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MSII Pathology > Damjanov - Chapter 1 - Laboratory Medicine > Flashcards

Damjanov - Chapter 1 - Laboratory Medicine Flashcards

1
Q

what are acute phase proteins?

A

positive and negative
+ appear in increased concentration in blood in response to inflammation (C-reactive PRO, transferrin, ceruloplasmin, fibrinogen, alpha1-antitrypsin)
- concentrations decrease in response to inflammation (albumin)

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2
Q

what is alkaline phosphatase? when is it elevated?

A

hydrolyzes orthophosphoric esters in many cells of the body and in serum
-elevated in biliary obstruction, growing bones, remodeling bones (Paget’s), osteoblastic metastases, and bone-forming tumors

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3
Q

what is aminotransverase/transaminase? what are two important ones?

A

a group of enzymes transferring amino groups from one AA to another
-ALT and ASP are important in liver function tests

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4
Q

what is BUN for?

A

blood nitrogen present as urea

  • elevated in renal failure (but less specific than elevated creatinine), but falls rapidly after renal dialysis b/c highly diffusible
  • increased in heart failure, shock, dehydration
  • doesn’t measure N included in proteins (18% of total blood N)
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5
Q

what forms the most powerful of body’s buffer systems?

A

CO2 and HCO3-

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6
Q

what is the creatinine level in renal failure (azotemia)?

A

elevated

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7
Q

why is lactate dehydrogenase important?

A

ubiquitous enzyme involved in removing H from lactate

-elevated in conditions with widespread cell destruction

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8
Q

sensitivity VS specificity

-when do you want them to be high?

A

sensitivity: correctly identify who has the disease (positivity in health; “true positives, false negatives”)
- high in screening tests

specificity: correctly identify who doesn’t have the disease (negativity in health; “true negatives, false positives”)
- high in final diagnosis

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9
Q

what is serum best defined as?

A

defibrinated plasma

-does not clot, can’t be used for study ofcoagulation factors and substances entrapped in fibrin meshwork of clot

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10
Q

under what 4 things is Na+ balance under control of? how do they work?

A
  1. thirst (increases if one ingests too much Na or loses too much water; osmoreceptors in hypothalamus increase osmolality of plasma to activate thirst)
  2. ADH (increased osmolality releases ADH from hypothalamus to resorb water in kidney)
  3. aldosterone (loss of ECV decreases GFR,, releasing renin to act on angiotensinogen to increase aldosterone from ZG of adrenal cortex, to promote exchange of Na+ for K+ or H+ in distal renal tubules to retain Na+)
  4. ANP (stimulates kidneys to increase excretion of Na+ in urine)
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11
Q

what is the primary determinant of serum osmolality?

A

sodium concentration

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12
Q

when does dilutional hyponatremia happen?

A
  1. increased water intake
  2. infusion of water
  3. decreased excretion of water (water retained in ECS)
  4. hypoproteinemia (inadequate production of serum PRO in cirrhosis; loss of PRO in nephrotic syndrome or gastroenteropathy)
  5. shift of water from cells into the ECV (hyperglycemia of DM, paraproteinemia, hyperlipidemia has osmotically active substances in blood)
  6. SIADH (water poisoning when tumor secretes ADH)
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13
Q

when does depletional hyponatremia happen?

A
  1. gastrointestinal loss (vomit, diarrhea, sequestration of fluid in intestine, GI fistulas)
  2. renal loss (glycosuria of DM, hypercalcemia, salt-wasting kidney disease, diuretics, Addison’s)
  3. dermal loss (burns)
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14
Q

what is the most common cause of hyponatremia?

A

combined loss of Na+ and water, where lost Na+ is not adequately replaced

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15
Q

how can there be renal loss of water?

A
  • central and nephrogenic diabetes insipidus
  • renal tubular necrosis (postsurgical period)
  • loop and osmotic diuretics
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16
Q

explain the difference between central and nephrogenic diabetes insipidus

A

C: primary (related to injury of hypothalamus or posterior pituitary) or secondary (drug treatment)
N: consequence of end-stage renal disease

both lead to renal loss of water and hypernatremia

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17
Q

when does sodium retention occur? (3)

A
  1. adrenal cortical lesions (most common)
    - hypercorisolism due to benign or malignant adrenal cortical tumors
  2. corticosteroids (esp. long-term use)
  3. infusion of Na-rich solutions
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18
Q

what are signs of dehydration?

A
  • hypernatremia
  • high hematocrit
  • spurious hyperalbuminemia
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19
Q

explain hyperchloremic metabolic acidosis?

A

depletion of HCO3- in metabolic acidosis is usually accompanied by formation of organic anions to replace lost HCO3-

  • if this doesn’t occur, the gap is filled with Cl-
  • NOT accompanied by hypernatremia
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20
Q

explain hypochloremic metabolic acidosis

A

metabolic alkalosis caused by loss of Cl- in GIT is associated with anion gap filled with HCO3-
-Na+ concentration is normal

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21
Q

what does insulin do for potassium?

A

insulin promotes K+ flux across cell membrane into cells

-no insulin = efflux of K+ from cells

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22
Q

what is hypokalemia usually caused by?

A

increased loss of K+ in urine, GIT, or skin

  • also may be due to redistribution of K+ from ECF to ICF compartment
  • rarely reduced intake (unless starvation or alcoholics)
23
Q

explain increased GI loss of K+

A

all GI secretions have K+, so vomit/diarrhea causes K+ and Na+ loss

  • prolonged laxative use has same effect
  • increased mucus production in inflammed mucosa or villous adenomas
24
Q

how does prolonged loss of Na+ cause K+ loss?

A

prolonged Na+ loss causes secondary hyperaldosteronism and increased loss of K+ in urine

25
Q

explain increased renal loss of K+

A

occurs most in patients treated with diuretics or those who have osmotic polyuria (diabetes)
-rare cases are mineralcorticoid excess in primary hyperaldosteronism, or secondary hyperaldosteronism (in end-stage kidney disease or cirrhosis)

26
Q

explain redistribution of K+ and how it causes K+ loss

A

occurs during alkalosis, which favors entry of K+ into cells, replacing H+ that entered ICF

  • insulin administration promotes entry of K+ into cells
  • familial periodic muscle paralysis: rare condition where hypokalemia develops b/c of entry of K+ into muscle cells
27
Q

what are cardiac symptoms of hypokalemia?

A

arrhythmias and abnormal cardiac contractinos associated with EKG changes

  • flattening/inversion of T-waves
  • ST segment depression
  • appearance of U waves
  • digitalis toxicity increases
28
Q

what are neuromuscular symptoms of hypokalemia?

A

generalized muscle weakness and hypotonia

-lethargy, depression, and confusion

29
Q

what are GI symptoms of hypokalemia?

A

slow peristalsis, constipation, ileus

30
Q

what are metabolic/renal symptoms of hypokalemia?

A

alkalosis and polyuria due to decreased concentrating capacity of kidneys

31
Q

what is hyperkalemia most often caused by?

A

renal failure, metabolic disturbances, tissue damage
-reduced excretion of K+, massive release from injured/lysed cells, or redistribution of K+ from ICV to ECV (rarely from increased intake)

32
Q

explain how reduced excretion of K+ can pathological causehyperkalemia

A

in end-stage kidney disease (>80% of nephrons are lost/damaged)

  • metabolic disturbances causing ketoacidosis
  • Addison’s disease hypoaldosteronism occurs, to decrease K+ in urine
33
Q

explain how redistribution of K+ from ICV to ECV occurs

A

internal redistribution occurs most often in ketoacidosis of diabetes

  • lack of insulin and severe hyperglycemia may also cause hyperkalemia
  • hyperkalemic periodic paralysis is rare muscle disease characterized by hyperkalemia and mytonia
34
Q

what is spurious hyperkalemia?

A

release of K+ from hemolyzed RBC
-hemolysis and delayed separation of blood cells from serum are most common causes of hyperkalemia in hospital laboraties

35
Q

what are characteristic EKG details of hyperkalemia?

A
  • initially peaked T waves
  • P waves disappear and QRS complexes are widened (if K+ > 6 mmol/L)
  • causes ventricular arrhythmia, progressing to fibrillation
36
Q

how do you treat hyperkalemia?

A

immediate infusion of Ca gluconate to counteract cardiotoxic effects of hyperkalemia

  • followed by infusion of hypertonic glucose (release insulin and promote entry of K+ into cells)
  • can also add sodium bicarbonate to increase pH of ECF to promote K+ shift into cells
37
Q

explain metabolic acidosis and how it is compensated

A

accumulation of H+ and decrease in HCO3-

  • pH < 7.4, HCO3- < 24 mmol/L
  • loss causes anion gap that is filled with fixed acids
  • lungs compensate by exhaling CO2
  • -in compensated metabolic acidosis, PCO2 is reduced
38
Q

explain metabolic alkalosis and compensation

A

loss of H+ or retention of HCO3-

  • pH > 7.4, HCO3- > 24 mmol/L
  • compensation is fast by reduced CO2 expiration, which leads to increased PCO2
39
Q

explain respiratory acidosis and compensation

A

excessive retention of CO2 in lungs

  • pH < 7.4, PCO2 > 40 mmHg
  • kidneys compensate over time by retaining HCO3-, leading to rise of blood HCO3-
40
Q

explain respiratory alkalosis and compensation

A

excessive loss of CO2 through lungs

  • pH > 7.4, PCO2 > 40 mmHg
  • kidneys compensate over time by increasing excretion of HCO3-, thus lowering HCO3- concentration in blood
41
Q

causes of metabolic acidosis? and the mnemonic?

A
  1. loss of bicarbonate (often through GIT)
  2. inability to excrete H+ through kidneys (end stage kidney failure)
  3. excessive production of endogenous acids (uncontrolled DM, ketoacidosis)
  4. ingestion of fixed acids (poisoning)
DEKALS:
Diabetic acidosis
Ethylene glycol (antifreeze)
Kidney failure
Alcohols (ethanol, methanol)
Lactic acidosis
Salicylate poisoning
42
Q

what is lactic acidosis? Type A VS B?

A

chronic increases in lactic acid (normal 0.6 - 1.2 mmol/L, increases 10x with exercise normally, but chronically becomes lactic acidosis)

  • Type A: more common, caused by hypoxic cell injury (heart failure, shock), or sever exercise
  • Type B: severe liver disease and chronic alcohol abuse; related to ingestion of certain drugs and poisons
43
Q

in what cases is metabolic alkalosis persistent?

A

three conditions

  1. extracellular volume contraction (leads to reduced glomerular filtration and increased Na+ reabsorption)
  2. K+ deficiency (enhance HCO3- reabsorption)
  3. mineralocorticoid excess (promotes distal tubular reabsorption of Na+ and excretion of K+ and H+)
44
Q

how is hypocalcemia associated with hyperphopshatemia?

A

three ways

  • hypoparathyroidism: congenital or asquired after removing parathyroids
  • chronic renal failure: phosphate retention and inadequate hydroxylation of vit D
  • hypomagnesemia (rare): Mg++ is needed to make active PTH
45
Q

what are symptoms of hypocalcemia?

A
  1. neuromuscular symptoms (numbness, paresthesia, muscle spasm/cramps –> Chvostek’s facial muscle spasm, Trousseau’s carpal spasm)
  2. cardiac signs (abnormalities of cardiac rhythm and prolonged QT interval in EKG)
  3. behavioral changes (nonspecific)
  4. laryngeal stridor (related to laryngospasm)
46
Q

what are the most common, less common, and uncommon causes of hypercalcemia?

A

most: primary hyperparathyroidism and malignant tumors
less: granuloma, hyper vit D, hyperthyroidism, drugs
uncommon: Paget’s disease, adrenal failure, milk alkali syndrome, Li therapy, hyperMg++, immobiliation

47
Q

what is primary, secondary, and tertiary hyperparathyroidism?

A

1: often from parathyroid adenoma, less often primary parathyroid hyperplasia
2: parathyroid hyperplasia in patients with chronic renal disease
3: develops in context of secondary hyperparathyroidism
- secretion of PTH becomes independent of Ca++ levels in blood and cannot be medically regulated

48
Q

symptoms of hypercalcemia?

A

mostly vague

  1. renal (polyuria, polydipsia, renal calculi, nephrocalcinosis)
  2. musculoskeletal (bone pain, fractures, periarticular calcifications)
  3. neurologic (weakness, depression)
  4. GI (ab pain, pancreatitis)
  5. cardiovascular (arrythmia, extreme cardiac arrest)
49
Q

what is a major source of spurious hyperphosphatemia?

A

hemolyzed blood

50
Q

what is spurious hypoalbuminemia commonly seen in?

A

pregnancy

-related to increased plasma volume

51
Q

what are the alpha1-globulins?

A

a1-antitrypsin - serine protease inhibitor (90%)
a1-fetoprotein - prominent in serum of fetuses and infants; increased in liver cell carinoma, gonadal/extragonadal cell tumors, and pregnant women with Down syndrome fetus

also include a1-acid glycoprotein and a1-lipoprotein

52
Q

what are alpha2-globulins?

A

a2-macroglobulin - protease inhibitor and one of largest proteins in the blood; increased in nephrotic syndrome (not lost in urine)
haptoglobin - binds and clears free Hb during intravascular hemolysis
ceruloplasmin - Cu-containing with ferroxidase activity for Fe and Cu transport; acute phase protein

53
Q

what are the beta-globulins?

A

transferrin - major Fe-transporting protein (correlates with total iron binding capacity of serum) reduced in chronic anemia
complement C3/4 - inflammation/immune mediators reduced in autoimmune disorders
B2-microglobulin - light chain part of class I HLA; filtered in glomeruli, but reabsorbed (increased if B-cell pymphoma and leukemia)
fibrinogen - high molecular weight protein in coagulation

also includes C-reactive protein

54
Q

what are the gamma-globulins?

A

immunoglobulins (all 5 of them)

C-reactive protein (usually present in barely detectable amounts, but 1000x more in infection)

MSII Pathology (11 decks)

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