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65 Cards in this Set
- Front
- Back
Homeostasis definition |
The property of a system that regulates its internal environment and tends to maintain a stable, constant condition |
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List some defects of homeostasis |
Oxygen deficiency Fluid loss Blood glucose alterations Electrolyte and acid-base imbalances Accumulations of waste products Alterations in temperature |
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Why is oxygen important? what is its ultimate role? |
Required for oxidative phosphorylation and production of ATP (ENERGY!) We need energy to survive, dur |
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Only need _______% depletion of ATP to cause widespread cellular effects |
5-10 |
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Define oxygen deficiency and name two states |
Decreased delivery of oxygen to cells or tissues Partial = Hypoxia Complete = Anoxia |
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Mechanisms of oxygen deficiency |
-Inadequate oxygenation of blood -Loss or reduction of blood supply (ischemia) -Reduced transport of oxygen in blood -Interference with oxygen utilization by the cell |
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Organs most sensitive to oxygen deficiency |
Brain Heart Liver Kidney |
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Ex of disease/occurence leading to oxygen deficiency |
Diffuse pulmonary disease Ischemia Asphyxia during birth in foals (dummy foals) Anemia Cyanide poisoning |
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Cyanide poisoning |
Interferes with oxygen utilization by cell Death rapid inhibition of cytochrome oxidase in the mitochondria of brain neurons |
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4 mechanisms that cause oxygen deficiency |
1. Lack of oxygen intake (Lungs) 2. Ischemic change causing decreased perfusion 3. Decreased carrying capacity of oxygen 4. Interference with cells to use oxygen |
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Fluid loss can occur from which spaces? |
Intracellular Interstitial Intravascular |
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What clinical signs do you expect with loss of fluid from intravascular space? |
Hemorrhage Shock (tachycardia, low BP, increased RR) |
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What clinical signs do you expect with loss of fluid from interstitial and intracellular space? |
Vomiting and/or diarrhea
Dehydration, lethargy, weakness |
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Alteration in glucose: 2 states |
Hypoglycemia (low blood glucose levels)
Hyperglycemia (high blood glucose levels) |
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Why is it important to have fine control of blood glucose concentration? (normal range: 3.4-5.7 mmol/L) |
Glucose affects energy production and utilization |
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Which organs can ONLY use glucose to meet their energy requirements? |
**Brain Retina Germinal epithelium of gonads |
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Clinical signs of hypoglycemia |
Seizures Weakness/collapse Muscle fasciculations Depression Ataxia |
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Hypoglycemia: clinical diseases |
Insulinoma Hepatic insufficiency/failure Sepsis Bovine Ketosis/Ovine Pregnancy Toxemia Xylitol toxicosis |
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What is insulinoma? what happens? |
(Dogs, cats, ferrets)
Functional beta-cell tumours of pancreas that secrete insulin Hyperinsulinism leads to increased glucose utilization by hepatocytes, myocytes, adiposcytes and decreased glucose production by hepatocytes |
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Hepatic insufficiency/failure: what happens |
Too few functional hepatocytes to maintain normal fasting blood glucose concentration |
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Sepsis: what happens? |
Systemic response to bacterial infection likely due to decreased hepatic gluconeogenesis and increased glucose utilization by tissues |
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What happens with bovine ketosis/ovine pregnancy toxemia? |
Increased glucose demands associated with lactation/pregnancy that are not adequately supplied *Negative energy balance |
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What happens with Xylitol toxicosis? |
(dogs, cattle and goats)
Xylitol is a potent stimulant for insulin release and leads to increased glucose uptake and utilization by cells |
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Hyperglycemia can lead to? |
Cellular dehydration through loss of glucose in urine and subsequent osmotic diuresis that depletes fluids and electrolytes |
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Long term hyperglycemia can potentially lead to? |
Tissue and vascular injury |
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Organ systems affected by hyperglycemia? |
Endocrine/metabolic system Renal/urologic CNS Opthalmic |
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Most common cause for mild to moderate increases in blood glucose concentration? |
STRESS!!!!!!! Corticosteroids cause increased gluconeogenesis and subsequent increased release of glucose from hepatocytes They also inhibit glucose uptake by tissue cells |
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Clinical diseases leading to hyperglycemia |
Diabetes mellitus (absolute or relative insulin deficiency) Hyperadrenocorticism (Cushing's disease) |
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Diabetes mellitus (DM) in dogs -type -what happens -what causes it |
-Type 1 DM - insulin dependent -Beta cell destruction leads to absolute insulin deficiency -Often immune-mediated
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Diabetes Mellitus (DM) in cats -type -what happens -associated with |
-Type 1 or Type 2 (non-insulin dependent DM) -Type 2: insulin resistance leading to defects in insulin secretion or defects in receptors on target cells -Can be associated with obesity in cats |
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Hyperadrenocorticism: -which species? -What happens? |
-Dogs and horses -Long term increase in endogenous corticosteroids leads to insulin resistance |
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Mechanisms of abnormal electrolyte concentrations in blood |
1. Decreased or increased intake 2. Shifts to and from ICF 3. Increased retention via kidneys 4. Increased loss via kidneys, GIT, skin, airways 5. Disease conditions that alter electrolyte concentrations (can result in acid-base abnormalities) |
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Sodium: -Central role -Where most important -Main source -Regulated by |
-Water and osmotic regulation -Osmotically effective solute in ECF -Dietary -By kidneys via Ang II and aldosterone |
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Types of sodium imbalance |
Hypernatremia Hyponatremia |
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Hypernatremia: Relative sodium gain reasons |
1. Inadequate water intake 2. Panting, hyperventilation, fever (insensible losses) 3. Diabetes insipidus |
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Diabetes insipidus effects |
Decreased water resorption by kidneys due to lack of ADH or an inability of the kidneys to respond to ADH |
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Absolute sodium gain causes |
Iatrogenic: Na containing IV fluids Increased sodium intake without concurrent adequate water intake (salt water ingestion, play dough ingestion) |
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Causes of hyponatremia |
Decreased dietary intake Excessive loss |
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Decreased dietary intake: hyponatremia |
Seen mostly in ruminants |
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**Know Excessive Loss (with continued water intake) |
1. GI loss - vomiting, diarrhea, sequestration 2. Renal loss - Addison's, prolonged diuresis 3. Cutaneous loss - sweating 4. Third Space loss - pleural or peritoneal effusion |
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Potassium: -main source -where mostly found -regulated by |
- Dietary -ICF -Aldosterone; promotes renal K+ excretion |
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Potassium imbalance |
Hyperkalemia Hypokalemia |
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Causes of hyperkalemia |
Increased total body potassium Shifting of potassium from ICF to ECF with no change in total body K |
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**Know Increased total body potassium due to |
1. Decreased renal excretion -Renal failure -Urinary tract obstruction -Addison's disease 2. Iatrogenic: K rich IV |
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Causes of shifting of potassium from ICF to ECF |
1. Metabolic acidosis (ex. accumulation of inorganic acids) 2. Cell lysis (ex. rhabdomylolysis) |
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Causes of Hypokalemia |
Decreased total body Shifting from ECF to ICF |
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Causes of decreased total body potassium |
Decreased intake: anorexia Increased renal excretion (osmotic diuresis, drugs) Increased GI loss Increased cutaneous loss |
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3 fractions of Calcium in the body |
50% free calcium 40% protein bound (albumin) 10% non-protein bound (citrates & phosphates) |
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Net effect of PTH on calcium levels |
Increased serum Ca via Ca mobilization (bone, intestine, kidneys) Decreased serum P (P excretion at kidneys) |
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Net effect of Vitamin D on Calcium levels |
Promotes hypercalcemia |
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Hypercalcemia: increased mobilization or absorption due to? |
1. Primary hyperparathyroidism (^ PTH) 2. Hypercalcemia of malignancy (^ PTH-rp) 3. Hypervitaminosis D |
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Hypercalcemia: decreased urinary excretion due to? |
Renal failure in horses |
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Causes of hypocalcemia |
**1. Hypoproteinemia (hypoalbuminemia) 2. Inadequate immobilization or absorption 3. Excess renal excretion |
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Examples of inadequate immobilization or absorption |
Pregnancy, parturient or lactationsal hypocalcemia Chronic renal disease |
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Examples of excess renal Ca excretion |
Ethylene glycol toxicity (antifreeze) |
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What makes up increased plasma metabolites (waste products) |
Urea Creatinine |
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An increase in blood non-protein nitrogenous compounds (urea and creatinine) is called? |
AZOTEMIA |
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**Causes of azotemia |
Pre-renal Renal Post-renal |
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Azotemia always needs to be interpreted in conjunction with? |
Patients USG!! |
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Pre-renal azotemia signs |
USG > 1.030 *Concentrated urine *Any process that decreases renal blood flow (hypovolemia due to dehydration, shock) |
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Renal azotemia signs |
USG: 1.008 - 1.012 *Any renal disease causing major GFR decrease *ex. Renal failure |
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Post-renal azotemia signs |
USG variable *Any disease/disorder to distal to the nephron that interferes with urea and creatinine excretion *Ex. urinary tract obstruction, uroabdomen |
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Increased body temperature causes |
1. Pyrogenic hyperthermia or Fever/Pyrexia 2. Non-pyrogenic hyperthermia |
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Pyrogenic hyperthermia |
Higher tha normal body temperature due to a changed thermoregulatory set-point in hypothalamus **Controlled hyperthermia |
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Non-pyrogenic hyperthermia |
Increased temperature due to failure thermoregulation **Uncontrolled hyperthermia |