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Internal Medicine Review > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Part of the nephron responsible for concentrating the urine

A

Loop of Henle

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2
Q

70% of all solutes are reabsorbed in this tubule

A

PCT (proximal convoluted tubule)

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3
Q

powerhouse of the nephron

A

TAL of Henle

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4
Q

creates a hypertonic environment of the medulla

A

TAL of Henle

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5
Q

aldosterone sensitive Na/K exchangers (2)

A

DCT
Collecting Tubule

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6
Q

Mainly adjust Na reabsorption using thiazide sensitive NA Cl symporter

A

DCT

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7
Q

Where vasopressin acts on aquaporin to allow passage reabsorption of intraluminal water

A

collecting duct

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8
Q

Hormone that has an effect in the efferent arteriole causing increase GFR but with compensatory Na reabsorption

A

angiotensin

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9
Q

facilitate dilation of the afferent arteriole causing increase GFR but no sodium reabsorption

A

ANP (prostaglandin)

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10
Q

Hormone responsible between the play of calcium and phosphate

A

parathyroid hormone

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11
Q

causes sodium reabsorption and K, H secretion at the distal nephrone

A

aldosterone

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12
Q

normal values of potassium

A

3.5-5mg/dL

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13
Q

most frequent cause of hyperkalemia

A

decrease secretion of potassium via renal/kidneys

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14
Q

Classic ECG changes in hyperkalemia

A

Tall peak T waves
Widened QRS
Loss of P waves

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15
Q

Drug to give when there is hyperkalemia

A

calcium gluconate

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16
Q

What is the mechanism of action for calcium gluconate?

A

Raises AP (action potention) threshold to usual 15 mV difference between resting and threshold potential

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17
Q

Treatment for Hyperkalemia classified as membrane stabilizers

A

calcium gluconate
Hypertonic normal saline (3%)

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18
Q

Treatment for hyperkalemia classified as shifters

A

Insulin
Albuterol

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19
Q

Treatment for hyperkalemia classified as excreters

A

furosemide
sodium bicarbonate
sodium polystyrene sulfonate

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20
Q

How does hypomagnesemia cause hypokalemia?

A

ROMK is a channel that secretes K to the renal tubule. Magnesium acts as an inhibitor for this channel.

Decrease magnesium -> increase potassium excretion -> decrease potassium in body

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21
Q

Patient profile:
male, hypokalemia and leg weakness.

This patient likely has?

A

Grave’s disease

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22
Q

ECG changes in hypokalemia

A

U waves

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23
Q

Tapping the front of the ear stimulates facial nerve depolarizations

A

Chvostek’s sign

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24
Q

Tetany in hand especially after decrease perfusion to hand. This sign is elicited via blood pressure cuff due to spontaneous action potentials from the median nerve

A

Trosseau’s sign

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25
Q

First tetanic sign to develop with hypocalcemia

A

Trousseau’s sign

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26
Q

ECG changes in hypocalcemia

A

QT prolongation

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27
Q

Normal values of sodium in blood

A

135-145mg/dL

28
Q

Levels of calcium to define it as hypocalcemia or hypercalcemia

A

Hypercalcemia: serum Ca > 2.5mmol/L
Hypocalcemia: serum Ca < 2.5mmol/L

29
Q

Treatment for hypocalcemia

A

Calcium gluconate

30
Q

Chronic hyponatremia should be corrected slowly to avoid this condition

A

ODS (osmotic demyelination syndrome)

31
Q

4 principle causes of high anion gap acidosis

A

lactic acidosis
ketoacidosis
toxins
renal failure

32
Q

2 causes of hyperchloremic or anion gap acidosis

A

bicarbonate loss form GI tract
renal tubular acidosis

33
Q

METABOLIC ACIDOSIS:
Specific causes of High Anion Gap Metabolic Acidosis

A

“MUPILES”
methanol
urea
DKA
paraldehyde
propylene glycol
iron, isoniazid, idiopathic acidosis
lactic acidosis (sepsis, shock)
ethylene glycol, ethanol
salicylic acid

34
Q

METABOLIC ACIDOSIS:
Specific causes of Normal Anion Gap Metabolic Acidosis

A

“HARD UP”
hyperalimentation
acetazolamide
RTA
diarrhea
uteroenteric fistula
pancreticoduodenal fistula

35
Q

Definition of AKI

A

urine output <0.5ml/kg/hours for 6 hours

serum creatinine increase by 0.3mg/dL within next 48 hours

0.5 times increase in baseline serum creatinine within the next 7 days

36
Q

Most common electrolyte abnormality in a patient with AKI

A

hyperuricemia
hyperphosphatemia
hyperkalemia
hypocalcemia

37
Q

Which classification of AKI is the most common?

A

Pre-renal

38
Q

Most common cause of intrinsic AKI are ___. (3)

A

sepsis
nephrotoxin
ischemia

39
Q

Complete anuria is uncommon in AKI except in the following conditions (4)

A

complete urinary tract obstruction
renal artery occlusion
overhwhelming shock
severe proliferative GN

40
Q

Features of amphotericin B nephropathy (4)

A

Hypomagnesemia
Hypocalcemia
NAGMA
Polyuria

41
Q

Features of aminoglycoside nephropathy

A

Hypomagnesemia
Non oliguric AKI

42
Q

Remarkable in electrolyte abnormality in Platin based therapy

A

Hypomagnesemia and hypokalemia

43
Q

Cause of Chinese herb nephropathy Balkan nephropathy

A

Aristolochic acid

44
Q

Contaminant in foodstuffs leading to nephrolithiasis, AKI

A

Melamine

45
Q

Features of artheroembolic disease

A

Eosinophiluria
Peripheral eosinophilia
Livedo reticularis

46
Q

Definition of CKD

A

eGFR of <60 mL/min/1.73 m2 for at least 3 months

47
Q

Cast found in CKD

A

Broad waxy casts
Isosthenuria

48
Q

Casts found in AKI

A

Muddy brown cast (for ATN)

49
Q

Definition of oliguria

A

< 400 mL/day

50
Q

Definition of anuria

A

< 100 mL/day

51
Q

Definition of polyuria

A

> 3000 mL/day

52
Q

Definition of hematuria

A

2-5 RBCs/hpf

53
Q

Features virtually diagnostic of GN

A

Hematuria with dysmorphic RBC
RBC cast
CHON excretion > 500mg/day

54
Q

Features of pyelonephritis

A

WBC casts
Bacteriuria

55
Q

Characterized by solute diuresis with an appropriate free eater excretion

A

post obstructive diuresis

56
Q

Identify:
> 500 mOsm/kg

A

Suggestive of prerenal disease and hypovolemia

57
Q

Identify:
< 250 mOsm/kg

A

True solute diuresis
post AKI / post obstructive

58
Q

Identify:
> 1000 mOsm/kg

A

Too concentrated urine found in profound hypovolemic states

59
Q

Identify:
< 30 mOsm/kg

A

Characteristic of total absence of ADH

60
Q

Absolute indications for dialysis:

A

“AEIOU”
Acidosis
Electrolytes
Intoxication
Overload
Uremia

61
Q

Bilaterally small kidneys support the diagnosis of CKD except: (4)

A

Diabetic nephropathy
Amyloidosis
HIV nephropathy
Polycystic Kidney Disease

62
Q

Leading cause of morbidity, mortality in CKD

A

Cardiovascular disease

63
Q

Stages in CKDA that are asymptomatic

A

Stage 1 and 2

64
Q

CKD Staging:
Clinicwl and laboratory complications are prominent

A

Stage 3 and 4

65
Q

CKD Staging
Normocytic normochromic anemia observed as early as

A

Stage 3

66
Q

CKD Staging
Peripheral neuropathy becomes clinically evident at:

A

Stage 4

67
Q

CKD Staging:
Gadolinium should be minimized at?
Gadolinium should be avoided at?

A
  1. Stage 3
  2. Stage 4 and 5

Internal Medicine Review (4 decks)

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