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Can the body correct a metabolic alkalosis when hypochloremia is present? Why?
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ClinPath Final
final exam
| Question | Answer |
|---|---|
| Can the body correct a metabolic alkalosis when hypochloremia is present? Why? | No, because bicarbonate will be excessively reabsorbed when chloride is depleted. |
| Body buffer systems | 1. bicarbonate system 2. red cell hemoglobin 3. plasma and intracellular proteins 4. organic and inorganic phosphates 5. bone carbonate |
| Respiratory component of bicarbonate buffer system | pCO2 |
| Metabolic component of bicarbonate buffer system | HCO3 |
| Analytes in a standard blood gas | pH, pCO2, HCO3, TCO2, pO2 |
| What is necessary to determine if a patient is acidemic or alkalemic? | pH |
| Respiratory acidosis is characterized by ____, which is caused by ____. | -increased pCO2 -caused by hypoventilation |
| Respiratory alkalosis is characterized by ____, which is caused by ____. | -decreased pCO2 -caused by hyperventilation |
| Metabolic acidosis is characterized by ____, which is caused by _____. | -decreased plasma HCO3 concentration -due either to bicarb loss or bicarb buffering of XS acid |
| Metabolic alkalosis is characterized by ____, which is caused by ____. | -increased plasma HCO3 concentration -loss of H+ ion |
| Base excess | the mEq/L of strong base or acid added to the sample that would produce a neutral pH |
| Positive base excess indicates... | metabolic alkalosis |
| Negative base excess indicates... | metabolic acidosis |
| Causes of hypoxemia | -hypoventilation (usually hypercapnic, too) -low concentration of inspired O2 -ventilation/perfusion mismatch -impaired alveolar gas diffusion -R to L shunting (does not respond to O2 therapy) |
| 3 components of total CO2 | -dissolved CO2 -H2CO3 -HCO3 ion |
| How to calculate anion gap | (Na + K) - (HCO3 + Cl) |
| Unmeasured anions | -negatively charged proteins -phosphates and sulfates (renal acids) -lactic acid -ketoacids -exogenous acids (ethylene glycol) |
| 2 Causes of metabolic acidosis | 1. accumulation of acids (increased anion gap) 2. loss of bicarb (normal AG and hyperchloremia) |
| 5 ways acids accumulate | 1. lactic acidosis due to hypoxia or mm damage 2. renal acidosis due to decreased GFR 3. ketosis 4. exogenous acid accumulation (ethylene glycol) 5. hyperalbuminemia |
| How does loss of bicarb create a metabolic acidosis with hyperchloremia? | -loss of bicarb from the GI or kidneys creates an acidosis, and the kidneys must reabsorb Na with Cl -results in hyperchloremia and normal AG |
| When does hyperkalemia occur with metabolic acidosis? | -usually occurs during inorganic or mineral acidosis due to renal failure or loss of bicarb in diarrhea |
| Things that can create a metabolic alkalosis | 1. loss of H ion: vomiting, abomasal displacement, Cl-losing diarrhea 2. enhanced HCO3 resorption: volume loss, Cl or K depletion (diuretics) 3. secondary to respiratory acidosis |
| How does the anion gap change during a simple metabolic alkalosis? | IT DOESN'T CHANGE! |
| How is metabolic alkalosis self-perpetuating? | -the kidney needs to conserve Na and water, and if Cl is not present to be reabsorbed with Na, then HCO3 goes in its place regardless of the alkalosis -if K is also lost, then H+ enters cells, addding to the alkalosis |
| Describe the primary mechanisms that create paradoxical aciduria | 1. HCO3 is reabsorbed with Na in the PCT, creating a more acidic tubular fluid 2. Hypokalemia will cause conservation of K in the DCT, and secretion of H+ into the urine |
| Common causes of respiratory acidosis | 1. widespread pulmonary dz, causing decreased CO2 loss by the lungs 2. intrathoracic lesions 3. lesions or drugs affecting the CNS respiratory center 4. poor ventilation during anesthesia |
| How does the body try to compensate for a respiratory acidosis? | Metabolic alkalosis: increased renal acid excretion and HCO3 reabsorption |
| Common causes of respiratory alkalosis | Hyperventilation: pain, psychological stress, panting, forced respiration during anesthesia, drugs/lesions stimulating the CNS respiratory center |
| How does the body try to compensate for a respiratory acidosis? | Renal excretion of HCO3 (metabolic acidosis) |
| What is the most common mixed acid/base disturbance? | -azotemia (increased AG and metabolic acidosis) with vomiting (metabolic alkalosis) |
| 3 fractions that comprise Ca concentration on chem panel | 1. Free calcium (active) 2. Protein-bound calcium (mostly albumin) 3. calcium bound to non-protein anions |
| 3 hormones involved in calcium regulation | 1. PTH 2. vitamin D (calcitriol) 3. calcitonin |
| Which hormones involved in calcium regulation also regulate phosphate? | PTH and calcitonin |
| Which hormones increase calcium concentration? | 1. PTH (ALSO INCREASES PO4) 2. Vitamin D |
| Which hormone causes hypocalcemia? | 1. Calcitonin (ALSO DECREASES PO4) |
| What pre-analytical error can cause falsely low calcium values? | Use of blood anticoagulated with anticoagulants that chelate calcium (EDTA, citrate, oxalate). |
| What are the major factors affecting serum/plasma total calcium concentration? | 1. age 2. protein status 3. gut absorption 4. bone resorption/deposition 5. kidney resorption 6. acid-base status |
| How does acid/base status affect total calcium concentration? | -Acidemia increases free calcium fraction due to competition for binding sites by H ion. --Organic acids bind free calcium -Alkalemia causes increased PTH secretion, and decreases free calcium. |
| Why is it important to remember that the amount of protein in plasma affects calcium concentration? | Because low protein may cause low TOTAL calcium concentration, but the animal may have a NORMAL free calcium concentration. (To supplement or not to supplement) |
| Things that cause hypercalcemia | "Hogs in yard" 1. hyperparathyroidism 2. osteolysis 3. granulomatous dz 4. spurious 5. idiopathic 6. neoplasia 7. young animal 8. addison's dz 9. renal failure 10. vitamin D xs |
| When is an animal at risk for metastatic mineralization? | When the calcium x phosphate > 70. Can cause renal failure! |
| Common causes of hypocalcemia | 1. hypoalbuminemia 2. post-parturient paresis (milk fever) in dairy cattle 3. equine colic 4. chronic renal dz (except horses) 5. acute pancreatitis 6. ethylene glycol toxicosis 7. rumen overload 8. myopathies |
| Virtually all phosphorous in plasma is... | inorganic phosphorous |
| 3 fractions comprising total phosphate concentration | 1. free phosphate 2. protein-bound phosphate 3. phosphate bound to non-protein cations |
| Serum/plasma phosphate can be artifactually increased by... | -delayed separation of serum from the clot -intravascular hemolysis (or during blood draw) -hyperbilirubinemia -monoclonal gammopathy |
| Factors affecting phosphate concentration | 1. age 2. dietary intake/absorption 3. resorption from bone 4. shifting of phosphate from ECF to ICF (insulin) 5. hormonal imbalances affecting calcium (PTH is phosphaturic) |
| Severe hypophosphatemia causes what life-threatening condition? | RBC hemolysis!! (<1.0 mg/dL) |
| Causes of hyperphosphatemia | (anything that causes marked cell dmg) 1. intravascular hemolysis 2. muscle damage 3. tumor lysis syndrome |
| 3 fractions that comprise total magnesium concentration | 1. free 2. protein-bound (albumin) 3. bound to non-protein anions |
| Where is magnesium usually found within the body? | -bones, soft tissue, and ECF -primarily an intracellular ion (cytosol of RBC's, except in cattle) |
| What pre-analytical factors may alter magnesium concentration results? | -using a chelator tube (EDTA, citrate, oxalate) -delayed separation of serum from clot will falsely increase Mg, except in cattle |
| How is magnesium measured post-mortem? | Magnesium can be measured in the aqueous or vitreous humor post-mortem and reflects antemortem concentrations |
| Factors affecting magnesium concentration | 1. protein status 2. dietary intake and absorption 3. excretion and resorption in kidney 4. lactation 5. hormonal influence |
| What are 2 major functions of magnesium in the body? | 1. proper PTH release and function 2. proper renal handling of potassium |
| Hypomagnesemia may be accompanied by ___ and ___. | -hypocalcemia -hypokalemia -will NOT respond to treatment until Mg is corrected |
| Common causes of hypermagnesemia | -milk fever (increased PTH results in increased gut absorption) -decreased urinary excretion |
| Common causes of hypomagnesemia | -decreased intake (grass tetany in cattle) -excess urinary loss due to osmotic diuresis -hypoproteinemia |
| Common causes of hypophosphatemia and hypocalcemia | -milk fever or eclampsia -hypovitamin D |
| Normocalcemia with hypophosphatemia | -decreased dietary intake -hyperinsulinemia |
| Hypercalcemia with hypophosphatemia | -hyperparathyroidism -equine renal disease |
| Normophosphatemia with hypocalcemia | -hypoalbuminemia -acute pancreatitis in dogs |
| Normophosphatemia with hypercalcemia | -neoplasia (HHM) -Addison's disease -granulomatous disease -idiopathic in cats |
| Hyperphosphatemia with hypocalcemia | -hypoparathyroidism -ethylene glycol toxicicosis -phosphate enema |
| Hyperphosphatemia with normocalcemia | -decreased GFR -growing animal -serum left on clot -rhabdomyolysis -tumor lysis syndrome |
| Hypophosphatemia with hypercalcemia | -hypervitamin D -puppies 6 to 24 weeks of age |
| What information is needed to categorize fluid? | -gross examination -total nucleated cell count -total protein -morphologic examination of any cells in fluid -BONUS: culture and chem panel |
| What kind of tubes should be used or fluid cytology? For culture? | -EDTA (purple) for cytology -red (glass) for culture |
| What are transudates the result of? | -disturbances of fluid circulation |
| 3 ways that fluids become deranged | 1. blockage of lymphatics 2. decreased oncotic pressure (albumin < 1.5) 3. increased hydrostatic pressure |
| 2 classifications of transudate | protein-poor (pure) and protein-rich (modified) |
| What determines protein-poor versus protein-rich transudate? | -type of capillaries affected -liver and lung are typically leakier i.e. protein rich (modified) |
| Presence of a protein-rich (modified) transudate in the abdomen should make you think about... | -congestion of the liver -can be caused by increased hydrostatic pressure in sinusoids AND/OR blockage of lymphatics in liver OR blocked VC/HV |
| Modified transudate in the abdomen could be a result of primary disease in ____ | -abdomen OR thorax! |
| Exudates form as a result of... | -disease of the pleural or peritoneal surface |
| Pathophysiology of exudate formation | -dz on pleural/peritoneal surface > increased vascular and mesothelial permeability > exudation of fluid, protein, cells > chemokines attract leukocytes > further leakage |
| Ddx for bicavitary effusions | 1. congestive heart failure (protein rich in abdomen, either in thorax) 2. generalized dz process affecting both cavities: disseminated cancer, FIP, coagulopathy 3. defects in diaphragm |
| Special fluids | -chyle -bile -urine -blood |
| What kind of effusion does uroabdomen cause? | -initially causes a transudate -over time will cause an exudate |
| What kind of effusion do chyle and bile in the abdomen cause? | -exudate |
| How can a hemorrhagic effusion be differentiated from blood? | -fluid will NOT contain platelets or clot |
| How are urine and plasma different on a chem panel? | -urine is higher in Cr and K, lower in Na and Cl -plasma is higher in Na and Cl, lower in K and Cr |
| [Cr]fluid > 2x[Cr]plasma | Diagnostic for uroabdomen |
| [Cr]fluid > [Cr]plasma | Suspicious for uroabdomen, should measure [K] |
| [Cr]fluid > [Cr]plasma AND [K]fluid > [K]plasma | Supports dx of uroabdomen, higher ratio is more supportive |
| [Cr]fluid > [Cr]plasma AND [K]fluid < [K]plasma | DOES NOT SUPPORT dx of uroabdomen |
| [Cr]fluid < [Cr]plasma | DOES NOT SUPPORT dx of uroabdomen |
| If fluid amylase/lipase activity > plasma/serum activity... | -abdominal effusion due to pancreatitis |
| If fluid [triglyceride] > plasma, but fluid [cholesterol] is < plasma... | -chylous effusion due to lymph duct rupture |
| If fluid [bili] is > plasma... | -abdominal effusion due to biliary tract rupture aka bile peritonitis -causes exudate |
| If fluid [glucose] < plasma, and [lactate] in fluid is > plasma... | -septic effusion |
| If fluid [lactate] is > plasma | -septic effusion in dogs/cats -strangulating obstructions in horses ***separate plasma from cells immediately!! |
| Blood glucose is altered if there is... | 1. altered dietary intake or absorption 2. altered gluconeogenesis 3. altered glycogenolysis |
| Hormones that regulate glucose | 1. insulin (pancreas): lowers 2. glucagon (pancreas): increases 3. growth hormones (pituitary): increases 4. catecholamines and cortisol: increase |
| How do ruminants generate glucose when fasting? | -use proprionate from the rumen or colon |
| Animals that are vulnerable to hypoglycemia during fasting | -animals with prolonged anorexia/starvation (glycogen stores depleted) -neonates (lack enzymes for gluconeogenesis) -end stage liver dz -glycogen storage dz |
| When can hypoglycemia occur without fasting? | -high producing dairy cows > neg. E balance > hypoglycemia and ketosis -ewes with twins (ovine pregnancy toxemia) |
| What artifacts can alter glucose measurement? | lipemia, icterus, hemolysis |
| What is the renal threshold for glucose? | 200 mg/dL |
| What types of preanalytical error can alter BG values? | -delayed sample separation -marked leukocytosis -erythrocytosis **RBC and WBC don't need insulin to use glucose! |
| Conditions causeing hyperglycemia | -physiologic rxn -diabetes mellitus (insulin deficiency or resistance) -drugs |
| Conditions causing hypoglycemia (11) | 1. pre-analytical error 2. analytical error 3. prolonged anorexia/starvation 4. sepsis 5. liver insufficiency 6. Addison's dz 7. Insulinoma 8. Paraneoplastic 9. Insulin overdose 10. Xylitol toxicosis 11. Bovine ketosis/ovine pregnancy toxemia |
| Ketogenesis is promoted by ___ and inhibited by ___. | -promoted by glucagon -inhibited by insulin |
| 3 ketone bodies | 1. acetoacetate 2. acetone 3. beta hydroxybutyrate |
| When are ketone bodies most commonly measured? | -screening for diabetes mellitus -screening dairy cows |
| 2 ketoamines | fructosamine and glycated hemoglobin |
| How are fructosamine and glycated Hb elevated? | -prolonged and consistent hyperglycemia (NOT stress) -fructosamine: 2-3 wks -Hb a1c: 60 days |
| When is insulin concentration most commonly measured? | -hypoglycemic patients suspected of having insulinoma -have increased [glucose] and increased insulin:glucose ratio |
| How to measure insulin:glucose ratio | [insulin] x 100/[glucose] |
| 2 fx of lipids in body | 1. energy storage 2. cell membrane structure |
| 4 body lipids (measured) | 1. cholesterol 2. triglycerides 3. free fatty acids 4. individual lipoproteins |
| Lipoproteins: least to most dense | chylomicron < very low density lipoprotein < intermediate density lipoprotein < low density lipoprotein < high density lipoprotein |
| Where does lipoprotein lipolysis occur? | -luminal surface of capillary endothelial cells -catalyzed by lipoprotein lipase, which needs insulin to work |
| How does heparin clear lipemia? | -activates LPL and hepatic lipoprotein lipase |
| What other compound can help clear lipemia? | -thyroxine |
| What is grossly visible lipemia caused by? | -chylomicrons or VLDL (triglycerides) -NOT cholesterol |
| Ddx for hypercholesterolemia | 1. increased production by hepatocytes (PLN) 2. increased production by enterocytes (post-prandial) 3. hypothyroidism 4. acute pancreatitis 5. cholestasis |
| Ddx for hypocholesterolemia | 1. PSS 2. PLE 3. hypoadrenocorticism |
| Ddx for hypertriglyceridemia | 1. equine hyperlipemia 2. post-prandial 3. hypothyroidism 4. nephrotic syndrome 5. acute pancreatitis |
| How should cholesterol be measured? | -serum sample after 12 hr fast |
| Methods of measuring triglycerides | -chylomicron test -total triglyceride measurement |
| How do FFA get outside of lipoprotein molecules? | hydrolysis of triglycerides > release of FFA to blood > bound to albumin > transported to tissues > used for energy |
| When are FFA usually measured? | -commonly measured in dairy cattle to assess energy balance -increase associated with negative energy balance -also increase with diabetes mellitus, hepatic lipidosis, obesity, food deprivation, after exercise |
| Pancreatic leakage enzymes | -amylase and lipase -must be at least 3-4 fold higher than URL to be suspicious (not very sensitive) -both are excreted by kidneys |
| Increased amylase activity may be caused by... | -pancreatic acinar damage -decreased GFR (prerenal, renal, postrenal) |
| Increased lipase activity may be caused by... | -pancreatic acinar damage -decreased GFR -dexamethasone treatment -pancreatic/hepatic neoplasia |
| Laboratory test of choice for pancreatitis | -pancreatic lipase immunoreactivity (PLI) -species specific ab's are used to measure lipase -independent of GFR status |
| What test is used to diagnose EPI in dogs and cats? | -trypsin like immunoreactivity (TLI) -decreased TLI = EPI |
| Causes of increased TLI | 1. pancreatitis 2. decreased GFR 3. dexamethasone tx 4. horses w/ strangulating obstruction and endotoxic shock |
| Conditions caused by chronic pancreatitis | -diabetes mellitus (islet cell destruction) -exocrine pancreatic insufficiency (acini destruction) |
| EPI | -exocrine pancreatic insufficiency -loss of acinar tissue -deficiency of digestive enzymes and secretions (HCO3) -leads to maldigestion of food -usually seen in German Shepherd, Rough Coated Collie, Greyhound |
| Signs of EPI | -chronic weight loss -accumulation of osmotically active particles w/in GI > movement of H2O into tract > osmotic diarrhea |
| Classic findings with pancreatitis | -increased amylase, lipase, PLI, and TLI -possible hypocalcemia, hypercholesterolemia, metabolic alkalosis, azotemia, cholestasis, DIC, hyperglycemia, abdominal effusions |
| Classic findings with EPI | -decreased TLI -possible decreased cobalamin and increased folate |
| Where does absorption of cobalamin usually occur? | -the ileum -decreased Cbl = distal intestinal dz |
| Causes of increased Cbl | -xs supplementation -hepatocellular dmg |
| Causes of decreased Cbl | 1. ileal mucosal dz 2. small intestinal bacterial overgrowth (SIBO) 3. EPI 4. Cobalt deficiency in cattle |
| How does SIBO cause decreased Cbl? | -increased numbers of enteric bacteria consume more Cbl, and it is not absorbed in the ileum |
| How does EPI cause decreased Cbl? | -interferes with modification of Cbl to absorbable state -also usually develop secondary SIBO |
| How does cobalt deficiency cause decreased Cbl? | -cobalt is needed for synthesis of Cbl by ruminal bacteria |
| Where is folate absorbed? | -proximal enterocytes -decreased folate = proximal intestinal dz -needs Cbl to be converted to its active form |
| Causes of increased folate | 1. SIBO (xs produced by bacteria, seen with EPI) 2. low intestinal pH (also seen with EPI) 3. xs dietary folate |
| What is fecal alpha-PI used to diagnose? | -PLE -leaky gut mucosal barrier allows it to enter GI |
| Tests for intestinal permeability | -D xylose absorption (horses; abnormal curve suggests dmg) -Urine sucrose concentration (test of absorption in horses; increase suggests dmg) -Iohexol (permeability in dogs; increases suggests dmg) |
Created by:
caldrid3