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Clin med sem 2 > Nephrology- Adults > Flashcards

Nephrology- Adults Flashcards

1
Q

Renal function- pathophysiology

A

Filtration of blood

  • removal of waste
  • maintain a proper concentration of electrolytes
  • acid/base balance
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2
Q

Renal function- cause

A

Regulating blood volume and BP

Producing erythropoietin

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3
Q

Renal function- epidemiology

A

Nephron- basic functionality unit of kidney
Glomerulus- site of blood filtration
Renal tubule- H20 & salt resorbed

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4
Q

Renal function- S/S & PE

A

Proximal Convoluted Tubule (PCT) - reabsorbs 60%

  • 65% -> Na, K, Ca
  • 80% -> Phosphate, H2O, Bicarbonate
  • 100% -> Glucose (>200, will see in urine), Amino Acids
  • Secretes drugs/toxins that are too big/protein bound to be filtered
  • H2O reabsorbed passively - osmotic gradient
  • Ammonia from glutamine (acidifies urine)
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5
Q

Renal function- diagnosis

A

Loop of Henle

  • 4 segments : thin descending, thin ascending, meduallary thick ascending, cortical thick ascending
  • Create concentration gradient and form concentrated urine
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6
Q

Renal function- labs & imaging

A

Distal Convoluted Tubule

  • Na and Ca reabsorption
  • Na - 5-10%
  • Ca - 10-15%
  • regulated by PTH and VitD
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7
Q

Renal function- treatment

A

Collecting Tubule

  • NaCl - reabsorbed
  • Bicarb - reabsorbed
  • H2O - rabsorbed - urine concentration
  • K - excretion
  • H+ - excertion
  • Urea - excreted
  • Regulated Urine volume
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8
Q

Acute renal failure/acute kidney injury- pathophysiology

A

Rapid worsening of renal function

  • quick rising BUN/Cr
  • accumulation of nitrogenous wastes in blood
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9
Q

Acute renal failure/acute kidney injury- cause

A

Prerenal
Postrenal
Intrarenal

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10
Q

Acute renal failure/acute kidney injury- epidemiology

A

No particular race/age
10% of people in hosp
2/3 pt in ICU
1% after surgery

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11
Q

Acute renal failure/acute kidney injury- S/S & PE

A 
Weakness/lethary
general malaise, drowsiness
Anorexia, N/V, diarrhea
Pruritis
Hiccups, SOB
Dizziness
Signs - point toward underlying cause
- prerenal - tachy, hypotensive
- Postrenal - distended bladder, CVA tenderness, enlarged prostate
Anuria, oliguria
Change in volume/wt
Change in Mental statu
Edema
Weakness
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12
Q

Acute renal failure/acute kidney injury- diagnosis

A

Criteria
- Abrubt (48hrs) absolute inc of serum creatinin of >0.3mg/dl above baseline
OR
- Serum Cr inc >50% w/in 7days OR
- Oligura (small amount of urine) <0.5mg/kg/hr for >6hr

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13
Q

Acute renal failure/acute kidney injury- labs & imaging

A

BMP - BUN, Cr
UA & urine microscopy - urine culuture
Urine output

Renal U/S - acute vs chronic
- small/shrunken kidney - chronic

Urine spot - osmolality, urine Na, Cr

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14
Q

Acute renal failure/acute kidney injury- treatment

A 
Depends on cause 
Dialysis if:
- serum Cr >5-10mg/dl
- unresponsive acidosis 
- severe electrolyte disorder 
- fluid overload
- uremic complications
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15
Q

Acute renal failure/acute kidney injury- prognosis

A

Complications - Dialysis Immediately

  • Hyperkalemia
  • Fluid overload
  • Signs of uremia - pericarditis, altered mental status
  • Severe metabolic acidosis (pH <7.1)
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16
Q

Prerenal Failure- pathophysiology

A

Most Common Cause of AKI

Reduced effective blood circulating to kidney

  • absolute reduction in fluid volume OR
  • Effective volume depletion - CHF, cirrhosis -> just perceived as this:: Respond by reabsorbing Na & others to inc vascular volume -> edema etc is made worse

No actual issue with Kidney

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17
Q

Prerenal Failure- cause

A

True intravascular volume depletion: hemorrhage, burns, diuretics, dehydration, GI loss, vomiting, diarrhea, anteric fistula

Dec Effective circulating volume: CHF, Cardiac tamponade, aortic stenosis, cirrhosis w/ ascites, nephrotic syndrome

Impaired renal blood flow: ACEI, NSAIDs, renal artery stenosis, renal vein thrombosis

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18
Q

Prerenal Failure- labs & imaging

A 
BUN:Cr ratio - >20:1
Urine Na - <20 meq/L
- not peeing it out 
Fractional Excretion of Na (FENa) - <1%
- measure % of Na filtered by the kidney & excreted in urine
Urine specific gravity - >1.020

Kidney is responding by inc reabsorption!!

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19
Q

Prerenal Failure- treatment

A

Correct underlying cause

  • CHF - diurese pt
  • Dehydration - IVF
  • Hemorrhage - Blood + Fluid
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20
Q

Postrenal failure- pathophysiology

A

Least Common

Ureters, bladder, urethra
- block here -> renal failure

Acute -> fix it - if don’t, can be permanent
- even then - might never be perfect

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21
Q

Postrenal failure- cause

A 
Nephrolithiasis
BPH
Obstructing tumor w/in GU system
Bladder outlet obstruction
Blood clots w/in urinary tract
Meds
Neurogenic bladder
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22
Q

Postrenal failure- S/S & PE

A

Abdominal or groin pain
Bladder discomfort
Anuria

Rectal exam
Pelvic exam

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23
Q

Postrenal failure- diagnosis

A

Post void residual >100mL -> bladder outlet obstruction

  • > 300 - more worried
  • U/S or Cath

U/S or Intravenous pylegram (IVP) - dilated ureters or renal pelvis

Abdominal CT - eval for mass

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24
Q

Postrenal failure- treatment

A

Relieve Obstruction!!

Cath
Nephrostomy tube
Stenting
Lithotripsy
Surgery - remove mass
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25
Q

Intrinsic Renal Failure- pathophysiology

A

One or both kidneys damaged and not working properly

Some quick, or develop over time

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26
Q

Intrinsic Renal Failure- cause

A

Acute Tubular necrosis - Most common
Nephrotoxins - NSAIDs, contrast agents, aminoglycosides, cyclosporine A, cisplatin, heme pigments (rhabdo)
Interstitial disease - acute interstitial nephritis, SLE, infection
Glomerrrulonephritis
Vascular dis - polyarteritis nodosa, vasculitis

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27
Q

Intrinsic Renal Failure- labs & imaging

A

BUN:Cr ratio - 10-15:1
Urine Na - >40 meq/L
FENa - >2%
Urine specific gravity - 1.010-1.020

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28
Q

Acute tubular necrosis (ATN)- pathophysiology

A

Most common cause of Intrinsic AKI

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29
Q

Acute tubular necrosis (ATN)- cause

A

Renal ischmia - all severe prerenal disease -> postischemic ATN

Nephrotoxins - aminoglycosides, heme pigmenst, cisplatin, radiocontrast media, pentamindine, mannitol, synthetic cannabinoids, tenofovir, IVIT

Sepsis

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30
Q

Acute tubular necrosis (ATN)- diagnosis

A

Classic UA - Muddy brown granular epithelial cell casts & free renal tubular epithelial cells

May have - hyperkalemia & metabolic acidosis

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31
Q

Acute tubular necrosis (ATN)- labs & imaging

A

BUN:Cr ratio - 10-15:1
Urine Na - >40 meq/L
FENa - >2%
Urine specific gravity - 1.010-1.020

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32
Q

Acute tubular necrosis (ATN)- treatment

A

Hold nephrotoxins
Treat underlying cause
Supportive management

Diuretics - for fluid overload
- not for oliguric

Most will spontaneously recover renal function - better if nonoliguric

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33
Q

Acute tubular necrosis (ATN)- prognosis

A

May never return to baseline

If during hosp -> higher in-hospital and long-term mortality

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34
Q

Acute Interstitial Nephritis (AIN)- pathophysiology

A

Immune mediated process of tubulointerstitial injury

- inflammatory infiltrate in interstitium

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35
Q

Acute Interstitial Nephritis (AIN)- cause

A

Meds - Cephalosporins, penicillins, allopurinol, diuretics, NSAIDs, sulfonamides

Illness - legionella, CMV, streptococcus, myocobacterium, EBC, vandida, SLE, sarcoidosis, Sjogren syndrome

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36
Q

Acute Interstitial Nephritis (AIN)- S/S & PE

A

Classic - fever, maculopapular rash, eosinophilia

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37
Q

Acute Interstitial Nephritis (AIN)- labs & imaging

A

UA - WBC, white cell casts, eosinophils, protein

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38
Q

Acute Interstitial Nephritis (AIN)- treatment

A

Stop offending med
Treat underlying cause
Glucocorticoids

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39
Q

Acute Interstitial Nephritis (AIN)- prognosis

A

Good

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40
Q

Glomerulonephritis- pathophysiology

A

Renal glomeruli damaged by deposition of inflammatory proteins in glomerular membrane

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41
Q

Glomerulonephritis- cause

A

Focal - Henoch-Scholeinpurpura, postinfectious, IgA nephropathy, hereditary nephritis, SLE

Diffuse - Postinfectious, membranoproliferative, SLE, vasculitis, rapidly progressive GN

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42
Q

Glomerulonephritis- S/S & PE

A

Heamturia
Edema of face/eyes - in morning
Edema Feet/ankles - evening
HTN

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43
Q

Glomerulonephritis- diagnosis

A

Hemeturia - tea or cola colored
UA - RBC, RBC casts, misshapen RBCs, proteins

Ranl biopsy

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44
Q

Glomerulonephritis- treatment

A

Steroids

Immunosuppressants/chemo meds

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45
Q

Chronic Kidney Damage (CKD)- pathophysiology

A

Kidney damage or dec kidney function for >3m

59% of americans develop CKD 3 or higher during life
50% w/ CKD - occurrence of AKI

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46
Q

Chronic Kidney Damage (CKD)- cause

A

DM

HTN

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47
Q

Chronic Kidney Damage (CKD)- epidemiology

A 
>60yo 
HTN, DM, CV
Fhx of CKD
Recurrent UTI
Prev AKI
Nephrolithiasis 
Transplant
Autoimmune
Smoking
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48
Q

Chronic Kidney Damage (CKD)- S/S & PE

A

Urine Microscopy

  • Squamous epithelial cell - sample contaminated
  • Renal tubular cells/cast - ATN or AIN
  • RBC casts - glomerulonephritis, AIN, vaculitis
  • WBC casts - interstitial nephritis, pyelo, inflammation
  • Fatty casts - nephrotic syndrome
  • Hyaline casts - nl
  • Muddy Borwn Casts - ATN
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49
Q

Chronic Kidney Damage (CKD)- diagnosis

A

Albuminuria
- specific to CKD
- nl - <30 mg/d
- Mod inc - 30-300 mg/day
- Severe inc - >300 mg/day
- Urine albumin:Cr ratio - prefered, yearly screening
- pathognomonic for kidney damage
- detects early CKD - before renal function change
- Higher -> quicker progression to failure
Early detection of med/sever inc in DM -> treat w/ ACEI or ARB and dec amount of albuminuria
- DM - target A1C 7% - prevent/delay progression CKD

U/S

  • nl kidney - 10cm
  • Shrunken = CKD
  • differentiate b/t actue and chronic
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50
Q

Chronic Kidney Damage (CKD)- labs & imaging

A

Creatinin - product of muscle metabolism, excreted by kidneys
- Nl - 0.6-1.2 mg/dl

GFR - plasma filtration by glomerulus

  • nl - >90 ml/min/1.73min2
  • inulin clear is gold for meas
  • MDRD and Cockcroft-Gault
    - MDRD - not used for AKI
    - use IBW - obese or fluid overload

Proteinuria - all types of proteins in urine

  • nl - <150 mg/d
  • gold - 24hr urine -> urine protine:Cr ratio
  • causes - Tubular damage, diabetic nephropathy, glomerulonephritis, rhabdo, bence jones proteins
  • less concerning - exercise, orthostatic porteinuria, acute sickness
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51
Q

Chronic Kidney Damage (CKD)- treatment

A

Staging - GFR and albuminuria

Meds to avoid - NSAIDs, contrast, Mg, Phophorous (Fleet’s enemas), Aluminum (Maalox, Rolaids), antimicrobials, DM meds, decongestants, antihypertensives, opioids, & gaba

RENALLY DOSE

Dialysis

  • start w/ GFR 10-15 - or unable to control volume status/hyperkalemia
  • ArteryVein Fistula needs 2m to mature
  • Hemodialysis - 3x/week
  • Peritoneal dialysis
    • Continuous ambulatotry PD - 4-5x/day
    • Continuous cyclic PD - machine cylces at night while asleep
52
Q

Chronic Kidney Damage (CKD)- prognosis

A 
Complications: 
HTN 
Hyperphophatemia
- Sevelamer - phosphate binders 
- foods to avoid - berry, whole grain, dark pop, porgessed foods 
Hyperparathryoidism 
- give Vit D
Anemia 
- Erthropoietin, aranesp, iron sup
- Goal Hgb - 10-11
Hyperkalemia  - Can be fatal!!
- low K diet, dialysis
- kayexelate - K binder 
Acidosis - Na bicarb
Uremic Encephaolopathy
53
Q

Nephrotic Syndrome- pathophysiology

A

Edema
Proteinuria - foamy urine
Low serum albumin
Hyperlipidemia

54
Q

Nephrotic Syndrome- cause

A

DM
Minimal change disease
Focal segmental glomerular sclerosis
Membranous nephropathy

55
Q

Nephritic Syndrome- pathophysiology

A

HTN
Hematuria
Proteinuria - less then nephrotic

56
Q

Nephritic Syndrome- cause

A

Post-inf glomerulonephritis
IgA nephropathy
Membranoproliferative glomerulonephritis

57
Q

Simple Cysts- pathophysiology

A

Thin wall without septa, calcifications or solid components

Epithelial cells from renal tubules and collecting ducts

58
Q

Simple Cysts- epidemiology

A

M>W

>50yo

59
Q

Simple Cysts- S/S & PE

A

“1cyst or multiple & bilateral

Asymptomatic
HTN

Rupture - hematuria, flank pain
- trauma or spontaneous
Infected - form renal abscesss

60
Q

Simple Cysts- diagnosis

A

US or CT - incidental finding

61
Q

Simple Cysts- treatment

A

Ruptures - IB or Tylenol for pain

62
Q

Complex Cysts- pathophysiology

A

Septa, calcifications, solid components

Risk of malignancy

Bosniak classification system

63
Q

Complex Cysts- diagnosis

A

CT w/ contrast

64
Q

Polycystic Kidney Disease- pathophysiology

A

Inherited disease - cause renal cyst
- progressive renal failure from enlargment of cysts

Autosomal dominant PKD - PKD1 & PKD2

65
Q

Polycystic Kidney Disease- epidemiology

A

50% ESRD by 60

Renal function decline by 4th ecade -> decline by 4-6ml/min/year
- progressively losing kidney function every year

66
Q

Polycystic Kidney Disease- S/S & PE

A

HTN

Hematuria
Proteinuria
Renal insufficiency found on labs
Flank pain - most common 
- due to renal hemorrhage, calculi or UTI
Nephrolithiasis - uric acid stones
- all the rest are Ca Oxalate
Renal Cell Carcinoma 
Extrarenal Manifestations:
Cerebral aneurysm 
- SAH or ICH most serious complication
- 5% younger 
- 20% >60yo  
Hepatic Cysts
Pancreatic cysts
Cardiac valve disease
Colonic divertifcula
Abdominal wal and inguinal hernia
67
Q

Polycystic Kidney Disease- labs & imaging

A

U/S

  • large kidneys and extensive bilateral cysts
  • Screen for those w/ pos FHx
  • US is less reliable in peds -> need genetic testing

CT or MRI - more sensitive

68
Q

Polycystic Kidney Disease- treatment

A 
HTN - rigorous control of BP
- ACEI 
- prevents progression of renal disease and dec 
Dietary Na restriction - <2gm per day
Statin
- treat HLD aggressively 
- Consider a coronary heart disease risk equivalent
- May preserve renal functiton

Tolvaptan - Ssamsca

  • 18-55 w/ GFR >25 at high risk for ESRD
  • Select via TKV, CT or MRI
  • Slow progression of PKD - disease modifying
  • Ensure adequate PO H2O intake
  • Contra - liver failure, hypovolemia, hypernatremia, dehydrated
  • SE - inc LFTs/liver tox, polyuria, polydipsia, chest pain, HA
  • Promotes excretion of free water - not losing electrolytes -> lose fluid, inc urin output, dec urine osmolality, restore serum Na level
  • Providerss must be registereed, shipped to pt via special pharm

Inc fluid intake
- supresses ADH levels-> inhibits cyst growth
- 3L/day
Dialysis
Kidney transplant
Pain - surgial aspiration or sclerosis of cysts

69
Q

Polycystic Kidney Disease- prognosis

A

Die from cardiac issues

Neuro deaths - ruptured intracranial aneurysm & HTN intracerebral hemorrhage

70
Q

Hypermagnesemia- pathophysiology

A

Plasma Mg > 2.5 mEq/L

Rare - renal impairment

Mg - is a CCB and block cardiac K channels

71
Q

Hypermagnesemia- cause

A

Oral ingestion - laxative abuse, accidental overdose of epson salts
Mg enemas
Mg infusion - preeclampsia or eclampsia
Renal insufficiency
- Mg excreted renally -> inc levels w/ CKD worsens
- Antacids or laxatives in regular doses

72
Q

Hypermagnesemia- S/S & PE

A

Asymptocatic -> <4
Neuromuscluar toxicity
4-6 : nasea, flushing, HA, lethargy, drowsiness, dec DTRs
6-10 : somnolence, hypocalcemia, absent DTRs, hypotension, bradycardia, EKG changes
>10: muscle paralysis -> flaccid quadriplegia, apnea, respiratory failure, complete heart block cardiac arrest

73
Q

Hypermagnesemia- labs & imaging

A

Mg - order by itself
BMP
EKG - dimished conduction, widened QRS, prolonged PQ interval

74
Q

Hypermagnesemia- treatment

A

Nl renal function:

  • stop offending agent
  • add diuretic to inc renal excretion of Mg - if still urinating

Ca gluconate - IV
- inc action potential threshold -> harder to depolarize -> more stable

Severe + renal impairment - hemodialysis

75
Q

Hypomagnesemia- pathophysiology

A

Plasma mg <1.8 mEq/L

76
Q

Hypomagnesemia- cause

A

Chronic diuretic therapy - loop, thiazide
Chronic alcoholism
Chronic diarrhea
Hypoparathryoidism
Nutritional deficiencies - prolonged TPN, malnutirtion
Uncontrolled DM
Chronic PPI usage - Cdiff + PPI -> gut flora changes

77
Q

Hypomagnesemia- S/S & PE

A

Neurologic

  • Tetany - Trousseau and Chvostek sign, muscle spasm, muscle cramps
  • seizures
  • involuntary movement

Cardiovascular - EKGs

  • Mod - Wide QRS & peaked T waves
  • Severe - Prolonged PR interval, QRS widening, diminished T wave
  • Freq PACs and PVCs -> sustained afib
  • Ventricular arrhythmias -> death
78
Q

Hypomagnesemia- diagnosis

A

Hypokalemia & Hypocalcemia!

Clinical - if not -> 24hr urine Mg excretion or fraction excretion of magnesium on random urine
- help diff b/t Gi and renal loss

79
Q

Hypomagnesemia- treatment

A

Severe - tetany, arrhythmias, seizures

  • IV Mg Sulfate
  • cont Cardiac monitoring
  • Reduce dose if CrCl <30

Asymptomatic/Minimal symptoms

  • PO replacement - MG Cl or Mg oxide
  • > diarrhea major SE
  • intracellular stores take longer to replete -> keep going to 1-2 days after labs normal

Correct underlying disease if possible

80
Q

Hypercalcemia- pathophysiology

A

Serum Ca >10.5 mEq/L
Mild - 10.5 - 12
Severe/life threatening >14

Nl - 9-10.5

81
Q

Hypercalcemia- cause

A

Malignancy

  • ectopic secretion of PTH by tumor
  • MM
  • Bone Mets

Endocrine

  • Hyperparathroid
  • MEN
  • hyperthyroid
  • Pheo
  • Adrenal insufficiency

Granulomatous dis - sarcoidosis, TB, histoplamosis, berryliosis, coccidiomycosis

Drugs - Thiazide, Vit A, Vit D, Estrogen, Milk-alkali syndrome, lithium

Misc - dehydration, porlonged immobilization, latrogenic, rhabdomyolysis, familial, lab error

82
Q

Hypercalcemia- S/S & PE

A

Asymptomatic till >12
Vague/ nonspcific
non-focal bdominal pain
Constipation, fatigue, diffuse body aches, anorexia, N/V
Intravascular volume depletion - tachy, orthostatic hypotension
Anxiety, depression, confusion, hallucinations

Severe::

  • lethargy, altered mental status, seizurres, coma
  • Cardiac conduction abnormalities - bradyarrhthmias, sinus arrest, AV blocks, AF, VT, LBBB, RBBB

Painful bones, renal stones, abdominal groans, psychic moans

83
Q

Hypercalcemia- diagnosis

A

EKG

  • ST elevation
  • Stort QT - classic - but not always seen
84
Q

Hypercalcemia- labs & imaging

A

Total Ca
- bound and unbound Ca

Ionized/unbound Ca - better represent

  • separate lab test OR
  • estimate

24hr Urine

Albumin

  • might have ““nl”” Ca if labumin is low or vice versa
  • correct Ca for albumin levels, or do an ionized Ca level
  • Corrected Ca = total Ca + (0.8 x (4-albumin))
1st Serum Ca - Elevated -> repeat ionized or total Ca + corrected albumin - HyperCa confirmed 
2nd - Measure PTH 
- High - primary hyperparathryoid
- low -> Check Vit D and PTHrP
PTHrP elevated - malignancy
85
Q

Hypercalcemia- treatment

A

Crisis - usually dehydrated

  • IV access and CV monitoring
  • Infuse NS ““wide open”” until BP and perfusion nl

Furosemide - NO LONGER RECOMMEND

  • can worsen hyperCa if not yet volumereplete
  • adversely affect hemodynamics and renal status

Osteoclast-inhibiting therapies

  • Bisphosphonates - hyperCa due to malignancy
  • Calcitonin - >14 and symptomatic -> dec serum Ca levels
  • Glucocorticoids - dec vit D

Severe - dialysis

Crisis due to primary hyperparathyroid - urgent parathyroidectomy

86
Q

Hypocalcemia- pathophysiology

A

Serum <8.5 mg/dL

Ionized <4.6 mg/dL

87
Q

Hypocalcemia- cause

A 
Hypoparathryoidism 
- genetic 
- postsurgical/radiation damage
- Hungry bone syndrome 
- Infiltration of parathryoid gland
- Autoimmune
Drugs
- Bisphosphonates
- Ca chelators - EDTA, citrate, phosphate
- Phenytoin
- Fluoride poisoning
Hypomagnesemia
Vit D def
PTH Resistance
Renal Dis
Loss of Ca from circulation 
- Tumor lysis
- Acute pancreatitis
- Osteoblastic mets
- Sepsis or acute severre illness
88
Q

Hypocalcemia- S/S & PE

A

Trosseau sign - carpal tunnel spasm after BP cuff applied for 3 min
Chvostek sign - spasm of facial muscle after tapping facial nerve in front of ear

Asymptomatic 
Mscule spasm orr muscle cramps
Tetany
Paresthesias
Confusion
Seizures
Dry skin, brittle nails, coarse hair
Anxiety, depression, dementia
Laryngospasm, bronchospasm
EKG - prolonged QT, flatened ST
89
Q

Hypocalcemia- labs & imaging

A 
Total Ca or Ionized Ca
Serum Phosphate
Vit D
Serum PTH
Mg
BMP
EKG
90
Q

Hypocalcemia- treatment

A

Acute & severe - IV calcium gluconate

  • treat emergent CV issues
  • Tetany, seizures <7.5

Mild - output
- Oral Ca + VitD - Calcitriol/VitD3

FIRST - Treat any concurrent hypomg -> then treat the hypoCa
- Ca problem won’t be fixed until Mg is fixed

91
Q

Hyperphosphatemia- pathophysiology

A

Serum >4.5 mg/dL

92
Q

Hyperphosphatemia- cause

A

Acute
Acute Renal Failure
Rhabdo
Tumor Lysis syndrome
Acute phosphate load - excess phosphate in TPN, rapid admin of phosphate rich drugs, phosphate containing laxatives, Vit D tox
Hypoparathryoid - parathroidectomy
- infiltration of parathyroid gland, metal overload
Extracellularr shift of phosphate - lactic acidosis, ketoacidosis, respiratory acidosis, crush injuries

Chronic
CKD!!
Hypoparathryoidsm - autoimmune, gene mutations
Pseudohypoparathryoidism

93
Q

Hyperphosphatemia- S/S & PE

A

Asymptomatic
Acute/severe -> hypoCa
- tetany, muscle cramps, perioral numbness or tingling, seizures
- Trousseau or Chvostek sign, hyperreflexia, carpopedal spasm, seizure

Uremia
- Fatigue, N/V, pruritis, SOB, sleep distrubances

Painful masses around joints, skin ulcerations, irritated conjunctiva
- ectopic calcifications

94
Q

Hyperphosphatemia- labs & imaging

A

Serum P
PTH
Serum Ca
Vit D

Renal U/S?

95
Q

Hyperphosphatemia- treatment

A

Acute w/ nl renal function
- Saline + Loop diuretic -> correct phosphaturia

Hypoparrthroid
- Ca + Vit D -> correct hypoCa

AKI::
Phosphate binders when level >6
- ionized Ca low -> Ca based binder - Ca Carbonate orr Ca acetate
- Ionized Ca high -> non-Ca based binder - sevelamer, aluminum hydroxide, lanthanum carbonate
Severe - P >12 or symptomatic
- Dialysis

CKD

  • start tx when levels above nl
  • Restrict dietary phosphate to 800-1000mg - dark colas, oysters, cheese, milk, organ meats, ice crem, chocolate, nuts/seeds
  • Phosphate binders - dec intestinal phosphate absorption
  • Dialysis - remove excess phosphate
96
Q

Hypophosphatemia- pathophysiology

A

Serum <2.5 mg/dL

97
Q

Hypophosphatemia- cause

A 
Resp alkalosis
Sepsis
Refeeding syndrome
Alcohol withdrawl
Renal transplant
HyperCa of malignancy
Hyperparthyroid
Hereditary rickets
Vit D
Inhibition of phosphate absorption
Inadequate intake
98
Q

Hypophosphatemia- S/S & PE

A 
Asymptomatic - unless <1mg/dL
Metabolic encephalopathy
Proximal myopathy
Impaired myocardial contractility
Dysphagia
Resp failure
Rhabdo
Hemolysis
99
Q

Hypophosphatemia- labs & imaging

A

Serum P

Urine P::
24hr or Random speciem + calculate fractional excretion of filtered phosphate
- Exc <100 mg or FEPO4 <5% -> low renal P excretion
-» internal redistubution or dec intestinal absorption
- Ex >100mg or FEPO4 >5% -> renal P wasting
-» Hyperparathyroid, VitD def, renal tubular defect

100
Q

Hypophosphatemia- treatment

A

Asymptomatic + P <2
- Oral P

Symptomatic

  • 1-1.9 = Oral phosphate - IV if rhabdo, CNS, hemolysis
  • <1 = IV phosphate - switch to PO once P >1.5

Urine P wasting - most diff to treat

  • Dipyridamole QID - inc P levels
  • inc renal P reabsorption
101
Q

Hyperkalemia- pathophysiology

A

Serum K >5.0 mEq/L
- not whole body K
Dangerous electrolyte abnormality!!

98% of K is intracellular
2% in blood stream
Nl 3.5-5 - tightly regulated by kidney

102
Q

Hyperkalemia- cause

A 
Inc intake 
- PO supplementation, IV K
Pseudophyerkalemia
- Mechanical trauma from venipuncture - see red serum 
- true severe intravascular hemolysis - see red serum
- Exercise - repeat clenching of fits durign venipuncture
- Cooling or deterioration of sample
- Thrombocytosis - Plt>500K
- Severe leukocytosis - CLL - cells fragile 
Dec Excretion
Renal Failure - acute or chronic
- kidney ubale to filter and excrete nl
Hypovolemia 
- dehydration, CHF, cirrhosis
- low flow to kidneys
Hypoaldosteronism
- RTA4
- Adrenal insufficiency 
Intra/extracellular Shifts
Any breakdown of cells
- broken cells release K when they lyses
- crush injury, trauma, rhabdo, TLS
- PseudohyperK
Acidosis - H+ moves from blood into cells exchange for K
Insulin deficiency or resistance
- insulin causes K entry into cells - DM
103
Q

Hyperkalemia- epidemiology

A

Meds

  • ACEI
  • ARBs
  • Spironalactone
  • Bactrim
  • K supplements
  • NSAIDs, BetaBlockerrs, digitalis, Succinycholine, Amiloride
104
Q

Hyperkalemia- S/S & PE

A

Cardiotoxicity

  • inc resting membrane potential of cardiac myocite -> membrane excitability
  • high levels - K causes depolarization threshold to rise -> depressed Cardiac function

Vague/varied symptoms
Asymptomatic
N/V, palpitations, lethargy, confusion, parethesias, muscle weakness, paralysis if advanced, arrhythmias/death

105
Q

Hyperkalemia- diagnosis

A

Emergency??

  • S/S - Most serious - muscle weakness/paralysis, arrhythmias
  • K >6.5
  • Mod >5.5 + sig renal impairment + ongoing tissue breakdown OR ongling K absorption OR signicant acidosis
106
Q

Hyperkalemia- labs & imaging

A 
K - repeat if any doubt
Serum K >5
BMP - renal function
EKG
ABG - acidosis?

EKG

  • 5.5-6.5 - Peaked T wave
  • 6.5-7.5 -> flattned P wave w/ prolonged PR or absent P wave
  • 7.5-8 -> Wide QRS
  • > 8 -> sine wave pattern - imminent cardiac arrest
107
Q

Hyperkalemia- treatment

A

Severe + EKG changes - IV calcium gluconate

Continuous cardiac monitoring

Options to drive K back into cell:

  • Insulin + glucose
  • Beta-2 adrenergic agonist - inhaled albuterol
  • IV Na bicarbonate - temp, not lasting solutions
Remove K from body:
GI cation exchanger 
- bind K in the GI tract in exchange for other cations -> excreted in feces
- Na polystyrene sulfonate - Kayexalate - poop it out 
- Patiromer - Veltassa
Diuretics - only if peeing
- Loop diuretic - Lasix + saline
Hemodiaylsis 
- HyperrKpt w/ severe renal impairment

Stop K supplements or meds that inc K

108
Q

Hypokalmeia- pathophysiology

A

Serum K <3.5

109
Q

Hypokalmeia- cause

A

Inc Loss

  • Renal - diuretics, hyperaldostteronism
  • GI - V/D

K from blood into intracellular compartment

  • Insuline excess - put more into cell
  • Beta agonist treatment
  • Alkalosis

Hypomagnesemia - fix mg first
- Mg & K lost together - diuretics, vomiting

Renal tubular acidosis
- type 1 (distal) & type 2 (proximal) -> K wasting

Meds

  • diuretis - except K sparing
  • antipsychotics - risperdal, seroquel
  • amphotericin B, barium or chlorquine intoxication

Very low cal diets - 200-800cal

110
Q

Hypokalmeia- S/S & PE

A

NO patho presenting S/S
Muscle fatigue or weakness
- starts in LE -> trunk/UE -> paralysis
Cramps, rhabdo, myoglobinuria
Resp muscle weakness -> resp failure/death
GI muscle invovement - ileus, constipation, n/v

111
Q

Hypokalmeia- labs & imaging

A 
BMP
Mg
EKG
- Flattened or inverted T wave
- Prominent U waves - V4-V6
- ST depression
- Prolonged QT interval -> QU - fusion of T and U wave
- Arrhythmia
112
Q

Hypokalmeia- treatment

A

Not emergent - unless cardiac menifest or <2.5
- IV K - can cause pain & phlebitis

PO K Cl - perfered for most others

Concurrent hypoMg -> needs to be repleted

Continuous Cardiac monitoring and frequent recheck of K levels

113
Q

Hypernatremia- pathophysiology

A

Elevated Serum Na >145 mEq/L

Na is main extracellular cation
Na is charged - need pump
H2O is the only that can freely move back and forth

As Na concentration inc and dec - fluid will follow

  • Ince - hypervolemia
  • Dec - hypovolemia
  • unchanged - euvolemia

Looking at Na in a blood draw, not the wholebody

114
Q

Hypernatremia- cause

A

Elderly patients w/ dec thirst and dec access to fluids - highest risk

Inadequate fluid intake
Excess H2O loss - skin, GI tract
- Urine - osmotoic diuresis, diabetes insipidus, diuretics can waste water and/or Na
Diabetes insipidus
- Central - dec pituitary excretion of ADH
- Nephrogenic - dec kidney sensation to ADH
(ADH inc absorption of H2O)

Hypervolemic hypernatremia

  • iatrogenic from hypertonic saline or dialysis
  • Hyperaldosteronism - inc aldosterone -> inc Na -> inc H2O -> inc volume

Hypovolemic hypernatremia

  • renal losses from renal disease or diuretics
  • Extrarenal losses
  • pt is dehydrated - look volume depleted

Euvolemic hypernatremia

  • hypodipsia - dec H2O intake or thirst - lesions
  • Diabetes insipidus
115
Q

Hypernatremia- epidemiology

A

Chronic - >2 days

  • less likely to provoke neurologic s/s
  • underlying neuro disease -> imparired thirst
  • undergo brain adaption to hyernatremia

Acute - hours
- more likely to provoke neurologic s/s

116
Q

Hypernatremia- S/S & PE

A

Early - anorexia, restlessness, N/V
Next - progressive AMS - lethary/irritabolity 1st -> stupor or comas
Neurologic - twitching, hyperreflexia, ataxia, tremor, seizures
- when Na >160
Dec brain volume
- Acute -> rupture of cerebral veins -> hemorrhaging
- OR Demyalating brain lesion
- Chronic - gets used to dec brain mass

S/S of dehyration - dry MM, tenting/poor skin turgor, lack of tears, dec salivation, tachy, hypotension, oliguira/anuria
- ask pt to stick out tongue - good indication

117
Q

Hypernatremia- diagnosis

A

Cause - Hx

118
Q

Hypernatremia- labs & imaging

A

BMP

  • Na >145
  • if pt is alert, not dementated, has water young, and Na >150 -> check for lesion

If Etiology unclear

  • Urine
  • Osmolality - solute per kg in solvant
  • looking for extrenal cause
  • plasma>urine osmolality -> DI
119
Q

Hypernatremia- treatment

A

Dilute fluids to correct deficit - replace ongoing losses

Chronic:
GO SLOW - if not, rapid fluid movement into brain -> cerebral edema -> seizures and coma
Dilute fluid needed - hypotonic
D5W - 1.34mL/hr x weight in kg
- 50kg pt -> 70ml/hr
- goal - lower serum Na by max of 10 mEq/L per 24hr
Recheck Na & glucose 4-6hrs after tx intitation
- correct if dec too fast/slow

Acute:
D5W - 3-6mL/kg per hour 
- can also use 1/2 or 1/4 NS
Monitor Na & glucose - Q1-2h until Na <145
- then dec rate to 1 ml/kg  per hr -> reach Na of 140
- checking glucose  b/c giving dextrose 
Goal - reduce Na by 1-2mEq/L each hour
- get back into a nl range w/in 24 hrs
120
Q

Hypernatremia- prognosis

A

High mortality - 40-60%
- w/ underlying disease

Inc M&M

  • perioperative 30d mortality
  • Perioperative major coronary events
  • Pneumonia
  • VTE
121
Q

Hyponatremia- pathophysiology

A

Na <135mEq/L

Most common electrolyte disorder seen in hosp pts

122
Q

Hyponatremia- cause

A

Hypervolemic

  • fluid overload
  • H2O is added or retained -> Na in serum is diluted
  • CHF, cirrhosis, IVF, nephrotic syndrome

Hypovolemic
- H2O and Na is lost - more Na then H2O
- renal losses - duretics -»> THIAZIDES
- Extrarenal losses - diarrhea, sweating, blood loss, fluid shifts
Fluid loss can lead to hypo or hyper Na - depends on how much Na is loss

Euvolemic
Adrenal insufficiency
Polydipsia - primary or psychogenic -
- urinating large amounts
Hypothyroidism
Syndrome of inapprepriate Antidiuretic Hormone (SIADH)
- Intracranial patho - tumor, hemorrhage
- Paraneoplastic syndrome - tumor secretes ADH
- Pulm dis - cancer, COPD, interstitial lung dis
- Meds - SSRI, cyclophsophamide
Resest osmostat - Kidney cant dilute urine
- threshold to release ADH is reset downwards

123
Q

Hyponatremia- epidemiology

A

Hypotonic - low solutes - osmolality <280

  • SIADH
  • Effective arterila blood volume depletion - CHR, cirrhosis, diuretics
  • Endocrine d/o: hypothyroid, adrenal insufficiency
  • advanced renal failure - extasy, exercise

Isotonic - nl solutes - osmolality 280-295
- Pseudohyponatremia - inc serum lipids or proteins can lead to an erroneous measurement of Na level -> get a fake low Na

Hypertonic - high solutes - osmolality >295
Significant hyperglycemia - cause a false low Na -> need to correct it
- for every 100mg above nl -> add 2ml to Na
Mannitol, maltose, sucrose retention - pulls H2O out of cells -> dilution

124
Q

Hyponatremia- S/S & PE

A

Not symptomatic until Na is 125-130

Anorexia, N/V, lethargy, disorientation, HA, seizures

Signs - weakness, agitation, hyporeflexia, orthostatic hypotension, delirium, coma, seizure, respiratory arrest, brainstem herniatiton

125
Q

Hyponatremia- diagnosis

A

When started:
Acute - w/in 24hr
Subacute - 24-48hr
Chronic - >48hr

Na level:
Severe - <120 - BE WORRIED
Mod - 121-129
Mild - 130-135

126
Q

Hyponatremia- labs & imaging

A

Find underlying cause!!

1st - BMP + serum osmolality
- osmolality can further direct you -> hypotonic, isotonic, hypertonic cause

Urine osmolality & electrolytes - helpful

Further looking::
TSH
Plasma cortisol
ACTH stimulation test
Brain/lung imaging
127
Q

Hyponatremia- treatment

A

Identify and treat underlying cause

Symptomatic - even mild - need emerg therapy

  • hypertonic saline - 100mL bolus
  • raise Na by 4-6 w/in a couple of hours
  • should alleviate symptoms & prevent hernia
  • check Na every 2H

Non-emergency - goal to Na up slowly

Over rapid correction -> osmotoic demyelination syndrome - central pontine myeinolysis

Hypovolemic - Isotonic saline

Hypervolemic

  • CHF, cirrhosis -> diuresis, fluid restrction, Na restriction – DO NOT TAKE SALT TABS
  • Renal Failure -> fluid restriction, dialysis, Na restrction

Euvolemic - Fluid restriction

  • SIADH - may add salt tabs and/or loop diuretic
    • Demeclocycline - off label use - if dont respond to salt tabs or loop diuretics - last ditch effort
      - SE: renal toxicity (esp cirrhosis), nephrogenic DI, intracranial hypertension

Clin med sem 2 (30 decks)

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