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SUM'20 - Anatomy & Physiology > Renal II > Flashcards

Renal II Flashcards

1
Q

drugs that dilate efferent arterioles causing; decrease GFR, decrease hyperfiltration resulting in nephropathy (in DM)

A

ACE inhibitors

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2
Q

Vasodilators of renal arterioles resulting in increased RBF

A

dopamine

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3
Q

RBF remain constant over the range of

A

80-200 mmHg(autoregulation)

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4
Q

Describe Myogenic mechanism of outoregulaton

A
  1. Increased blood flow 2. Increased stretch in afferent arteriole 3. Increase entry of Ca++ into vascular smooth muscles. 4. Vasoconstriction occurs to maintain constant blood flow
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5
Q

Describe tubuloglomerular feedback of outoregulation

A
  1. Increased blood flow 2. Increased fluid rush to macula densa. 3. vasoconstriction of afferent arteriole to maintain constant blood flow
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6
Q

4 Causes of edema

A
  1. High capillary hydrostatic pressure 2. Decreased plasma proteins 3. Increased capillary permeability 4. Blockage of lympatics
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7
Q

High capillary hydrostatic pressure conditions that cause edema (6)

A
  1. Excess fluid retention by kidneys 2. Acute or chronic kidney failure 3. Glomerulonephritis 4. Mineralocorticoid excess 5. Decreased arteriolar resistance (Vasodilator drugs, Autonomic insufficiency) 6. Increased venous pressure − Congestive heart failure − High output heart failure (e.g. anemia) − Venous obstruction − Venous valve failure − Cirrhosis
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8
Q

Decreased plasma proteins conditions that cause edema

A
  1. Low oncotic pressure 2. Loss of proteins ( Burns, wounds; Nephrosis; Gastroenteropathy) 3. Failure to produce proteins (Malnutrition (“kwashiorkor”), Cirrhosis, Albuminemia)
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9
Q

Increased capillary permeability conditions that cause edema

A
  1. Immune reactions (histamine) 2. Toxins 3. Burns 4. Prolonged ischemia 5. Vitamin deficiency (e.g. vitamin C) 6. Pre-eclampsia and eclampsia in pregnancy
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10
Q

Blockage of lymphatics conditions that cause edema

A
  1. Cancer 2. Surgery 3. Infections (Filariasis or Elephantitis)
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11
Q

Diagnosis for patient with significantly elevated ADH and urine osmolarity with decreased serum osmolarity and urine output

A

SIADH

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12
Q

Diagnosis for a patient with decreased urine output, high urine osmolarity, normal or high serum osmolarity and slightly high ADH

A

Water deprivation (lost in desert)

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13
Q

Diagnosis for patient with high urine output, ADH and serum osmolarity with decreased urine osmolarity

A

Nephrogenic Diabetes Insipidus

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14
Q

Diagnosis for patient with high urine output and serum osmolarity with low ADH and urine osmolarity

A

Central diabetes insipidus

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15
Q

Diagnosis for patient with high urine output and low serum osmolarity, urine osmolarity and ADH

A

1º polydipsia

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16
Q

Normal ABGs

A

pH 7.40 (7.35 - 7.45) [HCO3-] 24 (22 -26) mEq/L PCO2 40 (35 – 45)mmHg PO2 80-97 mmHg SO2 > 98%

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17
Q

The first and fastest line of defense against a change in hydrogen ion concentration is?

A

The chemical buffer system is the first and fastest line of defense against a change in hydrogen ion concentration, acting within seconds. Extracellular (HCO3-) Intracellular (Hb)

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18
Q

Second line of defense in acid base balance

A

Respiratory compensation is the second line of defense, acting within minutes

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19
Q

Third line of defense in acid base balance

A

Renal compensation is the third line of defense, acting within hours to days

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20
Q

Compensation in acute phase involves

A

In the acute phase (minutes to hours), the extra and intra-cellular buffer system (most importantly the HCO3- system) minimize the pH change - “first line of defense”

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21
Q

Compensation in chronic phase involves

A

In the chronic phase ( hours to days), renal or respiratory compensation partially or completely restore pH towards normal.

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22
Q

Can you have fully compensated metabolic

A

No Only respiratory acidosis and respiratory alkalosis can be completely compensated (not metabolic)

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23
Q

Body produces what amount of non-volatile acids

A

Our body produces 80 mmole of non-volatile acids (H2SO4, H3PO4). Kidneys get rids of these acids in pee

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24
Q

Body produces and excretes how much bicarb in a day

A

Production of ‘new’ HCO3- (~ 80 mmol/day) that can be increased in case of acidosis Excretion of HCO3- (1 mmol/day) that can be increased in alkalosis

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25
Q

H+ is excreted in the form of

A

Excretion of H+ as NH4+ (Ammonium ion) Excretion of H+ as titratable acid (H2PO4-)

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26
Q

Renal compensation in acidosis

A

Increased HCO3- reabsorption Increased H+ secretion Production of new HCO3-

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27
Q

Renal compensation in alkalosis

A

Decreased H+ secretion Loss of HCO3- in urine Decreased HCO3- reabsorption

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28
Q

Anian gap

A

Unmeasured anions = Na+ - (Cl- + HCO3-) = anion gap Normal anion gap = 8 to 16 mEq / L

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29
Q

Renal compensation for metabolic acidosis

A

Increase excretion of the excess fixed H+ as titratable acid and NH4+. Increase reabsorption of HCO3-, which replenishes the HCO3- used in buffering the added fixed H+. In chronic metabolic acidosis , an adaptive increase in NH3 synthesis aids in the excretion of excess H+

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30
Q

The serum anion gap represents?

A

unmeasured anions (phosphate, citrate, sulfate and proteins) in serum.

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31
Q

In metabolic acidosis, the serum anion gap is increased if?

A

the concentration of an unmeasured anion is increased to replace HCO3-

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32
Q

In metabolic acidosis, the serum anion gap is normal if?

A

the concentration of Cl- is increased to replace HCO3- (hyperchloremic metabolic acidosis) [e.g. Diarrhea, RTA, Carbonic Anhydrase inhibitors and Addison’s disease]

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33
Q

Renal compensation for metabolic alkalosis

A

Increased excretion of HCO3- because the filtered load of HCO3- exceeds the ability of renal tubules to reabsorb it. If accompanied by ECF volume contraction (e.g. vomiting) the reabsorption of HCO3- increases (secondary to ECF volume contraction and activation of RAII-Aldosterone system), worsening the metabolic alkalosis – “Contraction Alkalosis”

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34
Q

respiratory compensation for respiratory acidosis

A

There is NO respiratory compensation for respiratory acidosis

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35
Q

acute respiratory alkalosis compensation

A

renal compensation has not yet occurred

36
Q

chronic respiratory alkalosis compensation

A

renal compensation (increased HCO3- reabsorption) has occurred. Thus , arterial pH is decreased towards normal (i.e. a compensation)

37
Q

What causes the symptoms of hypocalcemia in chronic respiratory alkalosis

A

occur because H+ and Ca++ compete for binding sites on albumin. Decreased [H+] cause increased protein binding of Ca++ and decreased free ionized Ca++

38
Q

Difference btw acute and chronic respiratory acidosis

A

In acute respiratory acidosis, renal compensation has not yet kicked in. In chronic respiratory acidosis , renal compensation ( Increased HCO3- reabsorption) has occurred . Thus the arterial pH is increased towards normal (i.e. a compensation)

39
Q

Signs and symptoms of respiratory acidosis

A

CNS depression: drowsiness, disorientation unconsciousness (Elevated PCO2 - Increased cerebral blood flow - increased CSF pressure leads to CNS depression) low BP, headache, V fib, muscular twitching, convulsions

40
Q

Causes of increased anion gap acidosis include?

A

1 Methanol 2 Uremia (CRF) 3 DKA 4 Propylene glycol 5 Iron tab or INH 6 Lactic acidosis 7 Ethylene glycol 8 Salicylate/Sepsis Starvation MUD PILES anion gap = >12

41
Q

High anion gap metabolic acidosis: Diabetes ketoacidosis (DKA)

A

Increased serum ketones Serum ketones = acetoacetate and B-OH butyrate

42
Q

Diagnosis and treatment for patient with high anion gap metabolic acidosis, low carb ingestion leading to decreased insulin secretion and elevated ketoacid production

A

Starvation or alcohol abuse Give calories/carbohydrates

43
Q

Diagnosis and treatment for patient with high anion gap metabolic acidosis, tinnitus, delirium, elevated blood salicylate level

A

Salicylate Poisoning Treat with alkaline diuresis (I/ V NaHCO3 + Diuretics)

44
Q

Diagnosis and treatment for patient with high anion gap metabolic acidosis, alcoholism, acute blindness

A

Methanol (wood alcohol) and ethylene glycol (Anti-freeze) Poisoning

45
Q

Causes of Bicarb loss resulting in normal anion gap metabolic acidosis

A

Diarrhea– GI loss of HCO3- MCC Pancreatic; biliary or intestinal drainage Villous adenoma Diuretic (?)

46
Q

Fanconi’s syndrome

A

Type II RTA= Proximal RTA= inability to reabsorb filtered HCO3- Results in normal anion gap metabolic acidosis

47
Q

Type I RTA (Distal RTA)

A

inability to excrete H+ and therefore regenerate HCO3- Results in normal anion gap metabolic acidosis

48
Q

Type IV RTA

A
  • Low aldosterone impairs K+ and H+ secretion - Results in hyperkalemic non-anionic gap acidosis - Failure to excrete NH4+ (hyperkalemia inhibits NH3 synthesis) - Seen in diabetes mellitus due to destruction of juxta cells - Mild renal insufficiency
49
Q

Most common cause of metabolic alkalosis is?

A

volume and chloride depletion -Typically occurs with vomiting and diuretic use -In hypovolemia, kidneys avidly reabsorb NaCl and pee out H+ (trade off) -In these cases, urinary chloride is low and the alkalosis responds to NaCl repletion

50
Q

Other causes of metabolic alkalosis

A
  • Over use of antacids or soda bicarb “Arm and hammer ®”. - Hyperaldosteronism – leads to Na+ reabsorption and H+ excretion. -Hypokalemia– K+ conserved and H+ excreted Urinary chloride is normal and the alkalosis does not respond to NaCl repletion
51
Q

nice way to die

A

CO2 narcosis Supplemental O2 (if PO2 <60 mmHg) – watch for “CO2 retainers

52
Q

Causes of respiratory alkalosis

A
  1. Hyperventilation 2. High altitude (hypoxemia causes elevated ventilation rate) 3. Anxiety 4. Salicylate toxicity (direct stimulation of resp center); also causes metabolic acidosis 5. Sepsis 7. Pneumonia; PE (hypoxemia causes high ventilation rate) 8. Excessive mechanical ventilation
53
Q

Symptoms respiratory alkalosis

A
  • Lightheadedness - Perioral numbness - Paresthesias and even tetany due to fall of ionized calcium
54
Q

Tx of respiratory alkalosis

A

re-breathe own CO2 “paper bag”

55
Q

Effects of acidosis

A

Right shift of O-Hb curve CNS depression Decreased pulmonary blood flow Arrhythmias Impaired myocardial function Hyperkalemia

56
Q

Effects of alkalosis

A

Decreased Cerebral blood flow Left shift of oxy-Hb curve leading to decrease O2 delivery to tissue Arrhythmias Tetany , seizures

57
Q

hypoaldosteronism as a cause of metabolic acidosis

A
  1. The lack of aldosterone has 3 effects on kidney Decreased Na+ reabsorption , K+ secretion and H+ secretion
  2. This results ECF volume contraction ( by low Na+ reabsorption), hyperkalemia and metabolic acidosis with normal gap
  3. The ECF volume contraction is responsible of orthostatic hypotension. Increase pulse rate is via baroreceptor reflex
  4. ECF volume contraction also stimulate ADH secretion.
  5. ADH causes increase water reabsorption causing dilutional hyponatremia
  6. Hyperpigmentation is due to high ACTH (MSH-like activity)
58
Q

Can metabolic disturbance be fully compensated?

A
  • ONLY respiratory disturbance can be completely compensated
59
Q

Causes of Transient Urinary incontinence

A
  1. Delirium/confusion state
  2. Infection, urinary
  3. Atrophic uretheritis/vagintis CDIAPPERS
  4. Pharmaceuticals
  5. Psychological esp. depression
  6. Excessive urine output ( CHF, hyperglycemia)
  7. Restricted mobility
  8. Stool impaction
60
Q

Causes of stablished incontinence

A
  1. Detrusor overactivity
  2. Stress incontinence (outlet incompetence)
  3. Urethreral obstruction
  4. Detrusor underactivity “overflow incontinence”
61
Q

Diagnosis and treatment of incontinence overactive bladder and urgency

A

Detrusor over-activity as a cause cause of incontince and its treatment

  1. Associated with UTI
  2. Treatment: Anticholinergic; M3 blocker e.g. Tolterodine(Detrol ®); bladder training
62
Q

Incontince in a patient with BPH is due to? How do you treat

A
  1. In BPH
  2. Treatment: a adrenergic blocker e.g. prazosin, 5a-reductase inhibitor e.g. finasteride in BPH
63
Q

Diagnosis and treatment of incontinence with high intraabdominal pressure e.g. sneezing, coughing

A

Stress incontinence “outlet incompetence” as a cause of incontinence and treatment

2.Treatment: Kegel’s exercise, pessary, a agonist e.g. phenylpropanolamine

64
Q

Diagnosis and treatment of incontinence with Incomplete emptying

A
  1. = leak with overfilling
  2. Detrusor underactivity “overflow incontinence” and treatment
  3. Treatment: Intermittent catheterization, Bethanechol(cholinergic)
65
Q

Diuretics are

A
  1. Drugs inducing a state of increased urine flow are called diuretics
  2. Are ion transport inhibitors that decreases the reabsorption of Na+ at different sites in the nephron= Increased Na+ excretion along with water. Water chases sodium
66
Q

Carbonic anydrase inhibitor (acetazolamide) major effects

A
  • Increase HCO3- excretion = Metabolic acidosis with normal gap
  • Use to prevent mountain sickness
  • Inhibition of Carbonic Anydrase
67
Q

Loop diuretics (furosemide ) major effects, site of action and MOA

A
  • Increase NaCl excretion, K+ excretion, Ca++ excretion
  • Can treat hypercalcemia ©Loops Lose Calcium
  • S/E Ototoxicity, Hypokalemia, Hyeruricemia, Hypomagnesemia, Hypotension
  • MOA Inhibition of Na+-K+-2Cl- cotransport
  • Site of Action: Thick ascending limb of loop of Henle
68
Q

Thiazide diuretics major effects, site of action and MOA

A
  • MOA: Inhibition of Na+ reabsorption
  • Site of Action: Early DCT
  • Increase NaCl excretion, K+ excretion, decrease Ca++ excretion
  • Can treat calcium stone formation

S/E Hypokalemia, Hyponatremia Hypercalcemia, Hyperuricemia

69
Q

K+ sparing diuretics (spironolactone)/ aldosterone antagonist major effects, site of action and MOA

A
  • MOA: Inhibition of Na+ reabsorption, Inhibition of K+ secretion
  • Site of Action: Late DCT
70
Q

Prerenal causes of renal failure

A

Hypovolemia (dehydration, hemorrhage)

Cardiogenic shock

Sepsis

Drugs (NSAIDs)

Renal artery stenosis

71
Q

Renal (Intrinsic) causes of renal failure

A
  1. Renal ischemia
  2. Glomerulonephritis
  3. Nephrotic syndrome
  4. Nephrotoxic drugs ( NSAIDs, aminoglycosides)
  5. Thromoboembolism
72
Q

Postrenal causes of renal failure

A
  1. Renal ischemia
  2. Glomerulonephritis
  3. Nephrotic syndrome
  4. Nephrotoxic drugs ( NSAIDs, aminoglycosides)
  5. Thromoboembolism
73
Q

Acute renal failure is assymptomatic until ____% nephrone is lost

A

60%

74
Q

High mortality in renal failure is due to?

A

sepsis, CV dysfunction and pulmonary complications

75
Q

Etiology of acute renal failure

A
  1. Prerenal: (60% - 70%) decreased renal blood flow (hypoxia); Hypovolumia; low cardiac out put (in CHF); Sepsis, burns, renal a. stenosis. Reversible thing !
  2. Renal: damage to renal parenchyma; acute tubular necrosis (MCC); Nephrotoxic drugs e.g. aminoglycosides, CCl4, antifreeze poisoning, contrast dye, myoglobinuria
  3. Postrenal: Urinary tract obstruction (BPH, stone, neoplasm)

−FEFNa (Fractional excretion of Na) is high in renal and â in prerenal failure

76
Q

−FEFNa (Fractional excretion of Na) is _______ in renal and ______ in prerenal failure

A

is high in renal and low in prerenal failure

> 1% suggest renal etiology (ATN; Filter is broken)

< 1% suggest prerenal etiology

77
Q

Evaluation of acute renal failure

A
  1. UA (RBCs, casts, WBCs)
  2. Urine lytes
  3. Pass Foleys to rule out obstruction
  4. U/S

FEFNa (Fractional excretion of filtered sodium)

78
Q

Complications of acute renal failure

A
  1. Na+/water retention ® CHF, edema −Treat with diuretics
  2. Azotemia (High BUN and Cr) due to High GFR
  3. Hyperkalemia (therefore, avoid Ringer’s Lactate)
  4. Hypermagnesemia
  5. Hyponatremia
  6. Hyperphosphatemia : Low VitD3 and High phosphate (phosphate binds with Ca++) lead to hypocalcemia which causes secondary hyperparathyroidism
  7. Bone pain and fractures (renal osteodystrophy)
  8. Metabolic acidosis with high anionic gap
  9. Hyperurecemia
  10. Bleeding due to platelet dysfunction. (Platelets count , PT, PTT are normal). Also due to defective vWF
  11. Seizures ( due to hyponatremia)
  12. Hypocalcemia is due to low Vit D3 (Vit D3 promotes intestinal calcium absorption)
  13. −Hyperphosphatemia
79
Q

Treatment of acute renal failure

A
  1. Fluid and electrolyte balance −Calcium acetate
  2. Adjust medication dosage
  3. Dialyze
  4. Diuretics and IV hydration in ATN
  5. D/C offending medication
  6. Steroids for glomerulonephritis
80
Q

Can you give sux to patient with acute renal failure?

A

contraindicated in RF due to hyperkalemia

81
Q

What NMBD would be ideal for patient with Renal failure

A

Atracurium, vecuronium, mivacurim (no renal excretion)

82
Q

Irreversible, progressive reduction in GFR in chronic renal failure is due to?

A
  1. DM is MCC
  2. Hypertension
  3. Chronic glumerulonephritis
  4. Any cause of ARF
83
Q

diagosis for Irreversible, progressive reduction in GFR

A

Chronic renal failure

84
Q

Clinical presentation of a patient with chronic renal failure

A
  1. Neurological– lethargy , confusion, restless leg, seizures
  2. Cardiovascular– hypertension, CHF, pericarditis
  3. GI– anorexia, nausea, vomiting
  4. Metabolic—pruritus (uremia), bone pain (secondary hyperparathyroidism), hyperkalemia
  5. Renal osteodystrophy
  6. Anemia (low erythropoietin production)
  7. Bleeding disorders due to platelet dysfunction
  8. Sepsis –most serious problem as uremia inhibits immunity MCC cause of death
  9. Low Cr clearance
  10. More than 80% recover completely
85
Q

Therapy for chronic renal failure

A
  1. Dietary restriction (low salt and protein )
  2. ACE inhibitor ( S/E hyperkalemiaM )
  3. Renal replacement therapy −Hemodialysis, PD, Transplantation
86
Q

Replacement therapy indications for patient with chronic renal failure

A

−Hyperkalemia

−Clinical uremia

−Severe azotemia i.e. GFR < 10 cc/min

−Volume overload

−Acidemia

SUM'20 - Anatomy & Physiology (11 decks)

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