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Block 5 > Week 5 > Flashcards

Week 5 Flashcards

1
Q
  1. What are the phases of drug discovery and development (3) - describe each
A
  1. Discovery phase - bench scientific inquiry into drug targets and associated compounds
  2. PreClinical Phase - testing in animals, used to establish safety profile
  3. Clinical Phase - testing in humans, used to establish important characteristics of drug compound
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2
Q

What are the phases of clinical phase? (4)

A
  1. Phase I: non-blind / single dose (Ia) or repeated dose (Ib) in healthy volunteers / small # of subjects
  2. Phase II: single-blind or double blind / patients with target disease / moderate # of subjects
  3. Phase III: double-blind / patients with target disease / large # of subjects (1 - 4 years)
  4. Phase IV: post-approval, monitors drug safety / outcomes in the general population
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3
Q
  1. What is urine sedimentation useful for?
A
  1. visualize urinary analytes after centrifuging urine such as RBC, WBC, epithelial cells
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4
Q

what does it mean if you see these things in urine sedimentation?

  1. RBC - normal shape
  2. RBC - deformed shape
  3. WBC
  4. Tubular epithelial cells - excessive number
  5. Tubular epithelial cells - Oval Fat Body
A
  1. long differential like UTI, Stones, etc - but outside of glomeruli
  2. Glomerular disease
  3. suggests infection
  4. tubular damage
  5. epithelial cell laden with lipids creating the maltese cross- NEPHROTIC SYNDROME
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5
Q

RBC Casts

  1. What does it look like? (choose out of the following images)
  2. What does this mean?
A
  1. indicates glomerulonephritis (inflammation and damage to glomerulus) or hypertensive emergency
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6
Q

WBC Casts

  1. What does it look like? (choose out of the following images)
  2. What does this mean? (3)
A
  1. indicates tubulointerstitial inflammation (inflammation that affects the tubules of the kidneys and the tissues that surround them (interstitial tissue)
  2. Acute pyelonephritis - a bacterial infection causing inflammation of the kidneys
  3. Transplant rejection
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7
Q

Granular Casts

  1. What does it look like? (choose out of the following images)
  2. What does this mean?
A
  1. acute tubular necrosis (ATN)
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8
Q

Fatty Casts

  1. What does it look like? (choose out of the following images)
  2. What does this mean?
A
  1. indicates Nephrotic syndrome (assoc. with maltese cross)
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9
Q

Hyaline Casts

  1. What does it look like? (choose out of the following images)
  2. What does this mean?
A
  1. Solidification of Tamm-Horsfall mucoprotein - only casts that should be seen as normal in urine sample. They can be observed after intense exercise, in very concentrated low-volume urine, or during diuretic treatment.
  2. very large amounts of hyaline casts can indicate renal disease
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10
Q

Indicate what the name of each crystal is

A
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11
Q

Indicate what the name of each crystal is?

A
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12
Q

Crystals in Urine → Calcium Oxalate

  1. what disorders can lead to this crystal? (3)
A
  1. IBD, malabsorption of calcium, ethylene glycol poisoning
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13
Q

Crystals in Urine → Cystine

  1. what disorders can lead to this crystal? (1)
A
  1. cystinuria
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14
Q

Crystals in Urine → Struvite

  1. what disorders can lead to this crystal?
A
  1. indicates alkaline urine pH (associated with Proteus which is a urea splitting organism)
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15
Q

Crystals in Urine → Uric Acid

  1. what disorders can lead to this crystal? (2)
A
  1. indicates uric acid stones
  2. Urate nephropathy (Acute uric acid nephropathy is caused by deposition of uric acid crystals within the kidney interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter.)
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16
Q

Crystals in Urine → Calcium Phosphate

  1. what disorders can lead to this crystal?
A
  1. distal renal tubular acidosis
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17
Q

Crystals in Urine → Acyclovir

  1. what disorders can lead to this crystal?
A
  1. excessive dose of acyclovir which leads to renal dysfunction
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18
Q

Crystals in Urine → Ciprofloxacin/sulfa crystals

  1. what disorders can lead to this crystal?
A
  1. drug toxicity
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19
Q

Bright stones in kidney, ureter, and bladder can be seen in which type of imaging?

A

CT WITHOUT contrast

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20
Q

What type of imaging can differentiate between simple cyst and solid mass (malignant)

A
  1. CT WITHOUT contrast followed by CT WITH IV contrast
  2. cysts will show no change after contrast but masses will show increased density after contrast
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21
Q
  1. What is the optimal range of pH?
  2. What is the pH rangecompatible with life?
  3. Acidemia is considered pH
  4. Alkalemia is considered pH>?
A
  1. 7.35-7.45
  2. 6.8-7.8
  3. 7.37
  4. 7.43
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22
Q

The kidney repleneshis/controls levels of bicarbonate. It does so via reabsorption and generation

  1. where in the nephron does reabsorption of bicarb happen?
  2. where in the nephron does generation of bicarb happen?
A
  1. PCT
  2. Intercalated cells of collecting duct (secretion of H+ after H+ and HCO3- are made needs to be combined with urinary buffers to prevent acidic urine/nephron damages → where HPO42- or NH3 comes in)

both lead to bicarb going into interstitium

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23
Q

W/ bicarb generation - bicarb is absorbed into interstitium but this is paired with H+ secretion into lumen. This makes the urine acidic but this is where HPO42- and NH3 act like buffers.

  1. Which one is more readily available/limited?
  2. How is NH3 made?
A
  1. HPO42- is a fixed supply based on how much P is in diet
  2. NH3 - generated from gluatamine so there is an adaptable supply - this is the predominant form of acid excretion
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24
Q
  1. Where is ammonium generated?
  2. Where is ammonium reabsorbed?
  3. Where is ammonium secreted?
A
  1. Ammonium Generation: proximal tubule, divides glutamine into 2 NH4 / 2 HCO3 -
  2. Ammonium Reabsorption: thick ascending limb via NH4 + / Na + / 2 Cl - channel
  3. Ammonium Secretion: type A intercalated cells, used to carry H + out of the body
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25
Q

describe if these are respiratory/metabolic acidosis or respiratory/metabolic alkalosis

A

image

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26
Q

List some of the reasons for respiratory acidosis, metabolic acidosis*, respiratory alkalosis, or metabolic alkalosis

A
  • Metabolic acidosis - you need to check anion gap to further determine causes
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27
Q

Equation for anion gap?

A
  • Anion Gap = Na – (Cl + HCO3-)
  • you get values from your electrolyte panel/CBC
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28
Q

What is considered a

  1. high anion gap - what does this mean?
  2. normal anion gap
A
  1. >12 → this means that there is excessive H+
  2. 9-12
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29
Q

You have metabolic acidosis -

  1. What are the causes based on high anion gap
  2. What are the causes based on normal anion gap
A
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30
Q
  1. What are the compensation mechanisms of these 4 scenarios (respiratory acidosis, metabolic acidosis, respiratory alkalosis, or metabolic alkalosis)
A
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31
Q

How does levels of CO2 affect pH?

A

Remember the bicarbonate buffer system equation.

  1. With increase in CO2 → there is greater presence of H+ (decrease pH) (remember eqn wants to be in balance)
  2. When there is decrease in CO2 → there is less H+ (increase pH)
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32
Q
  1. What are mixed acid-base disorders?
  2. what patient stats can indicate this disorder? (2)
A
  1. two simultaneous metabolic/respiratory disturbances
  2. extreme pH deviation OR Pco2/HCO3- deviations with normal pH indicate possible mixed disorder
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33
Q

What is compensation vs correction of pH?

A
  1. Compensation is restoring pH to normal → will get close to normal pH
  2. Correction means pH is restored to normal due to correction of underlying disorder
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34
Q

What are the steps when determining what disorders are within mixed acid-base disorders?

  1. if initial label of pt is respiratory acidosis or respiratory alkalosis (5)
A
  1. see if its acidic or alkalosis by looking at pH
  2. Determine if this acidosis/alkalosis is due to respiratory or metabolic reasons
  3. determine if scenario is acute or chronic by looking at changes in Pco2 and how it goes along with patient changes in pH and HCO3- → this will tell you if patient has metabolic alkalosis or metabolic acidosis on top of original acid/base disturbance
  4. Metabolic alkalosis (nothing further after this)
  5. Metabolic acidosis → various steps
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35
Q

What are the steps when determining what disorders are within mixed acid-base disorders?

  1. if initial label of pt is metabolic acidosis (7)
A
  1. determine if there is or is not an anion gap
  2. if normal then non-AG metabolic acidosis → which can be caused by renal or gut issue
  3. Determining between renal or gut issue → you need to do Urine anion gap (UAG)
  4. Also do winters formula to determine if there is an additional resp. acidosis or resp. alkalosis
  5. (back to #2) - if there IS a larger anion gap then think MUDPILES as differential and calculate delta gap
  6. w/delta gap → if pts HCO3- > delta gap HCO3 then you also have metabolic alkalosis
  7. w/delta gap → if pts HCO3- < delta gap HCO3 then you also have NON-AG METABOLIC ACIDOSIS
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36
Q

What are the steps when determining what disorders are within mixed acid-base disorders?

  1. if initial label of pt is metabolic alkalosis
A
  1. nothing further in algorithm just check if chloride sensitive or resistant
  2. <10 is sensitive
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37
Q
  1. What is the winters equation?
  2. What does it determine?
A
  1. It determines if there is an additional resp. acidosis or resp. alkalosis on top of the Non-AG Metabolic Acidosis
38
Q
  1. What is normal HCO3- value
  2. Normal AG value
  3. Normal Pco2
A
  1. 24
  2. 12
  3. 40
39
Q
  1. (ACUTE) For every 10 change in pCO2 - (BLANK A) change in pH
  2. (CHRONIC) For every 10 change in pCO2 - (BLANK B) change in pH
A
  1. 0.08 increase
  2. 0.04 increase
40
Q

RESPIRATORY ACIDOSIS

  1. (ACUTE) For every 10 change in pCO2 - (BLANK A) change in HCO3-
  2. (CHRONIC) For every 10 change in pCO2 - (BLANK B) change in HCO3-
A
  1. 1 mEq/L INCREASE
  2. 3 mEq/L INCREASE
41
Q

RESPIRATORY ALKALOSIS

  1. (ACUTE) For every 10 change in pCO2 - (BLANK A) change in HCO3-
  2. (CHRONIC) For every 10 change in pCO2 - (BLANK B) change in HCO3-
A
  1. 2 mEq/L DECREASE
  2. 4 mEq/L DECREASE
42
Q
  1. What is urine anion gap equation?
  2. when is it used?
A
  1. UAG = (Na + K) - Cl
  2. when you have a non-AG metabolic acidosis and want to determine if cause is renal or non-renal
  3. remember negative UAG - gut/non-renal issue
43
Q
  1. What is delta qap equation?
  2. when is it used?
A
  1. calculatedAG - 12 = delta
  2. delta + labHCO3- = Y
  3. when you have AG metabolic acidosis and want to know if you also have metabolic alkalosis or Non-AG metabolic acidosis
  4. If labHCO3 > Y → metabolic alkalosis
  5. If labHCO3 < Y → NON-AG metabolic acidosis
44
Q

what are the differentials for High Anion Gap metabolic acidosis?

A

MUDPILES

  1. Methanol
  2. Uremia
  3. Diabetic Ketoacidosis
  4. Propylene glycol
  5. Iron poisoning OR Isoniazid
  6. Lactic Acidosis
  7. Ethylene Glycol
  8. Salicylates (aspirin overdose)
45
Q
  1. what is the cause of High Anion Metabolic Acidosis
  2. What causes there to be an anion gap?
A
  1. there is retention of acid and the body compensates this acidosis with an unmeasured anion which is why anion gap is present
  2. Acids (eg, lactate and pyruvate) are protons donors and must be buffered by bicarbonate. The consumption of bicarbonate by the unmeasured anions (which are present due to MUDPILES) will increase the anion gap by lowering the serum bicarbonate level.
46
Q
  1. How does methanol cause high anion gap metabolic acidosis?
  2. What is methanol found in?
  3. symptoms of methanol consumption
  4. tx?
A
  1. methanol is metabolized into formic acid which can lead to increase in molecules that “cancel out” bicarbonate and increase anion gap
  2. antifreeze, industrial cleaners, etc
  3. formic acid is CNS poison so it can show visual loss, confusion, coma
  4. ethanol (competes with alcohol DH), fomepizole (inhibits alcohol DH)
47
Q
  1. How does ethylene glycol cause high anion gap metabolic acidosis?
  2. What is ethylene glycol found in?
  3. symptoms
  4. tx?
A
  1. metabolized to glycolic acid, oxalic acid
  2. antifreeze / industrial cleaners / windshield wiper fluid
  3. Ethylene glycol is a kidney poison, presents with flank pain / oliguria / acute renal failure
  4. fomepizole (inhibits alcohol DH) / ethanol (competes with alcohol DH)
48
Q
  1. How does propylene glycol cause high anion gap metabolic acidosis?
  2. What is propylene glycol found in?
  3. symptoms
A
  1. metabolized to pyruvic / acetic / lactic acid
  2. antifreeze / solvent for IV benzodiazepines
  3. Presents with CNS depression / hemolysis / seizure / coma / organ failure (NO VISUAL / RENAL SYMPTOMS)
49
Q
  1. How does uremia cause high anion gap metabolic acidosis?
A
  1. inability to excrete organic acids, seen in advanced kidney disease
50
Q
  1. How does Diabetic Ketoacidosis cause high anion gap metabolic acidosis?
  2. symptoms
A
  1. overproduction of ketone bodies (acids) in type I diabetes
  2. Presents with polyuria / polydipsia / nausea / Kussmaul respiration (deep, rapid breathing)
51
Q
  1. How does lactic acidosis cause high anion gap metabolic acidosis?
A
  1. low tissue oxygen delivery leads to conversion of pyruvate → lactate
52
Q
  1. How does iron poisoning cause high anion gap metabolic acidosis?
  2. symptoms?
A
  1. high levels of ferric ions (Fe 3+) leads to massive production of H +
  2. Initially presents with GI pain, progresses to shock / coagulopathy / hepatic dysfunction / lung injury
53
Q
  1. How does isoniazid (INH) cause high anion gap metabolic acidosis?
A
  1. INH overdoses leads to seizures → overuse of muscles → lactic acidosis
54
Q
  1. How does aspirin overdose (salicylates) cause high anion gap metabolic acidosis?
A
  1. Aspirin directly stimulates cerebral respiratory centers and inhibits the citric acid cycle, causing uncoupling of oxidative phosphorylation which ultimately leads to lactic acidosis.
    * aspirin overdose first leads to respiratory alkalosis immediately after ingestion → hyperventilation*
55
Q
  1. What causes Normal AG Metabolic Acidosis?
  2. Why is there normal anion gap?
A
  1. acidosis is caused by the primary loss of HCO3-
  2. compensates with chloride retention
56
Q
  1. What are some causes of Normal AG metabolic acidosis? (6)
A
  1. diarrhea
  2. saline infusion
  3. hyperalimentation
  4. acetazolamide
  5. spironolactone/addison’s disease
  6. RTA
57
Q
  1. How does diarrhea cause normal AG metabolic acidosis?
  2. How does saline infusion cause normal AG metabolic acidosis?
  3. How does hyperalimentation cause normal AG metabolic acidosis?
A
  1. you lose HCO3- with diarrhea
  2. chloride toxicity - infusion of Cl drives HCO3- out of plasma
  3. artificial supply of IV nutrients (contains acidic compounds)
58
Q
  1. How does Acetazolamide cause normal AG metabolic acidosis?
  2. How does spironolactone/Addison’s Disease cause normal AG metabolic acidosis?
A
  1. inhibits carbonic anhydrase so formation and reabsorption of HCO3- is BLOCKED (less HCO3-)
  2. loss of aldosterone effects so H+ is retained and causes acidosis
59
Q
  1. What is the pathophysiology behind metabolic alkalosis?
A
  1. increased HCO3- in plasma
60
Q
  1. How does hypokalemia cause metabolic alkalosis?
A
  1. less K in plasma activates the H/K exchanger so K moves out of cell and H into cells (making plasma alkalotic)
61
Q
  1. How does contraction alkalosis cause metabolic alkalosis?
  2. How does RAAS system reinforce metabolic alkalosis
A
  1. Contraction alkalosis is a type of metabolic alkalosis caused by loop diuretics. Loop diuretics (at TAL) cause salt and water to be excreted in urine, whereas bicarbonate is retained. Loss of ECF volume increases plasma bicarbonate concentration. [[Also seen with thiazide diuretics]]
  2. w/decreased ECV the RAAS system is activate which leads to increased Na/HCO3- reabsorption in PCT AND increased aldosterone activity which leads to H+ secretion in collecting duct → BOTH CONTRIBUTE FURTHER TO METABOLIC ALKALOSIS
62
Q
  1. How does Milk-Alkali Syndrome cause metabolic alkalosis?
A
  1. excessive intake of Ca2+ and alkali (excessive tums or milk intake)
63
Q
  1. How does Bartter Syndrome cause metabolic alkalosis?
A
  1. congenital defect in NKCC transporter in TAL leads to decreased H2O reabsorption → increases RAAS and leads to alkalosis (as described in contraction alkalosis flashcard)
64
Q
  1. How does Gitelman Syndrome cause metabolic alkalosis?
A
  1. Congenital defect in NaCl reabsorption in DCT leads to less H2O reabsorption → decrease ECV activates RAAS → this leads to alkalosis (as outline in other flaschards)
65
Q
  1. How does Liddle Syndrome cause metabolic alkalosis?
A
  1. congenital increase in ENaC activity in Collecting tubule → acts similarly to aldosterone so this is increased secretion of H+
66
Q
  1. How does syndrome of apparent mineralcorticoid excess (SAME) cause metabolic alkalosis?
A
  1. remember this syndrome leads to elevated cortisol which has same effect as aldosterone → leads to increased H+ secretion → alkalosis
67
Q

Urine anion gap

  1. in acidosis excess (BLANK) is excreted in urine
  2. What RTA types will be seen with negative UAG
  3. What RTA types will be seen with positive UAG
A
  1. NH4+
  2. negative UAG represents normal renal response to acidosis so usually it is GI disorders → but can also be RTA type II
  3. RTA type I and type IV
68
Q

What is renal tubular acidosis?

A

When the kidneys do not remove acids from the blood into the urine as they should. The acid level in the blood then becomes too high, a condition called acidosis.

69
Q

DISTAL RTA (TYPE I) - worse one

  1. pathophysiology
  2. clinical presentation (4)
  3. tx
A
  1. defect in H+ secretion by distal nephron/alpha intercalated cells (inability to acidify urine). REMEMBER H+ secretion is necessary for bicarbonate generation → due to these two things you get metabolic acidosis
  2. chronic kidney stones, rickets, hypokalemia (because H secretion is paired with K absorption) , high urine pH
  3. sodium bicarbonate
70
Q
  1. Why does chronic kidney stones result from RTA type I? (Hint: they are calcium stones)
A
  1. Chronic Kidney Stones: acidosis increases Ca2+ release from bones / suppress bone resorption
  2. Alkaline urine precipitates calcium stones (may lead to bilateral kidney stones)
71
Q

What diseases is RTA type I associated with? (2)

A
  1. Autoimmune disease (Sjogren’s / rheumatoid arthritis)
72
Q

Proximal RTA (Type II)

  1. pathophysiology
  2. clinical presentation (4)
  3. tx (2)
A
  1. Defect in HCO3- reabsorption in PCT (mimics actions of acetazolamide) → this leads to increased HCO3- secretion and METABOLIC ACIDOSIS
  2. asymptomatic, mildly reduced HCO3-, hypokalemia, low urine pH
  3. sodium bicarbonate, thiazide diuretic (reduces H2O reabsorption in hopes that more is reabsorbed in PCT which is paired with HCO3- reabsorption)
73
Q
  1. How does hypokalemia happen in proximal RTA (Type II)
  2. What other disorders is this associated with? (2)
A
  1. loss of HCO3- reabsorption in PCT leads to loss of Na and volume → activation of RAAS → increases aldosterone which increases K secretion
  2. Fanconi syndrome (decreased PCT function), multiple myeloma
74
Q

Hyperkalemic RTA (Type IV)

  1. pathophysiology
  2. clinical presentation (3)
  3. tx (3)
A
  1. defect in renal response to aldosterone (hypoaldosteronism) → less H+ secretion PLUS less K secretion → hyperkalemia in plasma which decreases NH4+ production in PCT (less NH4+ excretion so this diminishes kidneys ability to excrete acid load)
  2. hyperkalemia, mild metabolic acidosis, low urine pH
  3. fludrocortisone (acts similarly to aldosterone), sodium bicarbonate, furosemide (decreases K+)
75
Q
  1. What does the BUN measure?
  2. What BUN value indicates renal failure?
A
  1. test measures the amount of urea nitrogen in your blood. Urea nitrogen is a normal waste product that your body creates after you eat. Your liver breaks down the proteins in your food – and while it does that, it creates blood urea nitrogen, also known as BUN. You shouldn’t have high levels because kidney should get rid of these toxins.
  2. >20 mg/dL
76
Q

Pre-Renal Failure (insufficient blood flow to kidneys)

  1. what happens to BUN
  2. Cr
  3. Uosm
  4. Una
  5. Fena (amount of filtered Na that is excreted usually very low <1%)
A
  1. ↑↑
  2. ↑
  3. ↑
  4. ↓
  5. ↓

you have decreased blood flow which makes body want to increase H2O reabsorption - bc water is reabsorbed you make concn urine

77
Q

What is normal

  1. BUN (mg/dL)
  2. Cr (mg/dL)
  3. BUN:Cr ratio
A
78
Q

Intrinsic Failure (dysfunction of nephron)

  1. what happens to BUN
  2. Cr
  3. Uosm
  4. Una
  5. Fena (amount of filtered Na that is excreted usually very low <1%)
A
  1. ↑
  2. ↑
  3. ↓
  4. ↑
  5. ↑
79
Q

Post-Renal Failure (bilateral obstruction of renal outflow)

  1. what happens to BUN
  2. Cr
  3. Uosm
  4. Una
  5. Fena (amount of filtered Na that is excreted usually very low <1%)
A
  1. ↑↑
  2. ↑
  3. ↓
  4. ↑
  5. ↑

high pressure disrupts the tubular reabsorption

80
Q
  1. BUN:Cr ratio of Pre-Renal Acute Renal Failure
  2. BUN:Cr ratio of Intrinsic Renal Failure
  3. BUN:Cr ratio of Post-renal Renal Failure
A
  1. >20:1
  2. 20:1
  3. >20:1
81
Q
  1. what is the leading cause of chronic kidney disease in the US
  2. 2nd leading?
  3. what is the main presentation of nephritic syndrome?
  4. what is the main presentation of nephrotic syndrome?
A
  1. diabetic kidney disease
  2. hypertension - High blood pressure can constrict and narrow the blood vessels in your kidneys, which reduces blood flow and stops the kidneys from working well
  3. hematuria + variable proteinuria (<3.5 g/day) + hypertension
  4. high grade proteinuria (>3.5 g/day) + edema
82
Q
  1. What does Tubulointerstitial Disease present with
A
  1. proteinuria, pyuria (increased WBC in urine), casts, concentrating defect → this is due to inflammation and damage to tubules of nephron. It can begin as AKI and then lead to CKD
83
Q

What are some issues that can lead to chronic kidney disease? (7)

A
  1. diabetic kidney disease
  2. nephrotic syndrome
  3. nephritic syndrome
  4. tubulointerstitial disease
  5. small vessel vasculitis
  6. hypertension
  7. renal cystic disease
84
Q
  1. what are the actions at the 5 different stages of kidney disease? (focus on stage 1, 4, and 5)
  2. What is a normal GFR?
A
  1. >90 is normal GFR
85
Q

What are consequences of renal failure? (Hint: MAD HUNGER)

A
  1. Metabolic Acidosis
  2. Dyslipidemia (especially elevated triglycerides)
  3. Hyperkalemia
  4. Uremia (leads to nausea / anorexia / pericarditis / encephalopathy / platelet dysfunction)
  5. Na + / H2O Retention (leads to HF / pulmonary edema / hypertension)
  6. Growth Retardation and Developmental Delay (occurs in children)
  7. Erythropoietin Deficiency (leads to anemia)
  8. Renal Osteodystrophy (skeletal abnormalities)
86
Q

Indications for Dialysis (Hint: AEIOU)

A
  1. Acidemia: inability to properly excrete H +
  2. Electrolytes: abnormal levels of ions, especially hyperkalemia
  3. Intoxication: toxicity of dialyzable substances (salicylates, isopropyl alcohol, ethylene glycol)
  4. Overload of Fluid: edema / CHF
  5. Uremic Symptoms (nausea, vomiting, bleeding, pericarditis, encephalopathy)
87
Q

What are the three methods for dialysis?

A
  1. Hemodialysis - pump blood from body → through filter → back to body (done in ‘sessions’)
  2. Peritoneal dialysis - fluid cycled through peritoneal cavity (acts as membrane, nightly - can do from home)
  3. Hemofiltration - constant filtering of the blood in critically ill patients
88
Q
  1. what is secondary hyperparathryoidism and tertiary hyperparathyroidism?
  2. How does renal failure cause this
  3. tx?
A
  1. In secondary hyperparathyroidism, the serum calcium is normal and the PTH level is elevated. Tertiary hyperparathyroidism is characterized by excessive secretion of PTH after longstanding secondary hyperparathyroidism, in which hypercalcemia has ensued.
  2. image - in tertiary there is increased Ca2+ because PTH forces excretion of calcium from bones
  3. phosphate binders
89
Q
  1. What is renal osteodystrophy?
  2. What is Osteitis Fibrosa Cystica?
A
  1. Renal Osteodystrophy: complication of untreated hyperparathyroidism → bone pain / fractures
  2. Osteitis Fibrosa Cystica: untreated, severely high PTH → bone cysts / Brown tumors
90
Q

How to diagnose between the RTA (1, 2, and 4)

A
  1. get if it is Non-AG metabolic acidosis
  2. check urinary anion gap (post means GUT issue like diarrhea)
  3. check urinary pH
  • >5.5 pH → it is RTA I (distal)
  • RTA II (proximal) is variable pH and HCO3 is between 12-20
  • RTA IV has pH <5.3 and HCO3- ~17

Block 5 (7 decks)

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