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Clin Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Type II RTA

A

Proximal

Defect in bicarbonate reabsorption, usually associated with features of Faconi syndrome, including glycosuria, aminoaciduria, phosphaturia, and uriscoruria(indicating PT dysfunction)

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2
Q

What causes isolated proximal RTA(type II)

A

Hereditary dysfunction of the basolateral sodium-bicarbonate cotransporter.

Faconi may be inherited or acquired due to myeloma, chronic IN, or drugs (tenofovir, ifofamide)

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3
Q

Treat proximal RTA ((type II)

A

Large doses of bicarbonate which may aggravate hypokalemia

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4
Q

Type IV RTA

A

May be due to hyporeninemic hypoaldosteronism or to resistance of the distal nephron to aldosterone.

Hyporeninemic hypoaldosteronism is typically associated with volume expansion nand most commonly seen in elderly and/diabetic patients with CKD

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5
Q

Hyperkalemia associated with NSAIDS and cyclosporine

A

Partially due to hyporeninemic hypoaldosteronism

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6
Q

Patients with hyporeninemic hypoaldosteronism are typically __kalemic; they may also exhibit ___ acidosis, with urine ph<5.5 and a ___ urinary ion gap

A

Hyper

Mild non anion gap

Positive

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7
Q

In type IV, acidosis often improves with reduction in serum _ (treatment)

A

K

Hyperkalemia appears to interfere with medullary concentration of ammonium by the renal countercurrent mechanism

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8
Q

How treat type IV if acidosis doesn’t improve with reduction of K

A

Oral bicarbonate or citrate

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9
Q

Type IV and various forms of distal tubular injury and tubulointerstitial disease (interstitial nephritis)

A

Associated with distal insensitivity to aldosterone; urine pH is classically >5.5, again with a positive urinary anion gap

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10
Q

Definition of urinary tract infection

A

Encompasses a variety of clinical entities: cystitis, pyelonephritis, prostatis, asymptomatic bacteriuria

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11
Q

Uncomplicated UTI

A

Acute disease in non pregnant outpatient women

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12
Q

Without an atomic abnormalities or instrumentation of the urinary tract; ____ ___ refers to all other types of UTI

A

Complicated UTI

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13
Q

Calculate and interpret anion gap in an acid/base disorder

Interpret blood gas and correctly name the acid/base disorder

Identify compensatory mechanisms for metabolic acidosis

Identify the most common causes of high anion gap metabolic acidossi

A

Know

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14
Q

Henderson hasselbalch equation

A

Bicarbonate and pCO2 are the drivers of pH

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15
Q

Acidemia

A

<7.35

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16
Q

Alkalemia

A

> 7.45

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17
Q

Acidemia metabolic acidosis or respiratory acidosis

A

Metabolic
HCO3<20

Respiratory
PCO2>45

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18
Q

Alkalemia metabolic or respiratory

A

Metabolic
HCO3>30

Respiratory alkalosis pCO2<35

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19
Q

Increased endogenous acids

A 
Ketoacidosis
Lactic acidosis
-diabetic
-alcoholic
-starvation
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20
Q

Increased ingestion of acids

A

Ethylene glycol
Methanol
Propylene glycol
Salicylate

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21
Q

Loss of bicarbonate

A

Diarrhea

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22
Q

Decreased secretion of acids

A

AKI
-defined by serum Cr

Chronic kidney disease
-defined as increase in GFR

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23
Q

Signs and symptoms of acidosis

A

Headaches
Ab pain
Malaise
“I have the flu”

Change in mental status-confusion, stupor, coma

Increased respiration’s

Variable changes in bp

Tachycardia-catecholamie release

Pulmonary need,s-changes in pulmonary compliance

Increased serum glucose-this is reactive be careful

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24
Q

Anion gap

A

Na-(Cl+HCO3)

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25
Q

BMP

A

Na K Bicarb CO2(when see CO2 it means bicarbonate)

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26
Q

Normal anion gap is 10, why positive

A

Albumin is primary unmeasured anion

* there are unmeasured anions!!!!!!

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27
Q

Total cations

A

Measured cations MC and unmeasured cations UC

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28
Q

Total anions

A

Measured anions MA and unmeasured anions (UA)

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29
Q

Normally MC+UC=MA+UA_> (Na+K)-(Cl+HCO3)

A

(MC+UC)-MA)=UA

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30
Q

Anion gap is a way of demonstrating accumulation of the __

A

UA

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31
Q

Elevation of anion gap suggests what

A

Metabolic acidosis itch circulating anion

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32
Q

Compensation

A

Respiration goes up under stress bc CO2 is very easy to blow off. It’s an immediate response

Respiratory changes take minutes
Metabolic take longer

So start blowing off CO2 with acidosis

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33
Q

Sometimes body will blow off so much CO2 that what happens

A

Get respiratory alkalosis-use equation for compensation

PCO2=(1.5xHCO3)+8(+/-2)

If calculated doesn’t match, then there is a respiratory alkalosis

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34
Q

Compensation always exists

A

However it will not completely reserve the primary problem. It is the normal physiologic response to attenuate the problem

Compensation can be appropriate, inadequate, or excessive

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35
Q

MUD PILES- most common causes of anion gap increase

A

Methanol, metformin
-wood alcohol-solvent

Uremia->renal failure

Diabetic ketoacidosis (type I, also includes starvation ketoacidosis

Paraldehyde, propylene glycol, phenformin

Isoniazid/iron toxicity

Lactic acidosis
->includes cyanide and CO poisoning, seizures, sepsis, ischemia
Ethanol/ethylene glycol

Salicylate

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36
Q

Glue a pain huffing?

A

Toluene first high anion gap then low! Weird acidosis picture

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37
Q

A 72 yo male presents with acute illness and leg pain. He sustained a cut on his lef while working in the years 10 days ago. Over 3 days, pain increased. He has fever, chills, nausea, and vomiting. He has only been able to tolerate small amounts of quirked over 24 hours he has not urinated for 12 hours.

BP 90/60, HR 125, RR 24, T 101.3

WBC up

Cloudy urine with pH 5.5, specific gravity 1.01

Casts muddy brown-tubular necrosis **-THIS IS WY GET URINE MICROSPY

PH 7.5, PCO2 30, CO2 15

BUN:Cr-prerenal?

Acid or base?

Why is Na high-Na not being reabsorbed have tubular dysfunction

A

1.01—-same concentration as serum, NOT CONCENTRATED!!! Something wrong with kidney

We would expect to be super concentrated

7.35 is normal—-compensation!!! Did you calculate PCO2?

Prerenal azotemia

High anion gap Metabolic acidosis, appropriately compensated (pH and pCO2 nearly the same-usually sign for scompensated but doesn’t always work use

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38
Q

Most likely cause high anion gap metabolic acidosis

A

Lactate acidosis with

39
Q

Does this patient need an IV

A

BUN Cr up tachycardia and hypotensive

Hydrate!

Normal saline bc isotonic want it to stay intravascular -we need to support his cardiovascular status

40
Q

Why does this patient have nausea and vomiting

A

Acidosis causes nausea as a compensatory mechanism for acidosis

41
Q

Every patient it’s acidosis will say they have what

A

Flu, nausea

42
Q

Uremia toxicity

A

80-100 BUN get symptoms

43
Q

Sepsis presentation

A

Acute fever, ill, tachycardia, hypotension

Multiorgan involvement in infection removed from the source!! (Wound on leg causes enough problems that get tachycardia, renal failur,e GI distress…)

Hypofunction of uninflected organs
Postulated that there is both overproduction of pyruvate and an inhibition of PDH activity (which you will recall. Is the rate limiting state in oxidative phosphorylation)

44
Q

What labs

A

Wound culture ?

45
Q

Rhabdomyolysis

A

Event that causes release of intracellular contents into extracellular space

Msucle aches-> hypotension and renal failure

Muscle fiber exhaustion
-seizure, extreme exercise, heat stroke, malignant hyperthermia

Physical injury
-trauma, crush injury, immobilization, compartment syndrome

46
Q

Drugs , supplements cause rhabdomyolysis

A

Statins

Selective serotonin reuptake inhibitors

Colchicine

Cocaine

Amphetamines

Heroin

Creatinine

Ephedra

47
Q

Toxins cause rhabdomyolysis

A

Alcohol
Toluene
CO

48
Q

Other causes of rhabdomyolysis

A

Hypokalemia, hypophosphatemia, excessive fluid shifts, vasculitis, ***influenza, dermatomyositis, polymyositis

49
Q

Diagnosis rhabdomyolysis HISTORRRRRY

A

Start with a complete history

Decreased urine output

Reddish brown color d/t presence of myoglobin

Dipstick: heme+but no rbc identified on microscopy +/- protein

Microscopy:granular casts

Serum labs: elevated creatine kinase, hyperkalemia, hypocalcemia, hyperphosphatemia

Acid/base disorder caused by release of lactate and other organic acids

50
Q

Diabetic ketoacidosis

A

Have typical symptoms of polyuria and polydipsia

Polyuria: osmotic diuresis due to high serum glucose->dehydration drives thirst (peeing all this stuff out and getting dehydrated which drives thirst…have intracellular hypoglycemia)

Ketones are rapidly excreted int he urine which also helps to maintain GFR and kidney perfusion

Abdominal pain and nausea are driven by acidosis

Vomiting drives a metabolic alkalosis (compensatory mechanism)

Vomiting expels H from gastric contents (which increases HCO3

Ketones are rapidly filtered in place of Cl

***differentiate polyuria from frequency!!!(high volume and a lot with polyuria, frequency just have to go a lot)

51
Q

Type I diabetic ketoacidosis

A

Intracellular hypoglycemia which activated FA degranulation which leads t large amounts of ketones

52
Q

Other : hyperkalemia and rhabdomyolysis

A

Treat with hydration it will wash out probably just intracellular falling out since membrane issue

53
Q

Early diabetic

A

Normal anion gap

As fluid decrease have high anion gap

54
Q

22 yo type I diabetic doesn’t check insulin but knows when they need it. Ow N/V and ab pain. This is early , vitals ok a bit of tachycardia

Na low
PH 7.3
CO2/bicarb-low
Glucose-HIGH
BUN-high
Cr-high end of Normal(prerenal bc diuresed.tachycardic bc now hypovolemia)
Ketone +

High K

How treat

A

HYDATE and insulin (tons-don’t stop insulin)

K goes down (was pseudo)

K and potassium goes back into cells and end up hypokalemic so need to replace after a few hours

55
Q

Alcoholic ketoacidosis

A

Stop eating during drinking binges or when vomiting begins

Alcohol levels are negligible upon presentation

Degradation of alcohol depletes NAD which curtails hepatic gluconeogenesis which leads to depletion of liver stores of glycogen

Metabolism of increases the NADH/NAD ration, favoring the conversion of pyruvate to lactate

Similar to DKA in that binge drinking leads to low insulin levels

Dehydration secondary to ADH suppression by etoh complicated by lack of intake but not as severe as DKA

Lactic acid builds up due to impaired hepatic conversion of lactate to glucose

56
Q

58 yo male ab pain
Low BMO alcoholic

Elevated glucose (not enough for DKA, this isn’t stress response 142 vs 475)

Creatinine up

Ketones positive
N/V
Anion gap-24 (not as high at ketoacidosis)

A

Normal anion gap 10, this one is 24 so delta gap is 14

Bicarb delta is 8,

57
Q

14>8 mixed metabolic acidosis

Delta gap 24-14

A

Ok

58
Q

Ethylene glycol

A

Sweet liquor foun in anti freez

100 ml can be fatal

Ethylene glycol is metabolized by alchol DH->glycolic acid->oxalis acid

Increased NADG levels encourage lactic acid formation ‘
Presented with intoxication, low blood alcohol level, and HAGMA without ketones

Calcium oxalate crystals in urine

Fluorescence under wood lamp

59
Q

Methanol

A

Found in solvents or impurity in alcoholic beverages

Less intoxication than either ethanol or ethylene glycol

30 ml can be fatal

Metabolized by alcohol DH->formaldehyde-> formic acid which causes MAGMA

NAD depletion favors lactate production

Blurry vision is characteristic or methanol ingestion

60
Q

Salicylate toxicity (tinnitus and tachypnea)

A

Presents with tachypnea as salicylate as a direct respiratoy stimulant

Tinnitus is present when serum salicylic acid levels reach 20-45 mg/sL

CNS manifestations: agitation, seizures, coma

Peak serum concentrations: 4-6 hours after ingestion

Tachypnea induces a respiratory alkalosis

Metabolic acidosis is the result of the acccumulation of both lactic acid and ketoacids

Salicylic acid contributes very little of the acid load

61
Q

Acute renal injury or disease

A

Staged according to the rate of rise in serum creatinine

62
Q

Chronic kidney disease

A

Uses GFR to define and stage CKD

63
Q

Renal failure

A

Decreased number of nephrons in CKD leads to:

Decreased ammoniagenesis int he proximal tubule

Result of decreased GFR(90 normal)

  • inability to secrete the daily production of fixed acids
  • decreased ability to filter and excrete various anions
  • accumulation of sulfate, phosphate and othe anions produce anion gap (AG)

-Harrison questions look at them !

64
Q

Ok

A

Ok

65
Q

62 yo man acute confusion . Can’t give history

Smells like alcohol

95/96
HR 96
RR18
Temp 97

PH 7.32
PCO2 30

CO2 low

A

Acidosis
Low bicarb

Metabolic acidosis

66
Q

What’s the differential for metabolic acidosis MUDPILES

A

High anion gap

  • uremia? (Look at BUN-get those symptoms at 100)
  • DKA-no glucose is normal
  • salicylate toxicity-tachypnic no
  • CO poisoning-he was outside in parking lot so not if in garage in car.
  • methanol, ethanol, lactic acidosis, ethylene glycol

-lets get serum alcoho,, look at urine (black light look for calcium oxalate crystals-ethylene glycol, and fluorescents under black light)

67
Q

Non anion gap metabolic acidosis is by definition hyper-chloremic acidosis

A

DKA-high anion gap

Loss of alkali (bicarb) can be from the GI tract or kidneys

Reciprocal changes in Cl and bicarb result in a normal AG

Pure non AG acidosis: increases in Cl equals the decrease in HCO3

68
Q

There is a change in the transport system that causes acidosis

A

Can be genetic or acquired

Transport systems have changes

*generalized tubular defect with obstruction

69
Q

Distal RTA

A

Type 1

70
Q

Type II

A

Bicarb transport change

71
Q

Type IV

A

Hypoaldosteronism

72
Q

Type I

A

Classic distal RTA

Hypokalemia, positive UAG, pH>5.5

73
Q

Type II

A

Proximal RTA
Faconi

Glycosuria, generalized aminoaciduria

74
Q

Type IV

A

Distal RTA

Hyperkalemia, positive UAG

75
Q

Classic distal type I

A

Inability of the distal tubule to acidity the urine

Familiala : defective HCO3/Cl exchanger and H ATPase

Associated with autoimmune disorders: SLE , Sjorgen syndrome, cryoglobinemia

Drugs: lithium, toluene, amphotericin

76
Q

RTA type I

A

Inability to secrete H leads to decreased NH4 in the tubules

Less NH4-> high urin pH>5.5

Positive UAG

Serum hypokalemia (augmented K secretion in lieu of H in exchange for Na reabsorption

Calcium oxalate crystals, osteomalacia, osteoporosis

Patients have hypocitraturia and hypercalciuria so they are prone to nephrolithiasis, nephrocalcinosis and bone disease

77
Q

Type IV

A

Hyperkalemia and metabolic acidosis

Asymptomatic with mild hyperkalemia and decreased bicarb

Decreased ammoniagenesis due to hyperkalemia

Urine pH normal

There is less sodium reabsorbed which means the lumen is less negative which results in less hydrogen secreted

But the hydrogen pump is still effective so the pH is maintained

Hypoaldosteronism->less sodium in tubular lumen, change H excretion!!! Los Na with Norma function of the proton pump maintains pH of urine

78
Q

Type IV RTA-related to transport system

A

Made worse by any drug that affects the RAAS: ACE inhibitors, ARBs, and NSAIDS
-need to know the mechanism of disruption of RAAS

Made worse by increased K intake and K sparing diuretics
-what are the K sparing diuretics

Usually a presumptive diagnosis bc it must be proven by low renin and aldosterone levels

What serum lab-24 hour urine?????? Potassium

79
Q

Causes of hyposaldosterone

A

Hyporeninemic hypoaldosteronism: type IV RTA

Drugs CKD and DM: potentially low renin state that leads to hypoaldosteronism

80
Q

K is _ with type IV

A

UP

81
Q

Proximal RTA II

A

Unable reclaim filtered HCO3 in proximal tubule

When serum HCO3 is less than 15 mmol/L, proximal tubule is unable to reclaim HCO2 the urine pH<5.5

When serum HCO3 is near normal there is HCO3 spillage into urine and pH>6.5

82
Q

Type 2 diagnosis

A

Can’t reclaim bicarb

Made by delivering HCO3 and measuring feactional excretion of HCO3

UFE HCO3>15% with bicarb

83
Q

Type II

A

Phosphaturia, aminoaciduria, glycosuria, bicarbonaturia

84
Q

Causes type II RTA

A

Carbonic anhydrase defiency (give for glaucoma)

Faconi

Wilson

Hyperparathyroidism, vitamin D defiency

Lead exposure

Drugs

85
Q

Generalized tubular defect

A

Both H and K secretion are impaired

Elevated K

Urine pH>5.5

Associated with interstitial kidney disease

  • SLE
  • sickle cell
  • obstructive uropathy
86
Q

Diarrhea

A

HCO3 loss in stool leads to acidosis and volume depletion

K is also lost ins tool

Net effect of hypokalemia and hypobiarbemia

The hypokalemia causes increased renal production of NH4 providing urinary buffer that increases. Urine pH

87
Q

How tell diarrhea from RTA??? With labs

A

Urine anion gap-looks at K

88
Q

Chronic progressive KD

A

Decrease in ammoniagenesis is proportionate to the loss of nephrons

GFR<40 unable to secrete the daily acid load

Less ammonia->less anion secretion
Result: hyperchloremic acidosis

89
Q

62 yo male woken up with big toe pain
Two bullet wound in army one. Removed other still in

After discharge tears out pipes and beams in old buildings

6 months headaches constipation, poor sleep, frequent urination

Big toe is swollen

A

Gout
Urine pH 5

Protein and glucose in urine

Gluco and proteinuria

CBC-low micro anemia, low platelets , peripheral smear see basophils stippling

PH7.29
PCO2 12
Normal anion, chronic kidney disease (BC GFR depressed)

BUN high Cr high (abnormal but proportionately so renal problem)

Uric acid high-
Waxy cast

90
Q

What does he have

A

Lead poisoning
With agitation insomnia urinary frequency

Kidney shriveled and shrunken CKD (cortical thinning and shrinking kidney)

91
Q

What expect in 24 hour urine

A

Ok

92
Q

Harmonic tubulointerstitial disease(lead poison)

A

Isothenuria with polyuria

Moderate proteinuria

Very few cells

Type I, II, or IV RTA

Broad waxy casts

Small kidney

93
Q

PROUD AMERICAN VETERANS LOVE GM

A 
Prostate
Analgesics
VU reflux
Gout
Myeloma
94
Q

Review

A

Acidosis
Metabolic or respiratory

Anion gap

Normal AG

Assess compensation

Clin Medicine (28 decks)

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