Nephrology Flashcards
Part of the nephron responsible for concentrating the urine
Loop of Henle
70% of all solutes are reabsorbed in this tubule
PCT (proximal convoluted tubule)
powerhouse of the nephron
TAL of Henle
creates a hypertonic environment of the medulla
TAL of Henle
aldosterone sensitive Na/K exchangers (2)
DCT
Collecting Tubule
Mainly adjust Na reabsorption using thiazide sensitive NA Cl symporter
DCT
Where vasopressin acts on aquaporin to allow passage reabsorption of intraluminal water
collecting duct
Hormone that has an effect in the efferent arteriole causing increase GFR but with compensatory Na reabsorption
angiotensin
facilitate dilation of the afferent arteriole causing increase GFR but no sodium reabsorption
ANP (prostaglandin)
Hormone responsible between the play of calcium and phosphate
parathyroid hormone
causes sodium reabsorption and K, H secretion at the distal nephrone
aldosterone
normal values of potassium
3.5-5mg/dL
most frequent cause of hyperkalemia
decrease secretion of potassium via renal/kidneys
Classic ECG changes in hyperkalemia
Tall peak T waves
Widened QRS
Loss of P waves
Drug to give when there is hyperkalemia
calcium gluconate
What is the mechanism of action for calcium gluconate?
Raises AP (action potention) threshold to usual 15 mV difference between resting and threshold potential
Treatment for Hyperkalemia classified as membrane stabilizers
calcium gluconate
Hypertonic normal saline (3%)
Treatment for hyperkalemia classified as shifters
Insulin
Albuterol
Treatment for hyperkalemia classified as excreters
furosemide
sodium bicarbonate
sodium polystyrene sulfonate
How does hypomagnesemia cause hypokalemia?
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
Patient profile:
male, hypokalemia and leg weakness.
This patient likely has?
Grave’s disease
ECG changes in hypokalemia
U waves
Tapping the front of the ear stimulates facial nerve depolarizations
Chvostek’s sign
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
Trosseau’s sign
First tetanic sign to develop with hypocalcemia
Trousseau’s sign
ECG changes in hypocalcemia
QT prolongation
Normal values of sodium in blood
135-145mg/dL
Levels of calcium to define it as hypocalcemia or hypercalcemia
Hypercalcemia: serum Ca > 2.5mmol/L
Hypocalcemia: serum Ca < 2.5mmol/L
Treatment for hypocalcemia
Calcium gluconate
Chronic hyponatremia should be corrected slowly to avoid this condition
ODS (osmotic demyelination syndrome)
4 principle causes of high anion gap acidosis
lactic acidosis
ketoacidosis
toxins
renal failure
2 causes of hyperchloremic or anion gap acidosis
bicarbonate loss form GI tract
renal tubular acidosis
METABOLIC ACIDOSIS:
Specific causes of High Anion Gap Metabolic Acidosis
“MUPILES”
methanol
urea
DKA
paraldehyde
propylene glycol
iron, isoniazid, idiopathic acidosis
lactic acidosis (sepsis, shock)
ethylene glycol, ethanol
salicylic acid
METABOLIC ACIDOSIS:
Specific causes of Normal Anion Gap Metabolic Acidosis
“HARD UP”
hyperalimentation
acetazolamide
RTA
diarrhea
uteroenteric fistula
pancreticoduodenal fistula
Definition of AKI
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
Most common electrolyte abnormality in a patient with AKI
hyperuricemia
hyperphosphatemia
hyperkalemia
hypocalcemia
Which classification of AKI is the most common?
Pre-renal
Most common cause of intrinsic AKI are ___. (3)
sepsis
nephrotoxin
ischemia
Complete anuria is uncommon in AKI except in the following conditions (4)
complete urinary tract obstruction
renal artery occlusion
overhwhelming shock
severe proliferative GN
Features of amphotericin B nephropathy (4)
Hypomagnesemia
Hypocalcemia
NAGMA
Polyuria
Features of aminoglycoside nephropathy
Hypomagnesemia
Non oliguric AKI
Remarkable in electrolyte abnormality in Platin based therapy
Hypomagnesemia and hypokalemia
Cause of Chinese herb nephropathy Balkan nephropathy
Aristolochic acid
Contaminant in foodstuffs leading to nephrolithiasis, AKI
Melamine
Features of artheroembolic disease
Eosinophiluria
Peripheral eosinophilia
Livedo reticularis
Definition of CKD
eGFR of <60 mL/min/1.73 m2 for at least 3 months
Cast found in CKD
Broad waxy casts
Isosthenuria
Casts found in AKI
Muddy brown cast (for ATN)
Definition of oliguria
< 400 mL/day
Definition of anuria
< 100 mL/day
Definition of polyuria
> 3000 mL/day
Definition of hematuria
2-5 RBCs/hpf
Features virtually diagnostic of GN
Hematuria with dysmorphic RBC
RBC cast
CHON excretion > 500mg/day
Features of pyelonephritis
WBC casts
Bacteriuria
Characterized by solute diuresis with an appropriate free eater excretion
post obstructive diuresis
Identify:
> 500 mOsm/kg
Suggestive of prerenal disease and hypovolemia
Identify:
< 250 mOsm/kg
True solute diuresis
post AKI / post obstructive
Identify:
> 1000 mOsm/kg
Too concentrated urine found in profound hypovolemic states
Identify:
< 30 mOsm/kg
Characteristic of total absence of ADH
Absolute indications for dialysis:
“AEIOU”
Acidosis
Electrolytes
Intoxication
Overload
Uremia
Bilaterally small kidneys support the diagnosis of CKD except: (4)
Diabetic nephropathy
Amyloidosis
HIV nephropathy
Polycystic Kidney Disease
Leading cause of morbidity, mortality in CKD
Cardiovascular disease
Stages in CKDA that are asymptomatic
Stage 1 and 2
CKD Staging:
Clinicwl and laboratory complications are prominent
Stage 3 and 4
CKD Staging
Normocytic normochromic anemia observed as early as
Stage 3
CKD Staging
Peripheral neuropathy becomes clinically evident at:
Stage 4
CKD Staging:
Gadolinium should be minimized at?
Gadolinium should be avoided at?
- Stage 3
- Stage 4 and 5
