicity
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-VERY nephrotoxic to cats!
-ALL parts of the plant are toxic -Unknown aqueous toxin -Causes seizures and pancreatitis -Poor survival rate, very lethal |
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Ethylene Glycol Toxicity
|
-Calcium oxylate crystals, cause tubular damage
-Can take months for the kidneys to repair -Can be removed with dialysis from blood before animal gets sick of happened recently |
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Leptospirosis and Acute Kidney Injury
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-Infectious cause of acute kidney injury
-Organisms replicate and persist in renal tubular cells -Pro-inflammatory cytokine production -Vasoconstriction -Intracellular Ca accumulation -Will see increased liver enzymes and thrombocytopenia |
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Pyelonephritis
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-Ascending bacteria from ureters make their way into the kidney
-Interstitial inflammation Causes tubular damage |
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Diagnostics of Intrinsic Acute Kidney Injury
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-Hemoconcentration from dehydration
-Anemia is possible -Leukocytosis -Azotemia of various degrees -Hyperphosphatemia -May or may not have hyperkalemia -Isosthenuria -Active sediment and casts in urine --anything but hyaline casts are abnormal -Urine culture and susceptibility is necessary! -Get images! (radiographs, ultrasound) |
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Leptospirosis testing
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-PCR from urine or blood
-Serum antibody titers -Make sure you use the same lab for both acute and convalescent titers |
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Treatment of Intrinsic Acute Kidney Injury
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-Take away all nephrotoxic drugs
-Restore renal perfusion --make sure fluids are right amount -Treat treatable things -Monitor very closely -Hemodialysis |
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Management of IV fluids for Kidney Disease
|
-GOAL IS TO RESTORE RENAL PERFUSION
-Initially use isotonic replacement crystalloid -Transition to maintenance crystalloids when volume is replete -Use hetastarch with caution -Do not give fluids to diurese the kidneys! Does not work! --aggressive fluid therapy will lead to volume overload --increases morbidity, mortality, and risk of acute kidney injury -Too much pressure will “blow up” the kidneys |
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Monitoring patients with Intrinsic Acute Kidney Injury
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-Monitor to avoid volume overload
-Multi-lumen central catheters -Monitor trends -Urinary catheters with closed collection system --record ins and outs -Keep tabs on body weight and electrolytes -Blood pressure is key! |
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Blood pressure monitoring with Intrinsic Acute Kidney Injury
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-37% of dogs with acute kidney injury had hypertension
-81% became hypertensive during hospitalization -Identify hypertension and treat! |
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Antibiotic treatment for Intrinsic Acute Kidney Injury
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-Amoxicillin-clavulonic acid for Leptospirosis
-Fluoroquinolone (enrofloxacin) for prostate issues -3rd generation cephalosporin (Cefotaxime) |
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Treatment for Intrinsic Acute Kidney Injury
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-Anti-emetics (for uremia)
-Antibiotics -Antacids -Nutrition: enteral is better than parenteral |
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Urine output for Patients with Intrinsic Acute Kidney Injury
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-Anuria and oliguria is associated with higher mortality rates
-May represent a more severe renal insult -Conversion from oliguria does not improve need for dialysis |
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Signs of Volume Overload
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-Conjunctival swelling (puffy eyes)
-Serous nasal and ocular discharge -Subcutaneous edema -Pulmonary edema -Ascites |
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Hypervolemia
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-Indication for hemodialysis and ultrafiltration
-Associated with hither morbidity, mortality, and no return to renal function -Hemodialysis is not very available to veterinary patients! -Polyuric patient is easier to manage |
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Furosemide and Hypervolemia
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-Inhibits Na/K/2Cl ATPase in thick ascending loop of henle
-Decreases cellular energy requirements -Increases urine flow to relieve an obstruction -No improvement in mortality or need for dialysis -Has been documented to convert oliguria |
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Mannitol and Hypervolemia
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-Osmotic diuretic
-Decreases cell swelling -Flushes tubular obstructions -Free radical scavenger -Not effective in preventing Acute Kidney Injury |
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Dopamine and Hypervolemia
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-Renal dose of dopamine results in renal vasodilation
-Increases renal blood flow -No proven benefit -Potential cardiotoxicity in critically ill patients -Not currently recommended in Acute Kidney INjury |
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Dialysis Indications
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1. Symptomatic uremia
2. Acidosis 3. Hyperkalemia 4. Volume overload 5. Azotemia refractory to medical management |
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Dialysis
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-Works based on concentration gradients
-Helps remove accumulated toxins --uremic toxins --accumulated water -Corrects acid/base abnormalities -Does not fix the kidney! Just gives the kidney time to heal -Can add different things to the dialysate to pull specific things out of the filtrate |
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Peritoneal dialysis
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-Uses peritoneum as semi-permeable membrane
-Pump fluid into the abdomen and allow exchange, then drain fluid -Low-tech approach -Can have multiple complications, putting fluid and dextrose directly into the abdomen! --peritonitis in 25% of patients --Excessive protein loss --pleural effusion |
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Hemodialysis
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-Uses synthetic semi-permeable membrane
-IHD or CRRT methods, no difference in survival rate between methods -40-60% survival rate in patients -Good for lily, ethylene glycol, currant or pyelonephritis treatment |
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Intrinsic Acute Kidney Injury Prognosis
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-Poor prognosis
-Need to intervene with small injuries before the animal becomes uremic -Canine mortality: 50% -Feline mortality: 47% -Hospital acquired canine mortality: 62% -Most deaths were in oliguric patients |
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Renal Recovery
|
-Takes time to repair the kidney
-Hematopoietic stem cells from the bone marrow repopulate and repair the damaged kidney cells -Hematopoietic cells help facilitate repair of injured tubular cells and microvasculature |
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Long Term Outlook for Intrinsic Acute Kidney Injury
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-19% of dogs and 25% of cats showed full recovery of renal function
-Usually took over 2 weeks for recovery, sometimes 60 days -Half of dogs and cats had persistent azotemia and chronic renal failure --kidneys never go back to normal, but animal feels fine -Survival times are often more than 2 years --variable timeframe |
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Acute Kidney Injury Conclusions
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-Potentially reversible if treated early
-Aggressive treatment and monitoring is recommended -Initiate dialysis early! -Conversion from oliguria may allow for easier patient management --Mannitol and furosemide can help -Prognosis is guarded, 45-60% mortality rate |
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When to refer Kidney patients
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-Refer EARLY!
-Any oliguric patient, needs 24 hour monitoring -Imaging should be performed by a radiologist -Hypervolemia is common, stop fluids! --do not give fluids and lasiks! --goal is to restore renal perfusion -Refer if owners are interested in dialysis |
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Chronic Kidney Disease
|
-Irreversible and progressive loss of renal function
--cannot be fixed, cannot increase the number of nephrons in the kidney -Can make patients feel better, but cannot fix them -Lots of breed predispositions |
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Causes of Chronic Kidney Disease
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-Most often unknown cause, by the time chronic kidney disease is present, inflicting cause is gone
-Infection -Inflammatory disease -Ischemia -Chronic obstruction -Vascular issues -Congenital causes |
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Self-perpetuation of Chronic Kidney Disease
|
-Once renal injury occurs, progressive damage follows
-Proteinuria, oxidative damage, hypoxia, glomerular injury -Occurs in response to damage to kidney tissue -Kidney cannot create new nephrons, can only increase the function of the ones already present -Response is to hypertrophy remaining nephrons |
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Glomerular Hypertrophy
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-Increased cell size or length of tubule
-increased function of all segments of the nephron -Glomerular hypertension occurs --capillary hydrostatic pressure increases, allows GFR to stay the same --causes hyperfiltration, more work being done by the healthy nephrons --can lead to proteins leaking out, proteinuria |
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Glomerular Hypertension
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-Increases GFR
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Glomerular hyperfiltration
|
-increased pressure in the glomerulus to maintain GFR
-Attempt to normalize the GFR -Results in proteinuria, proteins are forced through glomerulus -Scarring of the glomerulus and glomerulosclerosis --causes leaks, proteins can leak out -Results in accelerated progression of chronic kidney disease |
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Patchy ischemia of the Kidney
|
-Variable functions of nephrons
-As nephrons start to die due to ischemia, GFR should decrease -Remaining nephrons increase function, GFR is maintained --single nephron GFR increases -Results in glomerular hypertension and glomerular hyperfiltration -RAAS is activated -Good short-term fix, terrible long-term fix -Goal is to slow damage -50% reduction in renal mass results in 20% decrease in GFR --not proportional change! |
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Reduction in renal mass
|
-Results in smaller reduction in GFR
-individual nephrons start to filter more -Results in proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis -Progresses chronic kidney disease |
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Tubular Defects
|
-Injury or issue can be localized to a section of the nephrons
-Proximal tubule defects: --fanconi syndrome, glucosuria, cystinuria |
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Fanconi Syndrome
|
-Issue with proximal tubule
-Patient is unable to absorb glucose, amino acids, or phosphate from the filtrate -Can be congenital |
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Renal Tubular Acidosis
|
-Metabolic academia with abnormal renal acid-base function
-Kidneys are main site for bicarbonate absorption/recycling -Tubular acidosis results in systemic acidosis -Proximal renal tubule acidosis: type II --cannot resorb bicarbonate --distal tubule will resorb most, but not all -Distal renal tubule acidosis: type I --ineffective H secretion, body cannot get rid of H ions --urine will be alkaline |
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Nephrogenic Diabetes Insipidus
|
-Results from absent ADH receptors
-Congenital: abnormal or absent ADH receptors (rare) -Acquired: antagonization of ADH receptors (common) -Water is resorbed without salt in the collecting duct, works with ADH and ADH receptors -Problem in distal tubule will result in water staying in the tubule -Animal will have marked PU/PD and hyposthenuria |
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Clincial signs of Chronic Kidney Disease
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-Early signs: none
-PU/PD -Isosthenuria -By the time clinical signs manifest, majority of renal function is lost --takes A LOT of nephon loss to see isosthenuria (66%) -Vomiting, anorexia, diarrhea -Weightloss -GI signsa re due to uremia |
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Physical exam of a patient with Chronic Kidney Disease
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-Hydration status (animal is prone to dehydration)
-Body condition score -Renal palpation -Fundic examination (look to see if the retinal is coming off the back of the eye) --check BP -Bone and facial palpation |
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Questions to ask with Chronic Kidney Disease
|
-Duration of PU/PD
-Severity of symptoms -Appetite -Weight loss -Current diet and calorie intake |
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Initial diagnosis of Chronic Kidney Disease
|
-Chemistry panel with electrolytes
-CBC and reticulocytes (look for anemia) -Urinalysis --urine culture and protein:creatinine ratio -Blood pressure -Urinary imaging --radiographs and abdominal ultrasound are ideal --get radiographs at start and use as baseline to assess change |
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BUN and Creatinine
|
-NOT uremic toxins!
-Markers for other molecules that are retained/excreted --Uremic toxins are assumed to increase at the same levels as BUN and creatinine -Do not cause patients to feel sick -Factors other than kidney damage can cause BUN and creatinine to change levels --Creatinine: decreased with muscle loss, not reliable in face of muscle loss --BUN: increased with increased protein intake, decreased with malnutrition and low protein intake or synthetic liver failure |
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Staging Chronic Kidney Disease
|
-Tiered classification scheme helps provide info on current state
-Gives info for prognosis -Can inform treatment goals -Gives a standard for research |
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IRIS kidney Staging
|
-based on creatinine levels
-Stage 1: --dog= less than 1.4, cat = less than 1.6 -Stage 2: --dog= 1.4-2.0, cat = 1.6-28 -Stage 3: --dog= 2.1-5.0, Cat = 2.9-5.0 -Stage 4: --dog= more than 5, Cat= more than 5 |
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IRIS Substages
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-Proteinuric substage
--based on amount of protein in urine -Hypertension substage --based on BP |
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Chronic Kidney Disease treatment
|
-Correct complications of decreased GFR
-Minimize uremia, makes patient feel better -Provide adequate nutrition -Maintain acceptable quality of life |
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Uremia and uremic toxins
|
-Uremic toxins are products of protein metabolism
-Most important toxins are unknown -BUN and Creatinine are markers for toxin retention --NOT toxins themselves -Chronic Kidney Disease patients acclimate to azotemia --have milder clinical signs for the degree of azotemia compared to acute kidney injury |
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How to deal with uremia
|
-GFR cannot be increased, cannot grow new nephrons
-Avoid pre-renal azotemia! -maintain hydration, prevent a decrease in GFR via hypovolemia --feed canned food, add water to canned food --feeding tubes if needed --SQ fluids, but can be detrimental, only give if patient cannot maintain hydration on their own -Fluids will not help GFR, but will prevent dehydration and pre-renal azotemia |
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Nutrition and Uremia
|
-Give prescription diet
-Restrict protein, phosphorous, and Na -Reduces risk of uremic crisis by more than 70% -Slows progression of chronic kidney disease -Lower mortality, better quality of life |
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GI complications of Uremia
|
-Anorexia
-Nausea -Gastric hyperactivity, reduced excretion of gastrin -GI ulceration due to increased acidity --oral and GI mucosal ulcers |
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Treatment for Uremia
|
-Antacids: proton pump inhibitors are best
--omeprazole, NOT famotidine -Sucralfate for GI ulcers -Anti-emetics: maropitant, ondansetron, metoclopramide -Appetite stimulants: Mirtazipine |
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Hyperphosphatemia
|
-Serum phosphorous concentration is inversely related to the GFR
--decreased GFR, more phosphorous is retained in bloodstream -Inhibitis calcitriol synthesis via 1a-hydroxylase --cannot convert vitamin D to active form -Hyperphosphatemia stimulates PTH synthesis --PTH is uremic toxin, stimulates FGF-23 release, body’s response to get rid of extra phosphorous -Begins process of renal secondary hyperparathyroidism |
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Pathogenesis of Chronic Kidney Disease
|
-Early chronic kidney disease decreases GFR, leads to reduced
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Pathogenesis of Chronic Kidney Disease
|
-Early chronic kidney disease decreases GFR, leads to reduced Phosphorous excretion and increased P serum levels
-Increased P serum levels causes increased PTH and increased FGF-23 --FGF23 increases renal excretion of P and decreases calcitriol synthesis, attempts to normalize P levels |
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Renal Secondary Hyperparathyroidism
|
-Chronic Kidney Disease progresses and fewer nephrons remain functional
-Nephrons have diminished response to FGF23 and PTH -Decreased capacity for calcitriol synthesis -PTH increases, calcitriol synthesis increases to increase Ca concentration -More P is excreted -Mechanism becomes ineffective due to decreased functional renal mass and decreased GFR -Hyperphosphatemia results, is persistent -Bone is replaced with fibrous tissue as Ca is released for other purposes -Fibrous osteodystrophy |
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Hormone increases with Renal Secondary Hyperparathyroidism
|
-Elevations in PTH come before hyperphosphatemia
-FGF-23 is increased earlier than PTH -PTH and FGF-23 are both increased before Phosphorous |
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Preventing Renal Secondary Hyperparathyroid Syndrome
|
-Correct hyperphosphatemia!
--diet, give less phosphorous --phosphate binders, must be given with food and forms non-absorbable complexes with phosphorous -Can give calcitriol supplementation to dogs (no evidence that it works in cats) --P needs to be less than 5 before starting supplementation, otherwise P absorption will also be stimulated --very hard to control P levels enough to give calcitriol |
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Acidemia
|
-Tubules cannot process bicarbonate or toxins
-Metabolic Acidosis --uremic toxins --Dehydration can lead to lactic acidosis |
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Treatment for Acidemia
|
-Neutral pH diet
-Alkali supplementation, give a buffer --NaBicarbonate --K-citrate |
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3 Things that happen with Hyperphosphatemia
|
1. Inhibits production of calcitriol
-Inhibits enzyme that converts calcidiol into calcitriol 2. Stimulates PTH release 3. Stimulates FGF-23 When hormones are present, secondary parathyroidism appears PTH releases Ca from bone, replaces with fibrous tissue |
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Potassium Disorders
|
-Hypokalemia is very common, esp. in cats
--cannot resorb K that is filtered, is peed out -Can supplement orally --K-gluconate, K-citrate -Can give K IV -Hyperkalemia is an emergency situation if severe! More than 7 is severe --will make patient bradycardic and heart can stop --restrict dietary K --Give K binder |
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Anemia
|
-Lack of EPO production from the kidney results in non-regenerative anemia
--Normocytic, normochromic -GI ulcers can lead to blood loss --will be regenerative anemia -RBCs have shortened lifespan with uremia -Treat with Darbepoietin --treat before they are clinical --takes about 3 weeks to respond |
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Darbepoietin
|
-Synthetic human hormone EPO
-Has risk of an immune response, is a human hormone --animal will produce antibodies and hormone will be rendered ineffective -Hypertension is a possible side effect -Fe supplementation must also be administered --may cause anaphylactic reaction -Takes about 3 weeks to have desired change in PVC -Once started, animal is on for the rest of its life --can be tapered to maintenance dose, but cannot be stopped |
|
|
Hypertension and kidney disease
|
-Should be monitored often
-Can do fundic exams -Treat with ACE inhibitors (enalapril, benazepril) or Ca channel blockers (Amlodipine) |
|
|
Proteinuria
|
-Caused by glomerular and tubular injury
-Can be a manifestation of Chronic Kidney disease, also Accelerates progression of Chronic Kidney Disease -Treat by restricting protein in diet --decreases SNGFR and glomerular hypertension --slows progression of CKD, less protein going in results in less protein going out -Control hypertension -Can give ACE inhibitor, prevent constriction of efferent arteriole, will lower pressure in glomerulus and decrease amount of protein that is pushed through --GFR will also decrease, but is probably a good thing (reducing from hyperfiltration) |
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|
Treatment goals of Chronic Kidney Disease
|
-Goals change with IRIS stage
-Recheck often and regroup, restage -Do not give vitamin supplementation |
|
|
Azodyl
|
-Probiotic
-Minimizes urea absorption -Not effective, urea is not what makes patients feel sick --UREMIA is what makes patients sick -Does not matter -Only use if patient has everything else under control and fixed --almost not worth it -DO NOT USE AS PRIMARY TREATMENT |
|
|
Monitoring Chronic Kidney Disease
|
-Monitor every 4 months, minimum
-New treatment may be needed as time goes on -Recheck BP 1 week after meds are adjusted -Recheck UPC 2-4 weeks after meds are adjusted -30% of patients develop UTIs, most are asymptomatic --routine urine cultures are a good idea |
|
|
Prognosis for Chronic Kidney Disease
|
-Depends on stage
-Higher stage, shorter prognosis -Animal will progress, but try to slow it |
|
|
Treatments for Chronic Kidney Disease
|
-Cats can get transplants
-Transplants in dogs is limited -Chronic hemodialysis -Stem cell therapy? |
|
|
Stem cell therapy for Chronic Kidney Disease
|
-Still in trials |
|
|
Etiology of UTI
|
-Most are bacterial
-Fungal is rare -Viral UTI is super rare -27% of dogs will develop at UTI at some point -Most common source is ascending urethral infection -Hematogenous source is less common |
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|
Mechanisms that prevent UTI
|
-Urination
-Anatomic barriers that prevent bacterial from ascending into the bladder --length of the urethra --Urethral sphincted -Bladder mucosa prevents bacterial attachment with glycosaminoglycans -Urine is hostile to bacteria, poor environment for growth |
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|
Risk factors for UTI
|
-Disruption of Innate defenses
-Congenital abnormalities --recessed vulva --ectopic ureter -Urinary incontinence -Altered urinary composition --isosthenuria, dilutes bacteriostatic substances --Chronic kidney disease --Glucosuria -Systemic immunosuppression -Urethral catheterization |
|
|
Systemic immunosuppression and UTI
|
-Increased risk factor for UTIs
-Hyperadrenocorticism -Diabetes -Hyperthyroid cats -Neoplasia |
|
|
Urethral catheterization and UTIs
|
-BIG predisposing factor for UTI
-Nosocomial infections, resistant nasty infections -Important to have a closed collection system with catheters! -Routinely clean catheters |
|
|
Clinical signs of Lower UTI
|
-Bacterial cystitis
-“Noisy” lower urinary tract signs -Pollakiuria and stranguira -Hematuria -No polyuria, urine has already been made -NOT pathognomonic for infection!!! |
|
|
Pollakiuria
|
-Stranguria
-Increased frequency of urination -Decreased volume of urine -May or may not have blood in urine -Urine stream may be interrupted -Normal thirst |
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|
Polyuria
|
-No stranguria
-Moderately increased frequency of urination -Increased volume of urine per voiding -No hematuria -Normal urine stream -Increased thirst |
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|
Pyelonephritis
|
-Infection of the renal parenchyma
-Usually an ascending infection from bladder, up ureters, to kidney -May not have signs of lower UTI, may have already cleared -Intrinsic acute kidney injury! |
|
|
Clinial signs of Pyelonephritis
|
-Renal pain
-Fever -Lethargy, malaise, anorexia -PU/PD -Acute kidney injury and symptoms of uremia -In immunosuppressed patients, will not have lower UTI signs |
|
|
Prostatitis
|
-Intact male dogs
-Assume present in any intact male dog with UTI --prostate communicates with urethra -Possible, but less common in castrated dogs -Can produce systemic illness, looks similar to pyelonephritis -Requires specific antibiotics that cross blood-prostate barrier |
|
|
Rectal Exam
|
-ALWAYS needed!
-Only times to not do a rectal: --animal does not have a rectum --practitioner does not have any fingers |
|
|
Lower UTI DDx
|
-Urolithiasis
-Neoplasia -Sterile cystitis -FLUTD -Micturition disorders -Neurologic disease |
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|
Diagnosing UTI
|
-Urinalysis MUST be performed
-Cystocentesis is preferred method -Free catch will give 85% false positive -Catheterized will give 26% false positive -Do not do cystocentesis if there is a coagulopathy, thrombocytopenia, or bladder neoplasia |
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|
Urine Testing
|
-Specific Gravity
-pH -Glucose -Blood -Ignore urobilinogen, nitrate, leukocytes, USG on the dipstick -Cytology will give RBC, WBC, bacteria, casts, crystals |
|
|
Urine Culture and Sensitivity
|
-Should be performed on ALL patients with suspected UTI
-Documents organism, guides antibiotic therapy -Provides quantification of severity of infection |
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|
MIC testing for Urine
|
-Provides concentration where growth is inhibited
-Know which concentration of antibiotic stops growth of bacteria -Useful for determining dose of antibiotic |
|
|
Other diagnostics for UTI
|
-Urinary ultrasound:
--pyelonephritis, ureteral obstruction, urolithiasis, Transition cell carcinoma, prostatitis, prostatic neoplasia -Prostatic wash: --needed to investigate infection or neoplasia if urine culture is negative -Cytoscopy: --biopsy, culture, visualization of urethra, vestibule, vagina, etc. -CBC/Chem: --if pyelonephritis or prostatitis is suspected |
|
|
Asymptomatic Bacteriuria
|
-identification of bacteria within urine in a patient without symptoms of disease
-Patient has bacteria, but is not affected -Probably due to non-pathogenic bacteria strain --E. coli, enterococcus -Occurs in 29% of cats and 9% of dogs -Probably do not have to treat it, unless there is some other disease process going on concurrently |
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|
Encrusted Cystitis
|
-Bladder wall ulceration
-Mineral material is deposited in the bladder -Corynebacterium urealyticum --need 72 hours to culture -Staphylococcus |
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|
Uncomplicated UTI
|
-No structural, neurologic, or functional abnormalities
-Normal dog that is unlucky and got a UTI |
|
|
Complicated UTI
|
-Infection in patient with structural, neurologic, or functional problems
-Predisposes patient to persistent or recurrent infection -Predisposes treatment failure, makes therapy less likely to succeed -Chronic kidney disease -Diabetes M -Stones -Incontinence -Cats -Male dogs, intact females -Pyelonephritis and prostatitis |
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|
Choosing antibiotics for UTI
|
-Complicated vs. uncomplicated
--uncomplicated: 10-14 days --complicated: 4-6 weeks -Site of infection --kidney vs. bladder vs. prostate -Use “weakest” class of antibiotics based on susceptibility results |
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|
Antibiotics that can be used to treat prostate
|
-Fluoroquinolones
-Trimethoprim sulfate -Chloramphenicol -Macrolides |
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|
“Wimpy” antibiotics for UTI treatment
|
-1st tier: Amoxicillin, cephalexin, TMS
-2nd tier: clavamix, 2nd and 3rd generation cephalosporins, fluoroquinolones, nitrofurantoin -3rd tier: aminoglycosides, chloramphenicol. Carbopenems |
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|
Using MIC results for UTI
|
-Not typically needed for uncomplicated UTI
-Use with known urine concentration of antibiotics to determine dosing schedule |
|
|
Recurrent UTIs
|
-Reinfection: 2nd UTI within 6 months with a different organism
-Relapse: recurrence within 6 months with the same organism --suggests failure to completely eliminate the infection initially -Refractory: Persistent positive urine culture during treatment with appropriate antibiotis |
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|
Fungal UTI
|
-Uncommon in veterinary medicine
-Candida is most common --does grow on aerobic culture plates -History and PE findings are similar to bacterial UTI -Mostly in immunosuppressed patients -Treat if animal has clinical signs or organisms are persistent --Fluconazole is drug of choice for treatment --amphotericin B can also be used, is nephrotoxic though --IV clotrimazole can be used in refractory cases |
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|
Monitoring response to UTI therapy
|
-Clinical signs resolve within 2-3 days
--Dramatic improvement -Urine culture can be checked 5-7 days into treatment -Growth on urine culture should adjust treatment -Re-check culture 7-10 days after antibiotics are over -3 urine cultures! Really only with recurrent or complicated UTI |
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|
Urethral catheters
|
-Do not culture the catheter tip!
--has a biofilm -Wait 24-48 hours after removing a catheter to culture --let animal pee out biofilm before taking sample |
|
|
UTI treatment failure
|
-Wrong drug, wrong dose, wrong duration
-Drug does not reach sufficient concentration in the urine --GI disease, renal disease -Nidus is present for bacteria --stone, suture, neoplasia, urachal remnant -Anatomic or functional abnormalities or urinary tract -Homeopathic remedies do not really work for UTIs |
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|
Recurrent UTI infection
|
-Little evidence exists to support protocols |
|
|
Nephrolith
|
-Kidney Stone
|
|
|
Ureterolith
|
-Stone in the ureter
|
|
|
Cystolith
|
-Bladder stone
-Cystic calculi |
|
|
Urethrolith
|
-Stone in the urethra
|
|
|
Urolith Pathogenesis
|
-Urine contains thousands of dissolved solutes
-Some solutes form insoluble complexes --insoluble complexes form micro-crystals -Generally unknown why stones develop -Microcrystals combine to form macrocrystals, macrocrystals combine to form stones |
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|
Inhibitors to crystallization
|
-Undersaturation, not enough to form a crystal
-Inhibitory substances -Lack of scaffolding surface |
|
|
Relative supersaturation
|
-Solubility of an individual substance within urine
-Determined by concentrations of calculogenic molecules, inhibitory factors, or pH -Mathematical number, can be calculated -Relative supersaturation of more than 1 suggests supersaturation, likely crystallization -Relative supersaturation less than 1, undersaturation and unlikely to crystalize -Cannot use to supersaturation of one solute to calculate the value for a different solute |
|
|
“Stone”
|
-Can change in construction
-Forms in layers --if environment changes, layer that gets laid down next might be different |
|
|
Crystalluria is not a disease!
|
-not every crystal will precipitate to form a stone
-No treatment is necessary unless stones or urethral plugs have formed -Some crystals form naturally in urine --calcium oxalate --struvite -Some crystals need further evaluation --urate --cystine --xanthine |
|
|
Normal crystals in urine
|
-Struvite
-Calcium oxalate -Just because crystals are present does not mean a stone will form |
|
|
Abnormal crystals in the urine
|
-Urate
-Cystine -Xanthine -need further evaluation |
|
|
Historical info for patients with stone
|
-Variable, not specific to type of stone
-Lower urinary tract signs --pollakiuria --stranguria -Urethral obstruction -Ureteral obstruction and uremia |
|
|
Diagnostic Evaluation of Uroliths
|
-Abdominal radiograps
-Ultrasound --Best used together! Some stones do not show up on radiographs --Radiographs are not good for finding ureteral stones, too narrow/small -Urinalysis -Urine culture -Bloodwork --CBC/chem etc. |
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|
Uroliths on Abdominal Radiographs
|
-Calcium oxalate show up well
-Strivute are likely to be seen -Cysteine and urate stones will probably not be seen on radiographs -Cannot determine type of stone based on appearance on radiographs |
|
|
Uroliths on Abdominal Ultrasound
|
-Ureteroliths may not be seen on radiographs
-Might be able to see renal pelvis and ureteral dilation -Look for other causes for dysuria --neoplasia |
|
|
Urinalysis for Urolith diagnosis
|
-Can give a clue as to why the patient is forming a stone and what type of stone might be present
-Need to do at room temp! --crystals will precipitate in cool temps -Failure to see crystals does not mean that a stone is not present -Can help, but is not definitive |
|
|
Urine culture for Urolith Diagnosis
|
-Infection can cause a stone or infection can be caused by a stone
-Stone is an excellent nidus for bacteria |
|
|
Determining type of Urolith present
|
-Some breed predispositions exist
-Urinalysis can sometimes be helpful --Sometimes crystal can be misleading, not the same type as the stone present -Response to therapy can be indicative -Stone analysis is the only true method |
|
|
Calcium Oxalate Crystals
|
-Very common stone
--98% of stones in cats are CaOx --more than 50% of dog ureteroliths and nephroliths -Pathogenesis is unknown --probably multifactorial -Systemic hypercalcemia -Hypercalciuria -Hyperoxaluria from increased dietary intake or loss of oxalate-degrading bacteria |
|
|
Calcium Oxalate Monohydrate
|
-Forms with ethylene glycol toxicity
-Can form in patients with chronic kidney disease |
|
|
Calcium Oxalate Urolith Treatment
|
-NOT amenable to medical dissolution, cannot be dissolved
-have to remove surgically or ednoscopically -Therapy is aimed at prevention -Solubility is unaffected by urine pH -Acidosis causes hypercalciuria, may increase relative supersaturation |
|
|
Calcium Oxalate prevention
|
-Best method of treatment is prevention
-Correct systemic hypercalcemia -Increase the water intake, can decrease relative supersaturation --dilute urine decreases the concentration of Ca, increases voiding -Put animal on prescription diet, canned food with water -Target urine pH 6.5-7.0 -Target USG less than 1.020 |
|
|
Struvite Uroliths
|
-Magnesium ammonium phosphate (triple phosphate)
-Dogs: “infection stones” --have urease producing bacteria -Cats: sterile production |
|
|
Urease producing Bacteria
|
-Staphylococcus, Proteus, seudomonas, Klebsiella, Corynebacterium, Ureaplasma
-increases urine ammonia concentration |
|
|
Struvite Urolith Treatment
|
-Can be dissolved!
-Prescription dissolution diet -Antibiotics needed if there is an infection (dogs) --treat 1 month beyond radiographic resolution of stone -Urine should be pH less than 7, needs to be acidic --prevent ideal environment for pracipitation -Urine specific gravity should be less than 1.020 |
|
|
Struvite Treatment cats vs. dogs
|
-Cats: average time of dissolution is 13 days with the right diet |
|
|
Struvite Prevention
|
-Prevent UTI and bacteria from getting into area
-Dietary therapy is needed --urine pH less than 6.5 --urine specific gravity less than 1.020 -Urine acidifiers may ne needed |
|
|
Purine Uroliths
|
-Uric acid (urate) crystals are most common |
|
|
Causes for Purine Uroliths: Mutations
|
-Mutations are most common
--causes defect in urate transport in Dalmations and bulldogs -Have normal levels of enzymes, but the enzymes are mutated -Transport of uric acid into hepatocytes is reduced -Hyperuricosuria develops |
|
|
Causes for Purine Uroliths: Hepatic Dysfunction
|
-Portosystemic vascular abnormalities
-Could be congenital liver failure or acquired synthetic liver failure -Liver does not process purines, purines are excreted in the urine and cause stones -Hyperammonemia causes hyperammonuria and hyperuricuria -IN dogs with liver shunts, look for urate stones |
|
|
Purine Uroliths in Cats
|
-Unknown cause |
|
|
Treatment for Urate Uroliths
|
-Can be dissolved |
|
|
Allopurinol
|
-Xanthine oxidase inhibitor
-Helps prevent purines from becoming uric acid -Will see xanthine accumulate |
|
|
Xanthine Uroliths
|
-Typically seen in dogs being treated with allopurinol
--need to change therapy -Can also be seen in Cavalier King Charles -Most are secondary to allopurinol therapy |
|
|
Cystine Uroliths
|
-Cystine is dimer of cysteine amino acid
-Cystine is freely filtered across glomerular basement membrane, reabsorbed in proximal tubule -If proximal tubule is not working properly, will get cystinuria -Occurs in animals with genetic mutations, intact animals |
|
|
Cystine Urolith Treatment
|
-Can dissolve |
|
|
Tipronin
|
-Medical therapy for Cystine uroliths
-Prevented urolith recurrence in 86% of dogs |
|
|
Calcium Phosphate Uroliths
|
-Less common, very uncommon
|
|
|
Silica uroliths
|
-93% of affected dogs are male |
|
|
Dried solidified blood uroliths
|
-Reported in cats
-Not crystalline or gelatinous, just a dried rubbery blood clot -Not common, but happen -Unlikely to dissolve -Can be hard to diagnose, cannot find on radiographs |
|
|
Urolith Removal
|
-Move stone back into the bladder via catheterization |
|
|
Urohydropropulsion
|
-Voiding uroliths
-Can be done for small stones -Sedate animal, fill up bladder, squeeze bladder, and push stone out -Female dogs have highest success rates |
|
|
Intracorporeal Lithotripsy
|
-Use a laser to break up uroliths
-Energy breaks up stone -Can be used for uroliths in urethra, badder, possibly ureters and kidneys -Effective in 87% of patients |
|
|
Extracorporeal Shock Wave Therapy
|
-High energy shockwaves generated outside the body and focused on the stone
-In dogs can use in kidney and ureter -In cats can be done in ureter, NOT kidney |
|
|
Minimally invasive techniques for urolith removal
|
-Transvesicular percutaneous cystolithotomy
-Cystoscopy and basket retrieval |
|
|
Urolith post-procedure follow-up
|
-Radiographs to confirm complete removal
-Culture stone and urinary bladder in patients with negative urine culture -24% of patients have a positive culture despite negative UCS |
|
|
Ureterolithiasis
|
-One will not cause azotemia or isosthenuria because other kidney is functioning and voiding
-Will cause intrinsic damage -Diagnose with radiographs and abdominal ultrasound -Contrast studies may be needed -Renal pelvis and ureteral dilation may take days to develop -Clinical signs range from absent to severe uremia -The longer a full obstruction is there, the more damage will happen -Also cannot ignore partial obstruction, will also have loss of kidney function |
|
|
Treatment of Ureteroliths |
-medical management: IV fluids, mannitol, flucagon, prazosin
--ineffective, does nto work -Ureterotomy: best for a single stone within ureter -Nephrostomy tube: short-term fix -Ureteral Stents -Subcutaneous ureteral bypass |
|
|
Partial ureteral obstruction from urolith
|
-IT IS A PROBLEM! |
|
|
Goals of Dietary Management of Chronic Kidney Disease
|
-Supply daily calorie, protein, and micronutrient requirements
-Minimize disturbances associated with excesses or losses of nutrients -Modify progression of Chronic Kidney Disease -Need to avoid excess nutrients that animal cannot get rid of --phosphorous --protein --potassium |
|
|
Nutritional Adequacy of a diet
|
-Ideally should meet species and life stage nutritional requirements of the patient
--puppies, adults, and old dogs have different needs -Nutrient restriction in organ failure is an issue of tolerance -Nutritional restriction: how much? |
|
|
Causes of Weight Loss in Chronic Kidney Disease
|
-Metabolic derangement is seen with chronic disease
--animal is muscle-wasted, skinny -GI side-effects --ulcers -Therapeutic diets -Decreased Appetite |
|
|
Strategies to prevent Weight loss in Patients with Chronic Kidney Disease
|
-Appropriate diet choice
-Careful introduction of the new diet --needs consistency -Give clients a caloric goal and monitor response -Treat conditions that can lead to anorexia --anti-nausea etc. |
|
|
Conditions associated with Inappetence
|
-Dehydration
-Electrolyte disturbances -Pain -Nausea -B vitamin deficiencies -Medications and side effects -Environmental stress -Unpalatable diets -Learned food aversion |
|
|
Protein Restricted Diet with Chronic Kidney Disease
|
-No evidence that restricting dietary protein protects kidneys in cats and dogs
-Dietary restriction can be necessary to alleviate clinical signs of uremia -Some degree of protein restriction may be beneficial for patients with proteinuria |
|
|
Phosphorous in diet for Chronic Kidney Disease
|
-Major role in progression of CKD
-Direct data only exists in cats, evidence exists in dogs -Hyperphosphatemia is a big issue --secondary hyperparathyroidism, plays a role in CKD progression -Can feed P restricted diets -Can use intestinal phosphate binders |
|
|
Phosphate Binders
|
-Aluminum Salts
-Calcium salts -Epakitin -Lanthanum carbonate |
|
|
Target serum phosphorous concentration
|
-Normal range: 3-6.6
-Stage II: less than 4.5 -Stage III: less than 5 -Stage IV: less than 6 |
|
|
Calcitriol
|
-Active form of Vitamin D
-Reduced levels of calcitriol in CKD because of decreased conversion of calcidiol to calcitriol in kidneys -May be a factor that promotes renal secondary hyperparathyroidism -Consider an issue only if P levels are normal --can easily cause hyperphosphatemia and hypercalcemia |
|
|
Renal Secondary Hyperparathyroidism
|
-Need to treat hyperphosphatemia
-May give Vitamin D supplementation (calcitriol) -Ca supplementation should not be necessary unless pet is eating home-prepared diet |
|
|
Potassium
|
-30% of cats with hypokalemia have chronic kidney disease
-Acidifying diets with marginal amounts of K have been associated with CKD development -IN dogs with CKD can be normal, high, or low -Supplementation of K in cats with CKD and hypokalemia will stabilize or improve renal function -Unclear if hypokalemia is a cause or consequence of CKD |
|
|
Adverse Effects of Chronic Metabolic Acidosis
|
-Anorexia
-Nausea -Vomiting -Weakness -Muscle wasting -Weight loss |
|
|
Metabolic Acidosis and Chronic Kidney Disease
|
-80% of cats with CKD had metabolic acidosis
-No evidence that fixing metabolic acidosis with alkalinizing therapy will change progression of CKD |
|
|
Systemic Hypertension and Chronic Kidney Disease
|
-Hypertension is well-recognized complication of canine and feline CKD
-Unlikely to be Na responsive -Decrease Na gradually over 1-2 weeks |
|
|
Anti-oxidants and Chronic Kidney Disease
|
-No solid information on how much or how little anti-oxidants are needed
|
|
|
Evidence for efficacy of Therapeutic diet as treatment for Chronic Kidney Disease
|
-Significant difference between two groups of dogs, one fed prescription diet and one fed conventional diet
-Same findings for a group of cats --serum phosphorous and PTH was decreased in 76% of cats on CKD diet |
|
|
Interpretation of clinical trials for Chronic Kidney Disease diet assessment
|
-Therapeutic diets fed to dogs and cats have potential to delay onset of uremic crisis and mortality due to renal causes
-Don’t know which aspects of diets are beneficial |
|
|
Energy intake in animals with Chronic Kidney Disease
|
-Sufficient energy needs
-Prevent endogenous protein catabolism --will result in malnutrition and azotemia |
|
|
Selection parameters for a diet
|
-Degree of renal dysfunction
-Concurrent diseases -Body condition -Appetite and dietary preferences |
|
|
Protein restriction
|
-Not necessary until tolerance becomes an issue |
|
|
Indications for Abdominal Radiography
|
-Disease screening
-Confirm suspected clinical disease -Differentiation of suspected clinical diseases -Staging malignancies -Case management --prognosis, treatment, response to treatment |
|
|
Radiographic Positioning
|
-Obtained at end EXPIRATION
--(thoracic are peak inspiration) -Less superimposition of structures -Longer respiratory pause, easier to catch structures -Include the entire abdomen --cranial extent: diaphragm --caudal extent: greater trochanter |
|
|
Importance of Radiographic Positioning
|
-Proper positioning is important!
-Poor radiographs are inconclusive at best --at worst, are misleading |
|
|
Evaluating the Abdomen as a whole
|
-Look at body condition
-Abdomen wall -Peritoneum -Retroperitoneum --kidneys, ureters, adrenal glands, aorta, caudal vena cava, lymph nodes, cisterna chili |
|
|
Organs routinely seen on abdominal radiograph
|
-Spleen
-Liver (cranial most aspect) -Kidneys -Urinary bladder -Prostate in intact male dogs -GI tract |
|
|
Abdominal organs NOT visualized on radiographs
|
-Gallbladder
--can be seen in cats when distended -Pancreas -Lymph nodes -Adrenal glands -Ovaries -Uterus -Prostate in cats or neutered dogs |
|
|
Serosal Detail
|
-Subject contrast
-Differences in radiopacity affects visualization of abdominal organs -Most organs in abdomen are soft-tissue opaque, low subject contrast --everything blends together --Low subject contrast -Fat prevents silhouetting of adjacent structures --increases subject contrast, increases serosal detail |
|
|
5 radiographic opacities
|
-Metal
-Bone -Soft tissue/fluid -Fat -Air |
|
|
Definition of Serosal Detail
|
“The ability to see the serosal margins of the abdominal visceral due to the presence of outlining fat”
|
|
|
Causes of decreased serosal detail
|
-Poor technique, underexposure or motion artifact
-lack of abdominal fat -Immaturity (due to brown fat) -Peritoneal effusion -Mass effect: mass or enlarged structure results in displacement and silhouetting of adjacent organs -Peritonitis -Carcinomatosis |
|
|
Mottled Serosal Detail Differential Diagnoses
|
-Peritonitis
-Carcinomatosis -Peritoneal effusion (small volume or focal) -Abnormal fat --steatitis, fat inflammation --fat necrosis -Artifact --wet hair, subcutaneous edema or emphysema |
|
|
Determining the cause for poor serosal detail
|
-Peritoneal or retroperitoneal source
-Look at abdomen as a whole --abdominal distension? -Abdominal wall detail -Mass effect, organ displacement -Extra-abdominal signs |
|
|
Peritoneal Effusion and lack of serosal detail
|
-Very poor serosal detail
-Cannot see the margins of any organ -Distended abdomen -Generalized increase in abdominal soft-tissue opacity --abdomen looks very white |
|
|
Retroperitoneal Effusion
|
-Looks streaky, whispy soft-tissue opacities
|
|
|
Increased serosal detail
|
-Indicates pneumoperitoneum, free peritoneal air
-Air highlights our outlines adjacent structures -Enhanced serosal details leads to increased subject contrast |
|
|
Pneumoperitoneum
|
-Free air in the abdomen
-Often easiest to see in the cranial abdomen --least dependent, most upright region of the abdomen -Look adjacent to the diaphragm, between liver lobes -Can see free gas bubbles or pockets --not associated with GI tract or other organs -Will be able to see “both sides” of the diaphragm -Often hard to find on radiographs |
|
|
Horizontal beam Radiography for Pneumoperitoneum
|
-Increased sensitivity for detecting pneumoperitoneum
-VD view with animal in left lateral recumbency -Lateral view with animal in dorsal recumbency -Allows visualization of gas-fluid interface --on vertical beam, gas and fluid are superimposed |
|
|
Causes of Pneumoperitoneum
|
-Post-operative, 3-5 days
-Perforated viscus, especially in the GI tract -Penetrating abdominal wound -Post-abdominocentesis or cystocentesis -Very serious finding! Unless iatrogenic… |
|
|
Abdominal Mass Identification
|
-Look at location!
-Evaulate direction and degree of displacement of adjacent viscera --mass effect |
|
|
Mass Effect
|
-How a mass displaces the things around it and to what degree things are displaced
-Displacement and silhouetting of organs -Especially the displacement of the small and large intestines -Secondary to a space-occupying lesion --mass or enlarged organ -May or may not see the mass itself |
|
|
Abdominal Mass identification
|
-Can do special projections
--opposite lateral recumbent view --horizontal beam --oblique projections --compression view -Special procedures --contrast studies -Alternate imaging --ultrasound --CT, MRI |
|
|
Cranial Abdominal Masses
|
-Caudal displacement of small intestines and colon
-Can originate in: --liver --gallbladder --stomach --pancreas --spleen (portions) -Only the liver can caudally displace the stomach, the only thing that is cranial to it |
|
|
Liver Mass Effect
|
-Normal: within the costal arch
--gastric axis is parallel to ribs or perpendicular to the spine -Hepatomegaly: extends caudal to the costal arch --caudal displacement of the antrum -Only liver enlargement displaces the stomach caudally -Enlargement can be diffuse or focal -Microhepatica: small liver --cranial displacement of the antrum along gastric axis |
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|
Stomach Mass Effect
|
-gastric dilatation
|
|
|
Mid-abdominal masses
|
-Peripheral displacement of the small intestines and colon
-Small and large intestines -Spleen -Mesenteric lymph nodes -Ovary (when very large) -Uterine horns |
|
|
Splenic Mass Effect
|
-Location of splenic masses in mid-abdomen can vary
--Body and caudoventral extremity are mobile |
|
|
Caudal abdominal Masses
|
-Cranial displacement of the small intestines
--Can involve displacement of the colon -Urinary bladder -Descending colon -Uterus -Prostate -Paraprostatic cyst -Retained testicle |
|
|
Dorsal Abdominal Masses
|
-Ventral displacement of the small intestines and large intestines
-Need to figure out if it is peritoneal or retroperitoneal -Peritoneal: ovary -Retroperitoneal: kidneys, adrenal glands, sublumbar lymph nodes, muscles, vertebrae |
|
|
Fat Cats
|
-All of small intestines located in right mid abdomen
-Loose loops, not “bunched and scrunched” -Normal finding |
|
|
Roentgen Signs for Abdominal masses
|
-Location
-Number -Opacity -Size -Shape -Margin -Functional or functional implications |
|
|
CHANG lesions
|
-Differential diagnoses for abdominal masses
-Cyst -Hematoma -Abscess -Neoplasia -Granuloma -(physiologic enlargement, obstruction, organ torsion) |
|
|
DAMN IT lesions
|
-Differential diagnoses for abdominal masses
-Developmental, degenerative -Anomaly, autoimmune, artifact -Metabolic, mechanical -Neoplastic, nutritional -Infectious, inflammatory, iatrogenic, idiopathic -Traumatic, toxic |
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|
Renal Imaging
|
-Radiographs
-Contrast Radiographs -Ultrasound -CT -MRI -Scintigraphy |
|
|
Kidney location on Radiographs
|
-Retroperitoneal
-More mobile in cats -Ureters are not seen on radiographs -Right kidney is more difficult to visualize --adjacent to caudate liver lobe, silhouettes --more cranial than left kidney -Left kidney is further caudal |
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|
Abnormal kidney location on radiographs
|
-Most likely due to displacement and mass effect
-Excess retroperitoneal fat: ventral -Retroperitoneal mass: caudal -Hepatomegaly or liver mass: right kidney -Splenic mass: left kidney -Gastric distension: left kidney |
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|
Kidney shape and margins on Radiographs
|
-Smooth margins
-Symmetric -Dog: kidney-bean shaped VD, elliptical lateral -Cat: more rounded shape -Abnormal: irregular contour or margins, more rounded than normal --asymmetry |
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Kidney Size of Radiographs
|
-Dog: 2.5-3.5x length of L2
-Cat: --intact: 2.1-3.2x length of L2 --neutered: 1.9-2.6x length of L2 -Diseased kidneys can still be normal size |
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|
Renomegaly: Bilateral, normal shape, smooth margin
|
-acute nephritis or pyelonephrotos
-retroperitoneal effusion or inflammation -Neoplasia, lymphoma -FIP -Polycystic kidney disease -Amyloidiosis -Portosystemic shunt -Hydronephrosis |
|
|
Renomegaly: bilateral, irregular margins
|
-Polycystic Kidney Disease
-Neoplasia --lymphoma, metastatic disease, bilateral primary carcinomas -FIP -Perinephric pseudocyst -Subcapsular hematoma |
|
|
Renomegaly: Unilateral, normal shape, smooth margins
|
-Hydronephrosis secondary to urolith obstruction
-Compensatory hypertrophy -Neoplasia, lymphoma -Pyelonephritis -Perinephric pseudocyst (mostly in cats) -Subcapsular hematoma |
|
|
Renomegaly: unilateral, irregular margins, asymmetric enlargement
|
-CHANG lesions
-Cyst -Hematoma -Abscess -Neoplasia -Granuloma |
|
|
Small kidneys: unilateral of bilateral
|
-Chronic renal disease
--End stage nephritis -Congenital hypoplasia or dysplasia -Renal infarction |
|
|
Radiographic Opacities in Kidneys
|
Increased opacity:
--Renoliths --Cystic calculi -Decreased opacity: --gas in the renal pelvis and bladder --pyelonephritis and cystitis |
|
|
Mineralization in the Kidney
|
-Nephrolithiasis (renoliths)
--pelvic or parenchymal calculi, secondary to diet or infection -Dystrophic Mineralization --neoplasia, abscess, infarction -Nephrocalcinosis: metastatic mineralization --due to abnormal Ca:P ratio |
|
|
Metastatic Mineralization
|
-NOT metastatic neoplasia
-Due to an abnormal Ca:P ratio -Hyperadrenocorticism -Hyperparathyroidism -Hypercalcemia -Ethylene glycol toxicity -Hypervitaminosis D -Chronic Renal failure |
|
|
Decreased Renal Opacity
|
-Fat in the renal pelvis
-Air in the renal parenchyma or pelvis --gas-forming organism -Air in the renal pelvis secondary to vesico-ureteral reflux |
|
|
Absence of Renal Silhouete
|
-May be totally normal
--right kidney often silhouettes with the liver -May be aplasia, nephrectomy, end-stage nephritis, ectopic kidney, diaphragmatic herniation -If both kidneys are missing, probably due to contrast issue --cachexia, retroperitoneal effusion, mass |
|
|
Three Kidneys
|
-Adrenal mass
-Renal transplant -renal duplication (rare) |
|
|
Renal Function on Radiographs
|
-Evaluate via scintigraphy
--can assess GFR -IV urography |
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|
IV Urography
|
-Excretory urography, intravenous pyelography
-Based on kidney’s ability to take up concentrate, and excrete contrast -Iodinated contrast is given IV to animal --should b excreted by glomerular filtration --no significant tubular secretion or reabsorption -Provides info on morphology and function of kidneys --assess kidney, ureter, and bladder -Evaulate ectopic ureters and ureter patency -Kidney and ureter leakage/rupture |
|
|
IV urography Contraindications
|
-Dehydrated animal
-Otherwise no contraindications, as long as animal is normally hydrated -Avoid if animal is severely debilitated with poor renal perfusion |
|
|
IV urography Procedure
|
-IV contrast bolus and serial radiographs
-Vascular phase -Nephrogram Phase -Pyelogram phase |
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|
Vascular Phase of IV Urography
|
-Immediately after or during injection of contrast agent
-10 seconds -May not see the phase -Assesses renal arterial supply and vascular arborization |
|
|
Nephrogram Phase of IV urography
|
-Qualitative assessment of functional renal parenchyma
-Opacification, size, shape, general morphology -Duration of opacification -Degree of nephrographic opacification -Fading pattern of nephrogram -Allows assessment of degree of nephrographic and pyelpgraphic opacification and fading pattern of the nephrogram |
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|
Homogenous opacification on Nephrogram
|
-Normal
-Compensatory hyperplasia -Acute glomerular or tubulointerstitial disease -Perinephric pseudocyst -Hypoplasia |
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|
No opacification on Nephrogram
|
-Absent kidney
-Renal artery infarction or avulsion -Insufficient dose of contrast |
|
|
Focal, non-uniform opacification on nephrogram |
-Mass! CHANG lesions
--cyst, hematoma, abscess, neoplasia, granuloma -Infarct, not perfusing and not opacifying -Hydronephrosis |
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|
Multifocal, non-uniform opacification on nephrogram
|
-Polycystic disease
-Multiple infarcts -FIP -Acute pyelonephritis -Infiltrative neoplasia |
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|
Pyelogram phase of IV urography
|
-Assessment of the pelvis and ureters
-Pelvis should be distended -Can see filling defects -Diverticulae assessment |
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|
Radiography of the Ureters
|
-If normal, they are not seen on survey radiographs
-Can see on ultrasound, IV urography, retrograde vaginocystourethrogram, antegrade pyelography |
|
|
Antegrade Pyelography
|
-Method for visualizing the ureters
-Ultrasound-guided injection of contrast into a dilated renal pelvis -Can look at ureter on that side without worrying about systemic contrast administration |
|
|
Ureters
|
-Very small, 2-3mm in diameter
-Retroperitoneal except at the trigone -Caudal J-shape just before the trigone -Segmented due to peristalsis -Abnormal ureters can be ectopic, focal or diffuse enlargement, calculi, or rupture |
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|
Renal Ultrasound
|
-Complementary to radiographic studies
-Can look at size, shape, internal architecture and vasculature of kidneys -Operator dependent! -Equipment dependent -Cat kidney size: 3.8-4.4cm -Dog kidney size: 5.5-9.1 --evaluate relative to the aortic diameter -Cortex and medulla is hypoechoic --cortex is isoechoic to liver |
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|
Renal Architecture on Ultrasound
|
-Focal or multifocal changes in the parenchyma
--CHANG lesions, infarcts, mineralization -Diffuse parenchymal changes -Pelvic abnormalities |
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|
Renal Cyst on Ultrasound
|
-Variable in number and size
-Round, anechoic -Smooth, thin wall -Distal acoustic enhancement |
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|
Neoplasia, hematoma, absecess, and granuloma on renal ultrasound
|
-Very variable ecogenicity
--hypo, iso, hyper, complex -Can occasionally mimic cysts --usually lack one characteristic of the cyst -Often non-specific, need cytology or a biopsy |
|
|
Renal Infarcts on Ultrasound
|
-Produce wedge-shaped defects
--can be hyperechoic --can be concave cortical defect |
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|
Diffuse changes to the Kidneys on Ultrasound
|
-Increase in cortical echogenicity
-Decrease in cortical echogenicity -Reduced cortico-medullary boundary distinction -Medullary rim sign --hyperechoic medullary band --can be seen in normal dogs and cats |
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|
Acute nephritis on Ultrasound
|
-Kidney can be normal sized or enlarged
-May or may not have hyperechoic perirenal fat -retroperitoneal effusion |
|
|
Chronic Kidney Disease on Ultrasound
|
-Decreased cortico-medullary definition
--hard to tell cortex apart from the medulla -Kidneys can be small |
|
|
Renal Lymphoma in Cats on Ultrasound
|
-Lymphoma can do whatever it wants
-Nodules or masses -Irregular contour to the kidney -Increased or decreased echogenicity -Sub-capsular hypoechoic rim --lymphoma, FIP, fluid |
|
|
Renal Pelvis on Ultrasound
|
-Mineralization
-Dilation --pyelectasia (polyuria, pyelonephritis) --Hydronephritis (obstruction, pyelonephritis) --Echogenic urine, when normally anechoic |
|
|
Urinary Bladder
|
-Located in caudal ventral abdomen
-Cranial to pubis -Ventral to descending colon and rectum -Can be variable in size and somewhat variable in shape --round, tear shaped, pear shaped -Should be uniformly soft-tissue opaque -When enlarged, exerts mass effect --cranially displaces small intestine, dorsally displaces colon |
|
|
Urethra
|
-Not normally seen on survey radiographs
-Can see long bladder neck and proximal urethra in cats |
|
|
Enlarged/distended bladder
|
-Normal for animal?
-Obstruction -Neurologic issue, no contraction -Bladder atony |
|
|
Small bladder
|
-Can be normal
-Cystitis, animal is peeing frequently and so bladder is small -Herniated -Rupture -Congenital anomaly --ectopic ureters |
|
|
Abnormal bladder positions
|
-Cranial (most common)
-Caudal: retro-flexion -Ventral: inguinal hernia -Dorsal |
|
|
Urinary Bladder Decreased Opacity
|
-Iatrogenic introduction of air via catheterization or cystocentesis
-Emphysematous cystitis --gas in lumen and/or in wall |
|
|
Urinary Bladder increased opacity
|
-Calculi
-Dystrophic mineralization |
|
|
Urinary calculi on radiographs
|
-Mineral opaque:
--struvite --Calcium oxalate --Calcium phosphate --Calcium carbonate -Radiolucent calculi: cannot see on radiographs --cystine --urate --xanthines |
|
|
Calculi on Radiographs
|
-Evaluate urinary bladder and ENTIRE area of the urethra
-Include perineal area -In male dogs do flexed caudal abdomen/perineal projection --look for urethral calculi -Need to image entire area, whole outflow tract |
|
|
Radiolucent Calculi discovery
|
-Can do contrast studies of bladder or urethra
--cystography or cystourethrography -Can ultrasound the bladder |
|
|
Cystography
|
-Evaluate the bladder
-Assess bladder size, shape, position, integrity -Stranguria, dysuria -Look for mass lesions or filling defects -Crystaluria, hematuria, pyuria -Most commonly done to look at bladder integrity |
|
|
Positive contrast cystogram
|
-Most common
-procedure of choice for bladder location and integrity -Iodinated contrast -Look for bladder rupture or urethral rupture/tear |
|
|
Negative Contrast cystogram
|
-Least sensitive
-Can use room air or CO2 -Not very good alone |
|
|
Double contrast cystogram
|
-Use positive contrast and negative contrast
-Best to look at bladder wall itself --mass lesions or intraluminal abnormalities -Ultrasound is used more routinely than double contrast cystogram -Calculi will be centrally located -Blood clots will be in random positions, will be irregular -Air bubbles will be on periphery, on margins --smooth, round |
|
|
Cystic calculi
|
-Produce filling defects on cystogram
-Mineralopaque compared to fluid and air -Contrast solution is mineral-opaque, calculi will look like radio-lucent defects --too much contrast can obscure a small stone -Will be in dependent area of the bladder |
|
|
Cystogram for a Ruptured Bladder
|
-Decreased serosal detail from uroperitoneum
-Increased opacity and increased serosal detail from contrast in peritoneum |
|
|
Positive Contrast urethrogram
|
-Same principles as cystogram
-In male dogs the prostatic urethra will be mildly narrower -In females, do retrograde vaginocystourethrogram --foley catheter in distal aspect of vestibule, occlude back end |
|
|
Ultrasound of the Urinary Bladder
|
-Should be anechoic
-Bladder wall is generally less than 2-3mm thick |
|
|
Cystitis in Ultrasound
|
-Echogenic urine
--may see floating debris, or debris may settle out -Thickened wall, particularly cranioventrally --dependent area in the standing dog is thicker, where things settle -May see polypoid projections into the lumen --indicates polypoid cystitis --can look like neoplasia |
|
|
Bladder Calculi on Ultrasound
|
-Are bright with distal shadowing
-If small, might not shadow -Luminal -Dependent, sink with gravity -Move stones to see if they are single or multiple and sizes |
|
|
Bladder Neoplasia on Ultrasound
|
-Transitional cell carcinoma is most common
-Results in irregular areas of wall thickening -May have mineralization -Urine may be echogenic due to tumor cells or concurrent secondary cystitis (or both) |
|
|
Transitional Cell Carcinoma in Bladder
|
-Look for trigonal and urethral involvement
-Masses can obstruct urethra, patient will be unable to urinate -Can obstruct ureters, ureters will dilate and develop secondary jhydronephrosis -Evaluate for surgical resectability -Evaluate for mastitis in draining lymph nodes --sub-lumbar lymph nodes |
|
|
Prostate on Radiographs
|
-Caudal abdomen, cranial to the pelvic canal
--Ventral to colon and rectum -Look at “fat triangle” separating the bladder from the prostate -Not seen in cats or neutered dogs -May see in intact dogs |
|
|
Evaluating the Prostate on Radiographs
|
-Look at length or height
-Intact male dog: should be less than 70% of distance from sacral promontory to pubis -on VD should be less than 50% of pelvic inlet width |
|
|
Prostate on Ultrasound
|
-Intact male dogs: hyperechoic
--functional, brighter -Neutered dogs: much smaller, relatively hypoechoic --non-functional, less bright |
|
|
Mass effect of the Prostate
|
-Cranial displacement of the urinary bladder
-Dorsal displacement of the colon with compression |
|
|
Differentials for Prostatomegaly
|
-Benign hyperplasia in intact dogs
-Cysts -Neoplasia -Prostatitis -Prostatic abscessation -IN a castrated dog, primary differential is neoplasia |
|
|
Prostatic neoplasia
|
-In castrated male dogs, neoplasia is the primary differential for prostatomegaly
-Enlarged -Mineralized -Irregular -Also evaluate for urethral involvement (urethral obstruction) -Displacement or compression of the colon and rectum (tenesmus, obstipation) -Metastasis is possible --look at sublumbar lymph nodes, bones, lungs |
|
|
Prostatic neoplasia on Ultrasound
|
-Enlarged, asymmetric prostate
-Heterogenous irregular areas -Nodules, masses, cavitations -May or may not have mineralization -Also evaluate for urethral involvement or extent of involvement -Look for metastasis |
|
|
Paraprostatic Cysts
|
-Cyst outside of the prostatic parenchyma
-Not common, but do occur -Can be cystic vestive of mullerian duct, prostatic retention cyst, neoplasia -Stalk may connect it to prostatic parenchyma -May be infected -Variable in size, position, and shape --can look like “2 bladders” -May have eggshell mineralization |
|
|
Uterus on Radiographs
|
-Not usually seen in intact, non-pregnant animals
-May be seen in some obese animals between the bladder and the colon --should be small |
|
|
Uterine Enlargement
|
-Can be focal or diffuse
-Tubular soft-tissue mass, may be difficult to differentiate from small intestines, depending on size -Separates bladder and colon on lateral view -on VD view will be along left and right body walls --medially and cranially displaces small intestines |
|
|
Pyometra on Ultrasound
|
-Look between the bladder and the colon
-To find ovaries, find uterus first and then look for ovaries -Fluid in uterus will be echogenic with poymetra |
|
|
Diffuse Uterine Enlargement DDx
|
-Can be due to pregnanct or post-partum
-Fluid distended: pyometra, mucometra, hydrometra, hemometra --Endometritis --Endometrial hyperplasia --Uterine Torsion (less common in small animals) -Gas distended: Fetal necrosis, emphysematous pyometra -Bone distended: pregnancy or fetal mummification |
|
|
Fetal identification on Radiographs
|
-Fetal mineralization determines when fetuses can be viewed on radiographs
-Dogs: day 42-45 -Cats: day 35-39 |
|
|
Radiographic Signs of Fetal Death
|
-Abnormal position
--folded, extended --if proximal to pelvic canal, limbs should be extended out of pelvic canal -Overlapping calvarial bones --distortion of skull can occur during birth, but should not happen at any other point in gestation (indicates fetal death) -Gas within the uterus and/or fetus -Skeletal compaction (mummification) |
|
|
Uterus on Ultrasound
|
-Can identify normal, enlarged, or gravid uterus |
|
|
Kidneys
|
-Paired bean shaped organs
-Ventral to sublumbar muscles -Adjacent to dorsal abdominal wall -Retroperitoneal -Right kidney is more cranial than the left -Left kidney is entirely caudal to the last rib -Right kidney is attached to liver by the hepatorenal ligament -On left side, gonadal vessels drain into the renal vein |
|
|
Renal Vasculature
|
-Not typically one renal artery and one renal vein
-On right side, multiple renal veins is more common in cats -Dogs have multiple renal arteries, mostly on the left side -Even if there is a single artery, there will be various degrees of splits in the arteries |
|
|
Ureters
|
-Retroperitoneal
-Run from kidney down to urinary bladder, end up in trigone of the bladder -run through lateral ligaments of the bladder -Blood supply is from renal artery and from genital vessels --somewhat of a segmental blood supply |
|
|
Peritoneal vs. Retroperitoneal space
|
-Abdominal, pelvic, and scrotal cavities are lined by parietal peritoneum
-Visceral peritoneum is where parietal peritoneum reflects on organs --completely surrounded by visceral peritoneum -Kidney, aorta, ureters, and vertebrae are only covered by peritoneum on one side --“retroperitoneum” |
|
|
Urinary Bladder
|
-Apex, body, neck (trigone)
-Bladder can vary in location, depending on volume -Has ventral and lateral ligaments |
|
|
Ligaments of the bladder
|
-Ventral ligament: connects bladder to the linea alba and pelvic symphysis |
|
|
Urethra
|
-Extends from the bladder neck to the vagina or tip of the penis
-Shorter in female, longer in male -Membranous urethra and prostatic urethra in the male |
|
|
Bladder and urethra blood and nerve supply
|
-Blood and nerve supply enters dorsally
-Need to be careful during surgery, damage can cause incontinence -Main blood supply to bladder: caudal vesicular arteru --in female, branch of uterine artery --in male, branch of prostatic artery -Cranial vesicular artery -Pudendal nerve: somatic -Hypogastric nerve: sympathetic -Pelvic nerve: parasympathetic |
|
|
Imaging of the urinary tract
|
-Survey radiography is needed
-Ultrasonography -Excretory urography -Retrograde vaginourethrography -Voiding cystourethrography -CT -Nuclear scintigraphy |
|
|
Retrograde urethrocystography
|
-Evaluating bladder or urethral tears/ruptures
-Need to fill bladder completely or small leaks will be missed |
|
|
CT of the kidneys and bladder
|
-Can get 3D picture of urinary tract
- |
|
|
Congenital abnormalities of the Urinary Tract
|
-Renal agenesis |
|
|
Ectopic ureters
|
-Ureter does not enter the bladder normally
-90% of dogs are female -43% of cats are female -Can be one or both ureters --more often unilateral -Breed predisposition exists -Commonly associated with other congenital abnormalities --will have history of incontinence since birth --Usually constant incontinence, but may be intermittent |
|
|
Intramural Ectopic Ureter
|
-Ureters go through the wall of the bladder but do not open into the normal location
--runs through the wall of the bladder -Usually empties distal to the trigone region -Can empty in urethra, prostate, or vagina -More common |
|
|
Unilateral ectopic ureter vs. bilateral ectopic ureter
|
-Unilateral, animal will urinate normally some of the time
-Bilateral, animal will dribble all of the time |
|
|
Breed predispositions for ectopic ureters
|
-Siberian huskies
-Golden retrievers -Fox terriers -Labrador retrievers -Miniature poodles -Newfoundlands |
|
|
Physical Exam of animal with Ectopic ureters
|
-Animal lies down and urine pours out onto floor
-More prone to ascending secondary infections -Skin can be irritated from urine -Can have urine scalding |
|
|
Extramural ectopic ureters
|
-Ureter comes down from the kidney and never attaches anywhere near the bladder
-Completely bypasses the bladder and dumps distal to the bladder -More common in Cats |
|
|
Other abnormalities noted with ectopic ureters
|
-Double ureteral opening
--one opening into trigone, other opening distal to bladder --some urine is dumped normally, some is carried distal -Ureteral trough |
|
|
Sequelae from Ectopic ureters
|
-Ascending infections: 64-79% of cases, skips the bladder sphincter
--Pyelonephritis and cystitis -Hydronephrosis -Hydroureter: chronic infection, obstruction, or lack of ureteral peristalsis -Hypoplastic bladder causing lack of normal filling -Ureterocele -Vaginal abnormalities |
|
|
Diagnosis of Ectopic Ureters
|
-CBC/Chem
-Urinalysis and culture -Ultrasound -Excretory urography (multiple views) -Cystoscopy (most common) -Retrograde vaginourethrography -CT |
|
|
Treatment for Ectopic Ureters
|
-Surgery!
-Perform early to prevent secondary infections that can become chronic -Neoureterostomy performed for intramural ectopic ureters -Resection and reimplantation performed for extramural ureters |
|
|
Neoureterostomy
|
-Ventral midline cystotomy
-Inspect trigone for normal ureteral openings -Identify submucosal swelling or ridge within the bladder to find intramural ureter -Make hole through bladder mucosa into ureteral lumen -Place catheter distally to identify rest of the intramural ureter, ligate or resect --have to make a new hole and suture distal segment of the ureter |
|
|
Surgical correction for Extramural Ureters
|
-Tie off where ureter enters urinary tract
-Cut, attach anywhere on the bladder away from the trigone region --usually suture onto apex region |
|
|
Cystoscopic guided laser ablation of ectopic ureters
|
-Cystoscope guides surgery
-Cauterize “shelf” or tunnel where ureter travels through bladder wall |
|
|
Prognosis for Ectopic Ureters
|
-A lot of patients show continued incontinence
-Urethral sphincter mechansim incompetence goes along with ectopic ureters --innervation to the neck of the bladder is not normal --even if anatomic issue is fixed, incontinence remains -Test with urethral pressure polimetry |
|
|
Phenylpropanolamine
|
-increases urethral tone
-Medical management for incontinence |
|
|
Reasons for Persistent incontinence after surgery
|
-Urethral sphincter mechanism incompetence
-Re-canalization of a submucosal tunnel -Poor surgical technique -Decreased bladder capacity -Poor vaginal conformation -Pelvic bladder or short urethra -Underlying neurologic issue |
|
|
Hydraulic Occluder
|
-Small silicone cuff
-Placed around the urethra -Hooked to a port that goes subcutaneously under the skin -Increases tone around the urethra |
|
|
Ureterocele
|
-Congenital anomaly
-Can be associated with an ectopic ureter -Normal dilation of the ureter just where it enters the urinary bladder -Cystic structures can fill up with urine, puts pressure on the neck of the bladder --can develop into an obstruction -Resect abnormal portion of the ureter and re-attach to the bladder |
|
|
Persistent urachus
|
-Urachal remnants form ventral ligament of the bladder
-Urachal diverticulum at the cranial pole of the bladder -Acts as a nidus for infection -Can have persistence of entire urachal tract -Surgical fix |
|
|
Renal neoplasia
|
-Uncommon in dogs and cats
-Usually malignant -in dogs carcinomas are most common -in cats lymphoma and carcinoma are both common --Lymphoma can be primary or metastatic -Can also have benign lesions -Metastasis is common --non-specific signs, can go for a long time before diagnosis is made |
|
|
Clinical presentation of Renal Tumors
|
-Older male dogs
-No breed predisposition -Male cats -Lymphosarcoma in oriental and Siamese cats -Nephroblastoma is most common in young dogs and cats -Vague and non-specific signs --anorexia, lethargy, weight loss, hematuria -By the time signs show up, progression of disease is pretty advanced |
|
|
Physical examination of patient with Renal tumor
|
-Abdominal enlargement
-Palpable abdominal mass -Lameness |
|
|
DDx for Renal neoplasia
|
-Pyelonephritis
-Hematoma -Polycystic Kidney Disease -FIP in cats -Perinephric pseudocysts |
|
|
Lab findings for patients with Renal neoplasia
|
-CBC/chem
-Urinalysis and culture --hematuria, pyuria, and proteinuria are common -Secondary UTI is common -Renal failure may be present -Paraneoplastic syndromes --polycythemia --hypercalcemia, hypoglycemia --hypertrophic osteopathy |
|
|
Treatment of Renal neoplasia
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-Nephrectomy if unilateral and no evidence of metastasis
-Cats with lymphoma may respond well to chemotherapy |
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Prognosis for animals with Renal neoplasia
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-Depends on type, location, and extent of neoplastic involvement
-Carcinoma= 16 months -Sarcoma= 9 months -Metastasis is often present at time of diagnosis -Usually a poor diagnosis |
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Surgical approach to Renal Neoplasia
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-Ventral midline incision
-Xiphoid and caudal to the umbilicus or pubis -For right kidney elevate duodenum and displace intestine to left side -For left kidney, elevate mesocolon and retract small intestine to the right side -Isolate renal artery and vein |
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Calcium Oxalate Crystals
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-Common urolith in urinary tract
-Incidence has increased -Found in all parts of the urinary tract --kidney, ureter, bladder, urethra --more common in upper part -Cannot medically dissolve stones, need to intervene |
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When is surgery indiated for uroliths?
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-Infection that is unresponsive to medical management
-Obstruction -Medical management is not effective -Renal function is decreased in affected and contralateral kidney -Overall health of the animal |
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Recovery of renal function
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-Ability to recover from an obstruction is no determined
-Many obstructions are unilateral, do not know how long they have been obstructed -Pre-existing disease may have been present -Tubular dilatation and interstitial fibrosis occur with obstructions |
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Clinical Presentation of animals with Urinary tract Stones
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-Asymptomatic, often is an incidental finding
-Lethargy, weight loss, anorexia, vomiting -Fever -PU/PD -Hematuria may or may not be present due to irritation of stones -Anuria -Abdominal pain, splinting, renomegaly -Kidneys get enlarged and painful |
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Diagnostics for Urolithiasis
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-CBC/Chem
-Urinalysis and culture -Radiographs can be helpful to see location -Ultrasound gives good images of kidneys, bladder, ureter -Combination of radiographs and US is very effective in identifying location |
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Excretory Urography and Urolithiasis
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-If kidney is obstructed by a stone, do not get a good image
-No good contrast study -Tubular cells do to concentrate contrast well -No pyelographic phase |
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CT for urolithiasis imaging
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-Can see exactly where the obstruction is
-Do right around the time of surgery -Put contrast directly through the kidney into the renal pelvis |
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Presurgical considerations for Urolith removal
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-Do not know how an individual patient will respond to surgery
-Bilateral chronic interstitial nephritis is often present --Typically a bilateral disease, even if only one kidney is obstructed |
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Surgical Treatment for Uroliths
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-Indicated if there is an infection or obstruction
-Entire urinary system should be explored -Nephrotomy or pyelolithotomy -If bilateral issue, consider staging procedures -Culture urine from renal pelvis or ureter -Stone analysis is needed -Surgery may temporarily decrease renal function -Complications involve renal failure, hemorrhage, leakage |
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Surgical procedure for uroliths
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-Tie off renal artery, then vein
-Make a small incision in kidney, as small as possible -Flush calicies before closing to dislodge any small stones -Close with simple continuous with absorbable material |
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Surgical treatment of the Ureter
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-Tretment depends on location of calculi and whether or not obstruction is present
-Use an operating microscope, magnification is key -Pyelotomy: incision into the renal pelvis -Ureterotomy: incision into a ureter -Ureteral reimplantation -Ureteral stenting |
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Pyelotomy
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-Cutting into renal pelvis
-get stones located in the renal pelvis or proximal ureter -Isolate the kidney and work from dorsal side of the kidney -Make incision right into the area |
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Ureterotomy
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-Longitudinal incision into ureter
-Need magnification -Dilation usually indicates the location of the stone --make incision right in front of the dilation -If stone is embedded into ureter wall, cut over stone directly -Put tubing around surgical site to prevent retrograde movement of stone and urine into kidney -can flush down into the bladder -Close with simple interrupted |
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Ureteral reimplantation
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-Cut ureter and re-attach end to urinary bladder
-Used to take out urolith -Can only do if the stone is in the ureter very close to the bladder -If stone is higher up, can do renal descensus --dis-attach kidney from body wall attachments and re-attach further caudally |
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Complications with Upper Urinary Tract Stones
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-Post-operative leakage or stricture formation
-Uroabdomen -Persistent ureteral obstruction -Uroabdomen |
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Urolith Migration
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-Recurrent ureterolithiasis
-Once an obstruction in ureters is removed, allows things to flow from kidney |
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Ureteral stenting for Urolithiasis
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-Put a stent around the ureter
-One end sits in renal pelvis, other is in the bladder -Avoid stones in the ureter -Have complications, Can encrust or migrate, cause dysuria |
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Bladder and Urethral uroliths
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-Struvite calculi are most common in dogs
--associated with UTI -IN cats struvite calculi are not associated with UTI, more often calcium oxalate -Urate, ammonium biurate, silicate, cysteine stones are all possible -Always analyze whatever stone you remove! |
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Clinical signs of lower urinary tract urolith
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-Pollakiuria
-Stranguria -Hematuria -Partial or complete urinary obstruction --esp in males -Bladder distension -Abdominal pain -Uroabdomen |
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Radiographs of Bladder and Urethral calculi
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-Radiograph the whole abdomen!
-Look for stones in lower and upper urinary tract |
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Cystotomy
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-Common procedure
-Usually done along ventral surface of the bladder --avoid innervation and vasculature |
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Urohydropulsion
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-Push uroliths back into the bladder from urethra
-Create pressure by holding off in anus, release and flow should push stones through -Gets stones that have migrated during surgery back into bladder for removal |
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Urethrostomy
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-Urethral surgery
-Creates a permanent new opening for urine -Do when there is recurrent obstructive calculi, lodged calculi --urethral stricture, urethral or penile neoplasia, severe trauma, preputial neoplasia that needs amputation -Can make opening in scrotum, prescrotal, Perineal, or antipubic |
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Scrotal Urethrostomy
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-Preferred location for urethrostomy
--urethra is wider and more superficial -Surrounded by cavernous tissue -Neuter the animal at the same time -Urethral mucosa is sutured to the skin -Animal learns to posture differently to avoid urine scalding |
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Feline Perineal Urethrostomy
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-Treat obstructions that cannot be cleared by catheterization
-Prevents recurrence of obstruction in male cats -Cat presents anxious, restless, frequent urination attempts, abdominal pain --gets worse over time |
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Medical Management of Cat Uroliths in urethra
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-IV fluid therapy
-Clear obstruction if possible -Place in-dwelling soft urinary catheter -Treat hyperkalemia or other imbalances |
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Perineal Urethrostomy in Cats
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-Remove preputial skin and isolate the penis
--isolate as close to the pelvis as possible -break down ventral ligamentous attachments -Spatulate urethra, then suture to skin |
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Transpubic Urethrostomy
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-No normal urethral to work with |
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Prepubic Urethrostomy
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-Antepubic urethrostomy |
