Renal-Panre Flashcards
Primary Respiratory Acidosis
↑pCO2 due to hypoventilation
○ Causes: Anything that decreases respiration
■ Acute: CNS depression due to opioids/narcotics, pneumonia, cardiac
arrest
■ Chronic: COPD, Myasthenia gravis, Guillain Barre syndrome
Primary Respiratory Acidosis Compensation?
Kidneys slowly will retain HCO3 to help raise pH
Primary Respiratory Alkalosis
↓pCO2 due to hyperventilation
○ Causes: Anything that increases respiration
■ sepsis, PE, anxiety, pregnancy, pain, salicylates
○ S/S: Hyperventilation, tetany-like syndrome, paresthesias in extremities,
circumoral paresthesias
Primary Respiratory Alkalosis Compensation?
Kidneys slowly will excrete HCO3 to help lower pH
Primary Metabolic Acidosis
↓HCO3 will cause either:
○ ↑ H⁺ in blood → ↑Anion Gap Acidosis
○ ↑Cl⁻ → no change in anion gap aka Non/Normal Anion Gap Acidosis
■ Quick math equation : Anion Gap = Na⁺ - (Cl⁻ + HCO3⁻
Primary Metabolic Acidosis Causes
Causes of ↑ Anion Gap Acidosis MUDPILES ○ Methanol ○ Uremia ○ DKA ○ Propylene glycol, paraldehyde ○ Iron, INH, inborn error of metabolism ○ Lactic acidosis ○ Ethylene glycol ○ Salicylates ■ S/S: Neurologic symptomns (lethargy to coma) Causes of Normal Anion Gap (8-12 mEq/L) Acidosis ○ Diarrhea ○ RTA ■ Will see ↑Cl⁻ because kidneys hold onto (Na)Cl when (Na)HCO3 gets low
Primary Metabolic Acidosis
Compensation?
Respiratory response is quick →hyperventilation to blow off CO2
Primary Metabolic Alkalosis
↑HCO3
○ Common cause: Vomiting- loss of (H⁺)Cl⁻ so the kidney holds back HCO3
Primary Metabolic Alkalosis Compensation
No acute response from lungs, give patient back Cl⁻ and kidneys
will dump HCO3
Chronic kidney disease (CKD)
Irreversible condition (small, dysfunctional or nonfunctional kidneys) ● Leading causes: renal changes due to DM or HTN
Definition: >3mo of GFR <60mL/min or kidney structural/functional damage
Nephritic syndrome:
About glomeruli, can not filter kidneys due to being plug results swelling of body (increase bp)
Urine sediment (e.g. RBC casts)-spills blood
increase BP
Nephrotic syndrome:
Spilling proteins not retinaing fluid, urinating, But leaky protein increases swelling due lack of oncontic
Proteinuria > 3.5 g/24 hrs
Decreased BP
● Thrombosis(Blood clots-due to the loss of big proteins in urine which needs for clotting purpose)
Nephrotic syndrome Clinical features?
Clinical features: o Electrolytes (esp. K+) o Cardiac (pericardial effusion) o Heme (anemia [¯ erythropoietin]) o Neuro (risk of bleeding due to ¯ ability of platelets to aggregate) ● Caution when administering the following: o radio-opaque dyes o drugs o fluids o potassium
Nephrotic syndrome treatment
Treatment - renal replacement therapy:
o Dialysis: hemodialysis or peritoneal dialysis
o Continuous hemodiafiltration
o Transplant
Staged 0-5 based on GFR and kidney damage
Stage 0: at risk patients (DM, HTN, chronic NSAID use, non-white ethnicity, age
>60y, SLE, FHx)
● Stage 1: kidney damage (proteinuria , abnml u/a, as per imaging) with normal GFR
>90
● Stage 2: GFR = 89-60
● Stage 3a: GFR = 59-45
● Stage 3b: GFR = 44-30
● Stage 4: GFR = 29-15
● Stage 5: GFR <15, ESRD → dialysis and/or transplant
CKD Causes:
1 DM, #2 HTN, Glomerulonephritis, polycystic kidney disease
CKD s/s
Typically asymptomatic until GFR<30 then s/s uremia, fluid overload (N/V, fatigue,
easy bruising, uremic pericarditis, pulm edema, delirium, uremic encephalopathydarkening of skin, petechiae)
CKD common metabolic abnormalities
Azotemia, fluid retention, metabolic acidosis, hyperK, anemia, hypoCa, hyperphos,
impaired platelet aggregation, renal osteodystrophy
CKD labs
Proteinuria- #1 indicator of disease progression , U/A- broad waxy casts with ESRD,
estimated GFR, BUN/Cr
CKD treatment
Treat the metabolic derangements ● HTN- ACEI/ARB ↓ disease progression ● Erythropoietin for anemia ● Fluid restriction, ↓Na/K diet ● DDAVP for bleeding issues ● Dialysis and/or transplant for ESRD ● Prevent progression ○ Control HTN, DM, and protein intake
Hypernatremia
Na⁺ > 145 mEq/L
● Due to free water loss > extra sodium gain
Hypernatremia s/s
Thirst, neuro changes (weakness, confusion, coma, seizures)
○ CNS issues caused by shrinkage of cells due to hypertonicity shifting water
out of cells
Hypernatremia TX
Hypotonic fluids (PO water, D5W, 0.45%NS)
○ If hypovolemic with abnormal VS (circulatory collapse), use NS
○ Correct slowly over 48-72 hours
Hypernatremia causes
6Ds - Diuresis, Dehydration, DI, Docs, Diarrhea, Disease (hyperthyroid,
kidney, sickle cell)
○ Sustained hyperNa seen in those who have inability to maintain adequate
water intake (infants, elderly)
Hyponatremia
Na⁺ < 135 mEq/L
● Almost always due to ↑ADH → impairs kidney’s ability to excrete free water
Hyponatremia causes
Causes: SIADH, Drugs (thiazides, ACEI), vomiting/diarrhea, psychogenic polydipsia
Hyponatremia causes
S/S: Headache, N/V, muscle cramps, ↓DTRs, neuro changes (confusion, lethargy,
coma, seizure
CNS issues due to cerebral edema; hypotonicity cause water to shift into
cells
Hyponatremia labs
Labs, serum osmolality help determine if true hyponatremia
○ True hyponatremia is Hypotonic Hyponatremia
Hyponatremia TX
If hypervolemic/euvolemic: Water restriction +/- diuretics
○ If hypovolemic: Normal saline fluids (expands volume to ↓hypovolemic
stimulus for ADH secretion)
If hyponatremia is not corrected slowly what disorder can happen?
central pontine myelinolysis
Hyperkalemia causes
Spurious: Hemolysis of blood sample
○ ↓ excretion: Renal insufficiency, meds (ACEI, spironolactone), adrenal
insufficiency
○ Cellular shift: cell lysis (burns), tissue injury (rhabdomyolysis), tumor lysis
syndrome, metabolic acidosis (DKA), meds (𝛃-blockers)
○ ↑ intake: food (bananas, tomatoes
Hyperkalemia s/s
Asymptomatic or n/v, areflexia, weakness, flaccid paralysis, arrhythmias
Hyperkalemia dx
Repeat blood draw to confirm, check glucose and bicarb;
Hyperkalemia ekg
tall peaked T
waves, wide QRS, PR prolongation, loss of P waves
Hyperkalemia tx
ECG changes and/or K⁺ > 6.5 mEq/L → emergent treatment
○ C BIG K
■ C alcium gluconate to stabilize cardiac cell membranes
■ B icarb and/or I nsulin PLUS G lucose to shift K⁺ into cells most rapid
way to shift K⁺
■ K ayexalate to ↑ GI loss
○ Also can give 𝛃-agonist (albuterol) to ↑cellular reuptake of K⁺
○ Eliminate extra K⁺ from diet
○ Loop diuretics will ↑ urinary loss of K⁺
○ Dialysis in severe cases
C BIG K
K
■ C alcium gluconate to stabilize cardiac cell membranes
■ B icarb and/or I nsulin PLUS G lucose to shift K⁺ into cells most rapid
way to shift K⁺
■ K ayexalate to ↑ GI loss
Hypokalemia
K⁺<3.5 mEq/L
● Causes
○ Cellular shift: insulin, 𝛃2-agonists, alkalosis
○ GI loss: vomiting/diarrhea, chronic laxative use
○ Renal loss: diuretics (loop, thiazide)
○ Hypomagnesemia
Hypokalemia s/s
Fatigue, muscle cramp/weakness, ileus, ↓DTRs, paresthesias, rhabdomyolysis,
ascending paralysis
Hypokalemia dx
Labs-K, Mg, glucose, bicarb; ECG shows T wave flattening, U waves
Hypokalemia tx
Treat underlying cause, PO/IV K⁺ repletion
If hypoK is not responding to K⁺ repletion, check Mg level because ↓Mg will
make fixing K⁺ harder
Hypercalcemia?
Ca⁺⁺ > 10.2 mg/dL
● Causes: Hyperparathyroidism, malignancy
Hypercalcemia s/s
Stones, bones, abdominal groans, psychic moans
○ Kidney stones, osteopenia/fractures, constipation, weakness, fatigue,
altered mental status, depression, ↓DTRs
Hypercalcemia dx
Labs, Ca⁺⁺, ECG shows short QT interval
Hypercalcemia tx
Saline diuresis (NS, furosemide), “loops lose calcium” ○ Avoid thiazide diuretics as they ↑Ca reabsorption ○ If Ca⁺⁺ > 14 mg/dL, use calcitonin and bisphosphonates as well
Hypocalcemia? Causes?
Ca⁺⁺<8.5 mg/dL
● Causes: Hypoparathyroidism (post-surgical, idiopathic), vitamin D deficiency,
hypomagnesemia, pancreatitis, drugs (PPI)
Hypocalcemia S/s
Abdominal muscle cramps, tetany, perioral and finger paresthesias, ↑DTRs,
diarrhea; Chvostek sign: Facial spasm from tapping on facial nerve
○ Trousseau sign: Carpal spasm with BP cuff inflation
Hypocalcemia dx ? Ekg?
Ca⁺⁺, PTH and Mg, ECG shows prolonged QT interval
Hypocalcemia tx
Underlying disease, IV/PO calcium, Mg if needed
○ HypoCa will not correct in setting of hypoMg
Pyelonephritis (Level 2) causes
Causes: similar organisms to cystitis: E. Coli , gram neg uropathogens ( Proteus, Enterobacter
Pyelonephritis (Level 2) s/s
UTI symptoms + evidence of upper urinary tract disease
● Flank pain, CVA tenderness, fever/chills, tachycardia
Pyelonephritis (Level 2) dx
UA and culture, CBC, blood cultures
● Will see WBC casts
Pyelonephritis (Level 2) tx
Mild cases: Outpt with fluoroquinolone, push fluids, close f/u
● Complicated cases: Admission, IV antibiotics (fluoroquinolone, 3rd/4th generation
cephalosporin), IV fluids
○ Pregnancy, comorbid conditions, severe N/V, toxic appearing
Dehydration
Deficiency of water: ↓ in total body water → hypernatremia (hypertonic dehydration
Dehydration 2 types:
Clinically → often expanded to include 2 main types: Isotonic dehydration and hypertonic dehydration
Dehydration s/s?
Mild: headache, thirst, fatigue, sunken eyes, dry mucous
membranes, ↓ skin turgor, oliguria, concentrated urine
▸ Mod-severe: lethargy, muscle cramping, altered mental status, ↓
renal function, coma; Sx of hypovolemia → hypotension,
tachycardia, ↓ pulse, pre-syncope/syncope
▸ Infants: listlessness, sunken fontanelles, tearless crying, ↓ # of
wet diapers
Dehydration Tx?
Mild: oral rehydration
▸ Mod-severe: correct hypovolemia first with isotonic IV solution
(eg. normal saline, Ringers lactate), then correct any water deficit
with hypotonic solution (eg. 5% dextrose, 0.45% NaCl)
Dehydration Isontonic dehyrdation?
volume-deficit [hypovolemia]) How: ECF fluid & electrolytes are lost ≈ equal amounts Etiologies: Hemorrhage, burns, vomiting, diarrhea Labs: Na: 135-145 mEq/L
Dehydration hypertonic dhydration?
(water-deficit) How: ECF water loss > solute loss Etiologies:Watery diarrhea, profuse sweating Labs: Na: >150 mEq/L
HORSESHOE KIDNEY
Anomaly that usually occurs as a fusion of the lower poles of
both kidneys; both kidneys are typically functional & have their
own separate ureters
HORSESHOE KIDNEY Associated?
Associated conditions: hydronephrosis (80%) often due to
vesicoureteral reflux or ureteropelvic junction obstruction,
renal calculi, urinary stasis (↑ risk of infection), genital
anomalies (eg. bicornuate uterus), & several syndromes (eg.
Turner)
HORSESHOE KIDNEY s/sx?
S/Sx: most pts are asymptomatic & fused kidney is usually found incidentally (eg. antenatal U/S); pain & hematuria can occur with obstruction or infection
HORSESHOE KIDNEY Labs?
For obstructive uropathy →
postnatal U/S, creatinine
▸ UTI → U/A, urine culture, voiding
cystourethrogram
HORSESHOE KIDNEY tx?
most pts do not need any
therapeutic interventions;
urology referral for renal calculi,
obstructive uropathy, infections
