canine midterms

Functions to carry vital oxygen into the body and expel carbon dioxide, a metabolic waste, out of the body

2 portions:

• upper airways: nasal passage, sinus, pharynx and larynx

• lower airways: trachea, bronchi, bronchioles, alveoli, and lungs

Respiratory system

Rhinitis

Causes of Rhinitis

Fungal disease: _______________

Tooth rooth abscess

Foreign body

Parasitic: ___________

Neoplasia (i.e adenocarcinoma)

Allergy

Canine Distemper

Bordetella bronchiseptica

**case may progress into pneumonia when agents colonizes the lower respiratory tract

• Aspergillus fumigatus, Penicillum spp., Rhinosporidium seeberi, Blastomyces dermatitidis, Cryptococcus neoformans

• Pneumonyssoides caninum (nasal mite), Capillaria aerophagia

Rhinitis

Lab tests of Rhinitis

Rhinitis treatment

Depends on the underlying cause

Antibiotics: for primary and secondary bacterial rhinitis

Antifungals: for fungal rhinitis

1.-

2.-

3.-

• IV

• Nebulized

_______-

Steroid/ antihistamine: for allergic

rhinitis

Ketoconazole

Itraconazole

Flucoconazole

• Amphotericin B

Kennel cough

Kennel cough

Etiology of Kennel cough

Lab tests of kennel cough

Tx for Kennel cough

BOAS

BOAS

RISK FACTOR OF BOAS

LAB TESTS FOR BOAS

TX FOR BOAS

TRACHEAL COLLAPSE

TRACHEAL COLLAPSE

LAB TESTS FOR TRACHEAL COLLAPSE

TX FOR TRACHEAL COLLAPSE

PYOTHORAX

pyothorax

Etiology of Pyothorax

Lab tests for pyothorax

Tx for pyothorax

Functions of the Kidneys

• Waste Removal

• Fluid and Electrolyte Balance

• Acid Base Balance

• Hormone Production

• Blood Pressure Monitoring

• Conversion of Vit. D to its active

form

Waste Removal & Fluid and Electrolyte Balance

Blood Pressure Monitoring

Acide Base Balance

Source of EPO

Peritubular interstitial cells

(mainly in the renal cortex)

Stimulates bone marrow to produce red blood cells in response to hypoxia

EPO

Source of Renin

Juxtaglomerular (JG) cells

(afferent arteriole)

Triggers RAAS to increase blood

pressure and conserve

sodium/water

Renin

Source of Calcitriol (active vitamin D3)

Proximal tubule (via 1α-

hydroxylase enzyme)

Increases calcium and

phosphate absorption from gut,

reabsorption from kidneys;

regulates bone mineralization

Calcitriol (active vitamin D3)

Laboratory Tests

• Urine Specific Gravity

• Protenuria

• Creatinine

• UPC

• SDMA

• to help evaluate renal function by assessing whether water is being excrete or conserved appropriately, according to need.

• It is measured using a __________

Dogs:______________ (It is important to note that any USG value could be

considered 'normal' in a patient, depending on certain other factors, including the patient's _______ status)

• Specific gravity

• refractometer

• 1.015 - 1.045

• hydration

• Adequately concentrated urine

• Kidneys can concentrate → Likely pre-renal

  cause (e.g., dehydration) if azotemic

> 1.030

• Minimally concentrated

• May indicate early CKD if persistent and

  azotemia is present

1.013–1.029

• Isosthenuria (same as blood plasma)

• Suggests renal azotemia or loss of

  concentrating ability

1.008–1.012

• Hyposthenuria

• Indicates active dilution, seen in diabetes

  insipidus, psychogenic polydipsia, or early

  CKD

<1.008

• The presence of protein in the urine

• The urine of healthy dogs and cats contains only a small amount of ___________ and other proteins

• Persistent proteinuria with an inactive urine sediment is a marker of __________ in dogs and cats

• 2 major mechanisms:

  • Loss of selective glomerular filtration- resulting in an increased amount of plasma protein in the filtrate

  • Impaired tubular resorption of the filtered protein.

• Proteinuria

• albumin (< 1 mg/dl)

• chronic kidney disease (CKD)

• Non-proteinuric (NP)

• Normal — no significant protein loss in urine

< 0.2

• Borderline proteinuric (BP)

• Monitor — may be early or transient; consider

  rechecking

0.2 – 0.5

• Proteinuric (P)

• Abnormal — suggests glomerular or tubular

  dysfunction; requires further evaluation and

  often treatment

> 0.5

• A metabolic byproduct of muscle breakdown, excreted almost entirely by the kidneys. It is a traditional marker of renal function used to estimate the glomerular filtration rate (GFR)

• Limitations:

  • Affected by ________

  • not sensitive to _________

• Creatinine

• muscle mass

• early kidney diseases

• ___________ or “SDMA”

• A methylated form of the amino acid arginine, produced by all nucleated cells and primarily excreted by the kidneys.

• SDMA increases on average with______ and as little as _____ loss of kidney function versus___, which does not increase until up to 75% of kidney function is lost

• Symmetric Dimethylarginine

• 40%

• 25%

• creatinine

Detects early CKD

SDMA

Affected by muscle mass

Creatinine

Rises only after 75% GFR lost

Creatinine but SDMA rises at 40% GFR loss

Used for IRIS staging

Crea is primary, SDMA is supplementary

• A rapid and significant loss of renal function, leading to the accumulation of nitrogenous waste products, fluid imbalance and electrolyte disturbances (classically, ______)

• Reflects a wide range of parenchymal damage, from mild, hardly detectable nephron injury to severe, life-threatening failure of the kidneys

3 causes:

• Pre-renal: occurs when there is ________ to the kidney. This can be caused by severe hypotension, shock, and general anaesthesia.

• Renal: results from _____ to any part of the kidney itself. (i.e. toxins, medications and/or infection)

• Post Renal: occurs due to __________. In these cases the obstruction puts pressure on the kidneys, reducing glomerular filtration and causing __________

• AKI

• hyperkalaemia

• reduced blood flow

• injury

• urinary tract obstruction

• azotaemia

Causes Pre-renal ds:

• hypovolemia

• hypotension

• decreased cardiac output

• systemic vasodilation

Causes of renal ds:

• toxins

• ischemia

• infection

• glomerulonephritis

• immune mediated disease

Causes of post renal ds:

Obstruction (urolithiasis, prostatic hyperplasia, tumor/neoplasia)

Non-azotemic but ↑ SDMA, abnormal urine,

imaging, or renal biomarkers (e.g. proteinuria,

casts)

Grade 0 - normal

Clinical signs suggest AKI (e.g., PU/PD,

inappropriate USG, elevated SDMA)

Grade I - <1.4 (non-azotemic)

Mild azotemia, stable or worsening

Grade II - 1.4–2.0

Moderate azotemia

Grade III - 2.1–5.0

Severe azotemia

Grade IV - 5.1–10.0

Clinical Signs of AKI:

• Polyuria

• Polydipsia

• Lethargy

• Depressed mentation

• Hyporexia/ Anorexia

• *Oliguria (urine output <0.5ml/kg/hour)

• Stranguria

• Anuria

AKI in cases of UT obstruction

• Vomiting (the vomited material may have blood in it)

• Diarrhea (that may contain blood)

• A strange breath odor

• Ulcers in the mouth

• Seizure

Lab tests for AKI

• Blood test

• CBC

• Biochem: Comprehensive or Kidney specific profiling + SDMA

  • hyperkalemia is a common finding

  • decreased potassium excretion

  • metabolic acidosis

  • cell lysis: damaged cells release intracellular potassium

• Urinalysis

  • USG (Usually < 1.030)

  • UPC

• Radiograph

• Sonograph (Check renal structure)

Treatment for AKI

• IV fluid- Appropriate fluid therapy is probably the cornerstone of the medical therapy of AKI, and it aims at restoring hydration and normovolemia.

• Manage Hyperkalemia (i.e decreased renal excretion, oliguria/anuria, cell lysis, and/ or metabolic acidosis)

• Correction of fluids

• Insulin + Glucose: promoting the movement of potassium from the extracellular fluid (blood) into the intracellular space (inside cells)

• Sodium Bicarbonate

• Antibiotics- if with infection or secondary infection is expected

• Supportive medication (renal probiotics, supplements, etc.)

• Erythropoietin- If anemia is present

• Dialysis- process of externally removing toxins and accumulated waste products from the bloodstream when the kidneys stop functioning

  • hemodialysis

  • peritoneal dialysis

• Also known as renal failure and chronic kidney insufficiency

• Progressive, irreversible loss of kidney function over weeks to months

• Inability of the kidneys to efficiently filter the blood of waste products

• Risk factors:

  • Age

  • Breed

  • Diet (high protein levels)

  • Certain medications

  • AKI

  • Concurrent diseases (i.e Hypercalcemia, periodontal ds, Cardiac ds., etc.)

• Urine always in an isothenuric state (that is why urine of patients with CKD may always appear diluted) having a fixed specific gravity (1.008-1.0012)

• kidneys unable to concentrate or dilute urine

• occurs due to:

  • loss of nephron

  • tubular damages

CKD

Clinical signs of CKD

Polyuria

Polydipsia

Lethargy

Weakness

Dehydration

Anorexia/inappetence

Weight loss

Poor coat quality

Vomting

Marked weight loss

Uremic breath

Neurologic signs

• Laboratory Tests for CKD

• Blood tests

  • CBC- Anemia is a common finding

  • Biochem- Comprehensive or Kidney specific profiling + SDMA

• Urinalysis

  • low USG

  • Proteinuria

• Blood pressure monitoring

  • Hypertension

• Radiograph

• Sonograph

IRIS recommends confirming the stage with at least ______ fasting samples taken 2–4 weeks apart.

• 2

Creatinne

Stage 1(Creatinine

<1.4 mg/dL)

Stage 2 (Creatinine 1.4–2.0 mg/dL)

Stage 3 (Creatinine 2.1–5.0 mg/dL)

Stage 4 (Creatinine >5.0 mg/dL)

CKD Treatment

Treatment summary:

1.Diet- management- Low in phosphorus and protein

2.Control proteinuria- ACE inhibitors

3.Manage hypertension- add Amlodipine if ACE inhibitor is not enough

4.Phosphorus control- add phosphate binders

5.Hydration support- IVF, SQF, encourage drinking

6.Symptomatic care- antiemetics, potassium supplements, erythropoietin, etc.

7.Regular monitoring- usually done every month