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PANRE > Renal-Panre > Flashcards

Renal-Panre Flashcards

1
Q

Primary Respiratory Acidosis

A

↑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

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2
Q

Primary Respiratory Acidosis Compensation?

A

Kidneys slowly will retain HCO3 to help raise pH

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3
Q

Primary Respiratory Alkalosis

A

↓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

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4
Q

Primary Respiratory Alkalosis Compensation?

A

Kidneys slowly will excrete HCO3 to help lower pH

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5
Q

Primary Metabolic Acidosis

A

↓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⁻

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6
Q

Primary Metabolic Acidosis Causes

A 
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
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7
Q

Primary Metabolic Acidosis

Compensation?

A

Respiratory response is quick →hyperventilation to blow off CO2

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8
Q

Primary Metabolic Alkalosis

A

↑HCO3

○ Common cause: Vomiting- loss of (H⁺)Cl⁻ so the kidney holds back HCO3

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9
Q

Primary Metabolic Alkalosis Compensation

A

No acute response from lungs, give patient back Cl⁻ and kidneys
will dump HCO3

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10
Q

Chronic kidney disease (CKD)

A 
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

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11
Q

Nephritic syndrome:

A

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

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12
Q

Nephrotic syndrome:

A

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)

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13
Q

Nephrotic syndrome Clinical features?

A 
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
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14
Q

Nephrotic syndrome treatment

A

Treatment - renal replacement therapy:
o Dialysis: hemodialysis or peritoneal dialysis
o Continuous hemodiafiltration
o Transplant

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15
Q

Staged 0-5 based on GFR and kidney damage

A

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

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16
Q

CKD Causes:

A

1 DM, #2 HTN, Glomerulonephritis, polycystic kidney disease

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17
Q

CKD s/s

A

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)

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18
Q

CKD common metabolic abnormalities

A

Azotemia, fluid retention, metabolic acidosis, hyperK, anemia, hypoCa, hyperphos,
impaired platelet aggregation, renal osteodystrophy

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19
Q

CKD labs

A

Proteinuria- #1 indicator of disease progression , U/A- broad waxy casts with ESRD,
estimated GFR, BUN/Cr

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20
Q

CKD treatment

A 
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
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21
Q

Hypernatremia

A

Na⁺ > 145 mEq/L

● Due to free water loss > extra sodium gain

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22
Q

Hypernatremia s/s

A

Thirst, neuro changes (weakness, confusion, coma, seizures)
○ CNS issues caused by shrinkage of cells due to hypertonicity shifting water
out of cells

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23
Q

Hypernatremia TX

A

Hypotonic fluids (PO water, D5W, 0.45%NS)
○ If hypovolemic with abnormal VS (circulatory collapse), use NS
○ Correct slowly over 48-72 hours

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24
Q

Hypernatremia causes

A

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)

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25
Q

Hyponatremia

A

Na⁺ < 135 mEq/L

● Almost always due to ↑ADH → impairs kidney’s ability to excrete free water

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26
Q

Hyponatremia causes

A

Causes: SIADH, Drugs (thiazides, ACEI), vomiting/diarrhea, psychogenic polydipsia

27
Q

Hyponatremia causes

A

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

28
Q

Hyponatremia labs

A

Labs, serum osmolality help determine if true hyponatremia

○ True hyponatremia is Hypotonic Hyponatremia

29
Q

Hyponatremia TX

A

If hypervolemic/euvolemic: Water restriction +/- diuretics
○ If hypovolemic: Normal saline fluids (expands volume to ↓hypovolemic
stimulus for ADH secretion)

30
Q

If hyponatremia is not corrected slowly what disorder can happen?

A

central pontine myelinolysis

31
Q

Hyperkalemia causes

A

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

32
Q

Hyperkalemia s/s

A

Asymptomatic or n/v, areflexia, weakness, flaccid paralysis, arrhythmias

33
Q

Hyperkalemia dx

A

Repeat blood draw to confirm, check glucose and bicarb;

34
Q

Hyperkalemia ekg

A

tall peaked T

waves, wide QRS, PR prolongation, loss of P waves

35
Q

Hyperkalemia tx

A

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

36
Q

C BIG K

A

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

37
Q

Hypokalemia

A

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

38
Q

Hypokalemia s/s

A

Fatigue, muscle cramp/weakness, ileus, ↓DTRs, paresthesias, rhabdomyolysis,
ascending paralysis

39
Q

Hypokalemia dx

A

Labs-K, Mg, glucose, bicarb; ECG shows T wave flattening, U waves

40
Q

Hypokalemia tx

A

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

41
Q

Hypercalcemia?

A

Ca⁺⁺ > 10.2 mg/dL

● Causes: Hyperparathyroidism, malignancy

42
Q

Hypercalcemia s/s

A

Stones, bones, abdominal groans, psychic moans
○ Kidney stones, osteopenia/fractures, constipation, weakness, fatigue,
altered mental status, depression, ↓DTRs

43
Q

Hypercalcemia dx

A

Labs, Ca⁺⁺, ECG shows short QT interval

44
Q

Hypercalcemia tx

A 
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
45
Q

Hypocalcemia? Causes?

A

Ca⁺⁺<8.5 mg/dL
● Causes: Hypoparathyroidism (post-surgical, idiopathic), vitamin D deficiency,
hypomagnesemia, pancreatitis, drugs (PPI)

46
Q

Hypocalcemia S/s

A

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

47
Q

Hypocalcemia dx ? Ekg?

A

Ca⁺⁺, PTH and Mg, ECG shows prolonged QT interval

48
Q

Hypocalcemia tx

A

Underlying disease, IV/PO calcium, Mg if needed

○ HypoCa will not correct in setting of hypoMg

49
Q

Pyelonephritis (Level 2) causes

A

Causes: similar organisms to cystitis: E. Coli , gram neg uropathogens ( Proteus, Enterobacter

50
Q

Pyelonephritis (Level 2) s/s

A

UTI symptoms + evidence of upper urinary tract disease

● Flank pain, CVA tenderness, fever/chills, tachycardia

51
Q

Pyelonephritis (Level 2) dx

A

UA and culture, CBC, blood cultures

● Will see WBC casts

52
Q

Pyelonephritis (Level 2) tx

A

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

53
Q

Dehydration

A

Deficiency of water: ↓ in total body water → hypernatremia (hypertonic dehydration

54
Q

Dehydration 2 types:

A

Clinically → often expanded to include 2 main types: Isotonic dehydration and hypertonic dehydration

55
Q

Dehydration s/s?

A

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

56
Q

Dehydration Tx?

A

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)

57
Q

Dehydration Isontonic dehyrdation?

A 
volume-deficit
[hypovolemia])
How: ECF fluid &amp; electrolytes are lost
≈ equal amounts
Etiologies: Hemorrhage, burns, vomiting,
diarrhea
Labs: Na: 135-145 mEq/L
58
Q

Dehydration hypertonic dhydration?

A 
(water-deficit)
How: ECF water loss > solute loss
Etiologies:Watery diarrhea, profuse
sweating
Labs: Na: >150 mEq/L
59
Q

HORSESHOE KIDNEY

A

Anomaly that usually occurs as a fusion of the lower poles of
both kidneys; both kidneys are typically functional & have their
own separate ureters

60
Q

HORSESHOE KIDNEY Associated?

A

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)

61
Q

HORSESHOE KIDNEY s/sx?

A 
S/Sx: most pts are asymptomatic &amp; fused kidney is usually
found incidentally (eg. antenatal U/S); pain &amp; hematuria can
occur with obstruction or infection
62
Q

HORSESHOE KIDNEY Labs?

A

For obstructive uropathy →
postnatal U/S, creatinine
▸ UTI → U/A, urine culture, voiding
cystourethrogram

63
Q

HORSESHOE KIDNEY tx?

A

most pts do not need any
therapeutic interventions;
urology referral for renal calculi,
obstructive uropathy, infections

PANRE (15 decks)

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