Renal-Panre Flashcards

(63 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Primary Respiratory Acidosis Compensation?

A

Kidneys slowly will retain HCO3 to help raise pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary Respiratory Alkalosis Compensation?

A

Kidneys slowly will excrete HCO3 to help lower pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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⁻

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Primary Metabolic Acidosis

Compensation?

A

Respiratory response is quick →hyperventilation to blow off CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary Metabolic Alkalosis

A

↑HCO3

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Primary Metabolic Alkalosis Compensation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nephrotic syndrome treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CKD Causes:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CKD common metabolic abnormalities

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CKD labs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hypernatremia

A

Na⁺ > 145 mEq/L

● Due to free water loss > extra sodium gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Hyponatremia
Na⁺ < 135 mEq/L | ● Almost always due to ↑ADH → impairs kidney’s ability to excrete free water
26
Hyponatremia causes
Causes: SIADH, Drugs (thiazides, ACEI), vomiting/diarrhea, psychogenic polydipsia
27
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
28
Hyponatremia labs
Labs, serum osmolality help determine if true hyponatremia | ○ True hyponatremia is Hypotonic Hyponatremia
29
Hyponatremia TX
If hypervolemic/euvolemic: Water restriction +/- diuretics ○ If hypovolemic: Normal saline fluids (expands volume to ↓hypovolemic stimulus for ADH secretion)
30
If hyponatremia is not corrected slowly what disorder can happen?
central pontine myelinolysis
31
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
32
Hyperkalemia s/s
Asymptomatic or n/v, areflexia, weakness, flaccid paralysis, arrhythmias
33
Hyperkalemia dx
Repeat blood draw to confirm, check glucose and bicarb;
34
Hyperkalemia ekg
tall peaked T | waves, wide QRS, PR prolongation, loss of P waves
35
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
36
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
37
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
38
Hypokalemia s/s
Fatigue, muscle cramp/weakness, ileus, ↓DTRs, paresthesias, rhabdomyolysis, ascending paralysis
39
Hypokalemia dx
Labs-K, Mg, glucose, bicarb; ECG shows T wave flattening, U waves
40
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
41
Hypercalcemia?
Ca⁺⁺ > 10.2 mg/dL | ● Causes: Hyperparathyroidism, malignancy
42
Hypercalcemia s/s
Stones, bones, abdominal groans, psychic moans ○ Kidney stones, osteopenia/fractures, constipation, weakness, fatigue, altered mental status, depression, ↓DTRs
43
Hypercalcemia dx
Labs, Ca⁺⁺, ECG shows short QT interval
44
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 ```
45
Hypocalcemia? Causes?
Ca⁺⁺<8.5 mg/dL ● Causes: Hypoparathyroidism (post-surgical, idiopathic), vitamin D deficiency, hypomagnesemia, pancreatitis, drugs (PPI)
46
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
47
Hypocalcemia dx ? Ekg?
Ca⁺⁺, PTH and Mg, ECG shows prolonged QT interval
48
Hypocalcemia tx
Underlying disease, IV/PO calcium, Mg if needed | ○ HypoCa will not correct in setting of hypoMg
49
Pyelonephritis (Level 2) causes
Causes: similar organisms to cystitis: E. Coli , gram neg uropathogens ( Proteus, Enterobacter
50
Pyelonephritis (Level 2) s/s
UTI symptoms + evidence of upper urinary tract disease | ● Flank pain, CVA tenderness, fever/chills, tachycardia
51
Pyelonephritis (Level 2) dx
UA and culture, CBC, blood cultures | ● Will see WBC casts
52
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
53
Dehydration
Deficiency of water: ↓ in total body water → hypernatremia (hypertonic dehydration
54
Dehydration 2 types:
Clinically → often expanded to include 2 main types: Isotonic dehydration and hypertonic dehydration
55
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
56
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)
57
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 ```
58
Dehydration hypertonic dhydration?
``` (water-deficit) How: ECF water loss > solute loss Etiologies:Watery diarrhea, profuse sweating Labs: Na: >150 mEq/L ```
59
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
60
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)
61
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 ```
62
HORSESHOE KIDNEY Labs?
For obstructive uropathy → postnatal U/S, creatinine ▸ UTI → U/A, urine culture, voiding cystourethrogram
63
HORSESHOE KIDNEY tx?
most pts do not need any therapeutic interventions; urology referral for renal calculi, obstructive uropathy, infections