Renal II Flashcards
1
Q
drugs that dilate efferent arterioles causing; decrease GFR, decrease hyperfiltration resulting in nephropathy (in DM)
A
ACE inhibitors
2
Q
Vasodilators of renal arterioles resulting in increased RBF
A
dopamine
3
Q
RBF remain constant over the range of
A
80-200 mmHg(autoregulation)
4
Q
Describe Myogenic mechanism of outoregulaton
A
- 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
5
Q
Describe tubuloglomerular feedback of outoregulation
A
- Increased blood flow 2. Increased fluid rush to macula densa. 3. vasoconstriction of afferent arteriole to maintain constant blood flow
6
Q
4 Causes of edema
A
- High capillary hydrostatic pressure 2. Decreased plasma proteins 3. Increased capillary permeability 4. Blockage of lympatics
7
Q
High capillary hydrostatic pressure conditions that cause edema (6)
A
- 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
8
Q
Decreased plasma proteins conditions that cause edema
A
- Low oncotic pressure 2. Loss of proteins ( Burns, wounds; Nephrosis; Gastroenteropathy) 3. Failure to produce proteins (Malnutrition (“kwashiorkor”), Cirrhosis, Albuminemia)
9
Q
Increased capillary permeability conditions that cause edema
A
- Immune reactions (histamine) 2. Toxins 3. Burns 4. Prolonged ischemia 5. Vitamin deficiency (e.g. vitamin C) 6. Pre-eclampsia and eclampsia in pregnancy
10
Q
Blockage of lymphatics conditions that cause edema
A
- Cancer 2. Surgery 3. Infections (Filariasis or Elephantitis)
11
Q
Diagnosis for patient with significantly elevated ADH and urine osmolarity with decreased serum osmolarity and urine output
A
SIADH
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)
13
Q
Diagnosis for patient with high urine output, ADH and serum osmolarity with decreased urine osmolarity
A
Nephrogenic Diabetes Insipidus
14
Q
Diagnosis for patient with high urine output and serum osmolarity with low ADH and urine osmolarity
A
Central diabetes insipidus
15
Q
Diagnosis for patient with high urine output and low serum osmolarity, urine osmolarity and ADH
A
1º polydipsia
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%
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)
18
Q
Second line of defense in acid base balance
A
Respiratory compensation is the second line of defense, acting within minutes
19
Q
Third line of defense in acid base balance
A
Renal compensation is the third line of defense, acting within hours to days
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”
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.
22
Q
Can you have fully compensated metabolic
A
No Only respiratory acidosis and respiratory alkalosis can be completely compensated (not metabolic)
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
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
25
H+ is excreted in the form of
Excretion of H+ as NH4+ (Ammonium ion) Excretion of H+ as titratable acid (H2PO4-)
26
Renal compensation in acidosis
Increased HCO3- reabsorption Increased H+ secretion Production of new HCO3-
27
Renal compensation in alkalosis
Decreased H+ secretion Loss of HCO3- in urine Decreased HCO3- reabsorption
28
Anian gap
Unmeasured anions = Na+ - (Cl- + HCO3-) = anion gap Normal anion gap = 8 to 16 mEq / L
29
Renal compensation for metabolic acidosis
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+
30
The serum anion gap represents?
unmeasured anions (phosphate, citrate, sulfate and proteins) in serum.
31
In metabolic acidosis, the serum anion gap is increased if?
the concentration of an unmeasured anion is increased to replace HCO3-
32
In metabolic acidosis, the serum anion gap is normal if?
the concentration of Cl- is increased to replace HCO3- (hyperchloremic metabolic acidosis) [e.g. Diarrhea, RTA, Carbonic Anhydrase inhibitors and Addison’s disease]
33
Renal compensation for metabolic alkalosis
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”
34
respiratory compensation for respiratory acidosis
There is NO respiratory compensation for respiratory acidosis
35
acute respiratory alkalosis compensation
renal compensation has not yet occurred
36
chronic respiratory alkalosis compensation
renal compensation (increased HCO3- reabsorption) has occurred. Thus , arterial pH is decreased towards normal (i.e. a compensation)
37
What causes the symptoms of hypocalcemia in chronic respiratory alkalosis
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
Difference btw acute and chronic respiratory acidosis
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
Signs and symptoms of respiratory acidosis
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
Causes of increased anion gap acidosis include?
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
High anion gap metabolic acidosis: Diabetes ketoacidosis (DKA)
Increased serum ketones Serum ketones = acetoacetate and B-OH butyrate
42
Diagnosis and treatment for patient with high anion gap metabolic acidosis, low carb ingestion leading to decreased insulin secretion and elevated ketoacid production
Starvation or alcohol abuse Give calories/carbohydrates
43
Diagnosis and treatment for patient with high anion gap metabolic acidosis, tinnitus, delirium, elevated blood salicylate level
Salicylate Poisoning Treat with alkaline diuresis (I/ V NaHCO3 + Diuretics)
44
Diagnosis and treatment for patient with high anion gap metabolic acidosis, alcoholism, acute blindness
Methanol (wood alcohol) and ethylene glycol (Anti-freeze) Poisoning
45
Causes of Bicarb loss resulting in normal anion gap metabolic acidosis
Diarrhea– GI loss of HCO3- MCC Pancreatic; biliary or intestinal drainage Villous adenoma Diuretic (?)
46
Fanconi's syndrome
Type II RTA= Proximal RTA= inability to reabsorb filtered HCO3- Results in normal anion gap metabolic acidosis
47
Type I RTA (Distal RTA)
inability to excrete H+ and therefore regenerate HCO3- Results in normal anion gap metabolic acidosis
48
Type IV RTA
- 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
Most common cause of metabolic alkalosis is?
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
Other causes of metabolic alkalosis
- 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
nice way to die
CO2 narcosis Supplemental O2 (if PO2 \<60 mmHg) – watch for “CO2 retainers
52
Causes of respiratory alkalosis
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
Symptoms respiratory alkalosis
- Lightheadedness - Perioral numbness - Paresthesias and even tetany due to fall of ionized calcium
54
Tx of respiratory alkalosis
re-breathe own CO2 “paper bag”
55
Effects of acidosis
Right shift of O-Hb curve CNS depression Decreased pulmonary blood flow Arrhythmias Impaired myocardial function Hyperkalemia
56
Effects of alkalosis
Decreased Cerebral blood flow Left shift of oxy-Hb curve leading to decrease O2 delivery to tissue Arrhythmias Tetany , seizures
57
hypoaldosteronism as a cause of metabolic acidosis
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
Can metabolic disturbance be fully compensated?
* ONLY respiratory disturbance can be completely compensated
59
Causes of Transient Urinary incontinence
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
Causes of stablished incontinence
1. Detrusor overactivity
2. Stress incontinence (outlet incompetence)
3. Urethreral obstruction
4. Detrusor underactivity “overflow incontinence”
61
Diagnosis and treatment of incontinence overactive bladder and urgency
Detrusor over-activity as a cause cause of incontince and its treatment
2. Associated with UTI
3. Treatment: Anticholinergic; M3 blocker e.g. Tolterodine(Detrol ®); bladder training
62
Incontince in a patient with BPH is due to? How do you treat
1. In BPH
2. Treatment: a adrenergic blocker e.g. prazosin, 5a-reductase inhibitor e.g. finasteride in BPH
63
Diagnosis and treatment of incontinence with high intraabdominal pressure e.g. sneezing, coughing
Stress incontinence “outlet incompetence” as a cause of incontinence and treatment
2.Treatment: Kegel’s exercise, pessary, a agonist e.g. phenylpropanolamine
64
Diagnosis and treatment of incontinence with Incomplete emptying
1. = leak with overfilling
2. Detrusor underactivity “overflow incontinence” and treatment
3. Treatment: Intermittent catheterization, Bethanechol(cholinergic)
65
Diuretics are
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
Carbonic anydrase inhibitor (acetazolamide) major effects
* Increase HCO3- excretion = Metabolic acidosis with normal gap
* Use to prevent mountain sickness
* Inhibition of Carbonic Anydrase
67
Loop diuretics (furosemide ) major effects, site of action and MOA
* 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
Thiazide diuretics major effects, site of action and MOA
* 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
K+ sparing diuretics (spironolactone)/ aldosterone antagonist major effects, site of action and MOA
* MOA: Inhibition of Na+ reabsorption, Inhibition of K+ secretion
* Site of Action: Late DCT
70
Prerenal causes of renal failure
Hypovolemia (dehydration, hemorrhage)
Cardiogenic shock
Sepsis
Drugs (NSAIDs)
Renal artery stenosis
71
Renal (Intrinsic) causes of renal failure
1. Renal ischemia
2. Glomerulonephritis
3. Nephrotic syndrome
4. Nephrotoxic drugs ( NSAIDs, aminoglycosides)
5. Thromoboembolism
72
Postrenal causes of renal failure
1. Renal ischemia
2. Glomerulonephritis
3. Nephrotic syndrome
4. Nephrotoxic drugs ( NSAIDs, aminoglycosides)
5. Thromoboembolism
73
Acute renal failure is assymptomatic until \_\_\_\_% nephrone is lost
60%
74
High mortality in renal failure is due to?
sepsis, CV dysfunction and pulmonary complications
75
Etiology of acute renal failure
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
−FEFNa (Fractional excretion of Na) is _______ in renal and ______ in prerenal failure
is high in renal and low in prerenal failure
\> 1% suggest renal etiology (ATN; Filter is broken)
\< 1% suggest prerenal etiology
77
Evaluation of acute renal failure
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
Complications of acute renal failure
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
Treatment of acute renal failure
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
Can you give sux to patient with acute renal failure?
contraindicated in RF due to hyperkalemia
81
What NMBD would be ideal for patient with Renal failure
Atracurium, vecuronium, mivacurim (no renal excretion)
82
Irreversible, progressive reduction in GFR in chronic renal failure is due to?
1. DM is MCC
2. Hypertension
3. Chronic glumerulonephritis
4. Any cause of ARF
83
diagosis for Irreversible, progressive reduction in GFR
Chronic renal failure
84
Clinical presentation of a patient with chronic renal failure
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
Therapy for chronic renal failure
1. Dietary restriction (low salt and protein )
2. ACE inhibitor ( S/E hyperkalemiaM )
3. Renal replacement therapy −Hemodialysis, PD, Transplantation
86
Replacement therapy indications for patient with chronic renal failure
−Hyperkalemia
−Clinical uremia
−Severe azotemia i.e. GFR \< 10 cc/min
−Volume overload
−Acidemia
