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Medical School > MF2 RENAL > Flashcards

MF2 RENAL Flashcards

1
Q

Which kidney is higher

A

left

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2
Q

Describe the vasculature of the kidney

A

renal artery → segmental arteries → interlobar artery → arcuate artery → cortical radiate arteries → afferent arterioles → glomerular capillaries → efferent arterioles → peritubular capillaries and/or vasa recta → interlobar veins → arcuate veins → interlobar veins → segmental veins → renal vein

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3
Q

Risk factors of upper UTI

A
  • Female
  • Sexual intercourse
  • Indwelling catheter
  • Diabetes mellitus
  • Urinary tract obstruction
  • Vesicoureteral reflux: primary congenital defect, bladder outlet obstruction)
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4
Q

Risk factors of lower UTI

A
  • Sexual intercourse
  • Female
  • Post-menopause (decreased estrogen)
  • Foley catheter
  • Hyperglycemia
  • Impaired bladder emptying
  • Poor hygiene
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5
Q

Symptoms and Urinalysis for UTIs

A

SYMPTOMS
- Lower
> Dysuria
> Increased frequency
> Increased urgency
> Suprapubic pain
- Upper
> Fever
> Chills
> Flank pain (costovertebral engle)
- Kids
> Delirium
> Fatigue
> Incontinence
- Elderly
> Irritable
> Malodorous
> Fever even in lower

URINALYSIS
- WBCs
- Leukocyte esterase
- Nitrates
- Hematuria

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6
Q

Radiology for UTI diagnoses

A
  • Renal ultrasound: can be used with kids with kidney malformation that can lead to UTI
  • Bladder Ultrasound
  • Voiding (VCUG) cystourethrogram: radiocontrast on fluoroscopy to watch urination
    > Vesicoureteral reflux
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7
Q

Types of Kidney Stones

A

Nephrolithiasis: solutes in urine precipitate out and crytallize

  • Calcium stones: calcium oxalate (80%) or phosphate
  • Uric acid: lose too much fluid, high protein diet, diabetes, metabolic syndrome
  • Struvite: magnesium ammonium phosphate → upper UTI
  • Cysteine stones: rare disorder → cystinuria

Xanthogranulomatous peylonephritis: infected kidney stone causes chronic obstruction → infection and increased pressure

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8
Q

Kidney stones treatment

A
  • Shockwave lithotripsy
  • Medications
    > a-blockers/CCB
    > NSAIDs/opiates
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9
Q

Receptors in bladder and urethra

A
  • B3 on bladder wall: binds NE; relax bladder
  • M3 on bladder wall: binds acetylcholine; contract detrusor
  • Stretch receptors on bladder wall: detect rugae expansion
  • a1 on internal sphincter: binds NE; closes sphincter
  • N1 on external sphincter: binds Ach; closes sphincter
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10
Q

Nephrotic syndrome (subtypes, causes)

A

Massive proteinuria, hypoalbuminemia, hyperlipidemia, edema

  • Increased permeability through damaged glomerular basement membrane
  • PRIMARY (intrinsic kidney disease)
    > Membranous glomerulonephritis: white adults,
    thickened basement membrane from auto-Abs
    - HBV, SLE, solid tumors (lung, breast, GI)
    > Minimal change glomerulonephritis: children; if adult
    check hematological malignancy;
    - NSAIDs
    ***PERIORBITAL EDEMA IN KIDS
    > Focal segmental glomerulosclerosis:
    - African ancestry, obese, HIV, scaring/sclerosis of
    glomerulus
  • SECONDARY (systemic disease, congenital)
    > Nodular Glomerulosclerosis
    - DM: hyperglycemia → glycation → thickened
    basement membrane → hypertrophy, scarring,
    thickening
    - Amyloidosis: nodular deposits
    > Focal segmental glomerulosclerosis: podocytes
    - Inherited, heroin
    > Membranoproliferative GN
    - HCV, malaria, SLE, leukemia, lymphoma, shunt
    neprhitis
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11
Q

Factors affecting GFR

A
  • Pressure out
    > Glomerular hydrostatic pressure: out capillaries
  • Pressure in
    > Colloid pressure: by plasma proteins pulling water
    > Scapular hydrostatic pressure: fluid backup
  • KF
    > Surface area of glomeruli
    > Permeability of glomeruli
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12
Q

Diagnosing Nephrotic syndrome

A
  • Urinalysis
    > 3+ or 4+ proteinuria (dipstick)
  • Blood test
    > Hypoalbuminuria
    > Hyperlipidemia
    > HIV, Hep C (FSG)
    > Autoantibodies (membranous)
    > Cancer
  • Physical exam
    > Edema
  • Renal biopsy
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13
Q

Nephrotic syndrome treatment

A
  • Corticosteroids: immune suppression
    > Prednisone
  • Diuretics: loo diuretics for edema
    > Furosemide
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14
Q

Nephron - Proximal Convoluted Tubule

A
  • 3NA/2K pump, water follows
  • NaCl channel
  • Amino acids
  • SGLT2 transporter (glucose)
    > Jiardiance is an inhibitor; used for diabetes, HTN
  • HCO3 reabsorb, Na & H antiporter
    > Acetazolamide inhibits → Na/H2O excretion, acidosis
    > Impaired = type II renal tubular acidosis
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15
Q

Nephron - Loop Henle

A
  • Aquaporin I: water pump
    > Mannitol increases gradient → more reabsorption
  • Na/K/2Cl cotransporter
    > Loop diuretics inhibit (furosemide)
    > Barters type I syndrome
  • ROMK: K pump
    > Barter’s type III
  • IC-KB: Cl pump
    > Barter’s type II
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16
Q

Nephron - Distal Convoluted Tubule

A
  • NaCl pump
    > Thiazide diuretics inhibit (increased Ca absorb)
    > Gitleman’s syndrome
  • 3Na/2K pump, water follows
  • Ca channel
    > Hypercalcemia: cancer if admitted, hyperparathyroidism
    if outpatient
    > PTH activates this channel
  • Na pump
    > Aldosterone activates (activated by ACE)
  • K pump
    > Aldosterone activates (activated by ACE)
    -3Na/2K pump, water follows
    > Aldosterone activates (activated by ACE)

**K sparing diuretics inhibit aldosterone (receptor agonist)
> Spironolactone
**Type IV renal tubular acidosis inhibits aldosterone

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17
Q

Nephron - Collecting system

A
  • Intercalated A cells: secrete H
    > Inhibition is type IV renal tubular acidosis
  • Intercalated A cells: reabsorb H
  • Aquaporin II: pump water
    > Activated by ADH (activated by increased plasma
    osmolarity, decreased blood volume)
    > Activated in SIADH (urine concentrated, euvolemic; small
    cell lung cancer)
    > Inhibited by chronic lithium (bipolar meds, diabetes
    insipidus; urine dilute, inappropriate)
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18
Q

Barter’s Syndrome

A
  • Loop of Henle issue → acts like loop diuretic
  • Infants
  • Increased renin
  • Increased aldosterone
  • Decreased Na, K, Cl
  • Increased HCO3 → alkalosis
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19
Q

Gitleman’s sydrome

A
  • NaCl pump issue in DCT → acts like thiazide diuretic
  • Teenage
  • Alkalosis
  • Hypokalemia
  • Decreased Mg
  • Often asymptomatic; muscle weakness, fatigue, dizziness, vertigo, plyuria, nocturia
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20
Q

Hypernatremia and Hyponatremia

A

**Disorders of water balance

HYPERNATREMIA
- Decreased volume
> Dehydrated (less urination) or diabetes insipidus
(increased urination)
- Increased volume
> Excessive IV or hyperaldosteroneisma
- SYMPTOMS: tired, weak, altered mental status, seizures
***cerebral edema

HYPONATREMIA
- Hyperosmolar
> Hyperglycemia
- Iso-osmolar
> Lab error
> Multiple myeloma
- Hypo-osmolar
> Hypervolemic: CHF, cirrhosis, nephrotic syndrome
> Euvolemic: SIADH, Addison’s, hypothyroid, adrenal
insufficiency
> Hypovolemic: renal or GI fluid loss
- SYMPTOMS: neurological predominate (headache, nausea, malaise, lethargy, weakness, muscle cramps, anorexia, disorientation)
***cerebral demyelenation syndrome (“locked in”)

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21
Q

Hyperkalemia vs Hypokalemia

A

HYPERKALEMIA
- Increased intake
> IV
- Transcellular shift
> Cell injury
> Metabolic acidosis
> Tumor lysis
- Decreased loss
> Decreased GFR, hypoaldosterone
- SYMPTOMS: muscle weakness, arrhythmias, paralysis, nausea, palpitations, muscle stiffness
> ECG changes and cardiotoxicity (peaked & narrow T, loss
P, long PR, wide QRS, AV block)

HYPOKALEMIA
- SYMPTOMS: usually asymptomatic; muscle cramps, arrhythmias, fatigue, myalgia, constipation
- Decreased intake
> Anorexia
> Alcoholism
- Transcellular shift
> Alkalemia, insulin, hyperaldosterone
- Increased loss
> Renal: loop diuretics/Bartter’s, thiazide/Gittleman’s
> GI: vomiting (increase pH), diarrhea (decrease pH)

22
Q

Hypertension

A

ESSENTIAL (95%)
- Increased sympathetic NS activity
> Obesity (high catecholamines)
> High stress (high cortisol)
- Increased renin release
> Diabetes
> Obesity
- Increased Na retention (“low renin HTN”)
> African American
- Increased age (decreased compliance, increased TPR)

SECONDARY (5%)
- Renal
> Vascular: fibromuscular dysplagia, renal artery stenosis
> Parenchyma: diabetic nephropathy, glomerulonephritis,
polycystic kidney disease
- Cardiac
> Coarctation of aorta (diff BPs upper vs lower)
- Lungs
> obstructive sleep apnea
- Neuro (ICP)
> Cushings triad: high BP, low HR, irregular respiration
- Drugs
> Sympathomimetics (cocaine, NMDA, PCP,
amphetamines, ADHD meds)
> Estrogen contraceptives (estrogen increased liver AII)
> NSAIDs (inhibit COX2 → constrict afferent → low GFR)
- Pregnancy
> Preeclampsia: >20wks, HTN, proteinuria
> Eclampsia: >20wks, HTN, proteinuria, seizures
- Endocrine
> Adrenal
- Cortisol → Cushing’s syndrome
- Aldosterone → hyperaldosterone → high Na → BV
- Norepinephrine → pheochromocytoma
> Thyroid
- Hypothyroid
- Hyperthyroid
- Hyperparathyroid → increased Ca → vasoconstriction

23
Q

HTN medications

A
  • ACEi: avoid in asthma, african american, pregnant, renal arterial sclerosis
  • ARBS
  • Dihydropiridine CCBs: good in low renin HTN
  • Thiazide diuretics
  • B-blockers: careful in COPD, asthma
  • Aldosterone antagonists (K sparing diuretics)
  • Alpha 1 blockers/ alpha 2
24
Q

HTN meds in pregnancy

A
  • Hydralizine: vasodilator
  • Methyl-dopa: alpha-2 agonist
  • Lavetalol: beta blocker
  • Nifidipine: Ca channel blocker
25
Q

HTN emergency

A
  • Decrease BP 25% in 2hr → <160 in 24hr → baseline in 2 days
  • IV medications:
    > Nicardipine *
    > Nitroprusside
    > Nitroglycerine
    > Esmolol (aortic dissection)
    > Labetalol *
26
Q

Acidemia

A

—RESPIRATORY—
- Decreased resp rate → increased pCO2
> CNS depression
> Neuromuscular
> Obstructive lung disease
**Compensation HCO3:pCO2: acute 1:10, chronic 3:10

—METABOLIC—
**Compensation pCO2 = 1.5 x HCO3 + 8
- AGMA (>12)
> Ketoacidosis
> Uremia
> Lactic acidosis (decreased O, decreased clearance
[liver/renal failure], sepsis)
> Toxins
- Methanol
- Ethylene glycol (antifreeze)
- Propylene glycol
- Salicylates (tylenol, aspirin)
> Renal failure

***Delta ratio (AG/HCO3)
> 0.4 - 0.8: AGMA + NAGMA
> 1 - 2: pure AGMA
> 2+ : Metabolic alk + AGMA
> < 0.4: Hyperchloremic

  • NAGMA (<12)
    > Renal
    - Renal tubular acidosis (hypoK [type I, II], hyperK IV)
    - Renal Failure
    > Extrarenal
    - Saline infusion
    - TPN
    - Ureteral divergence
    - Pancreatic fistula
    - Addison’s, acetazolamide
    - Diarrhea
27
Q

Alkalemia

A

—RESPIRATORY—
- Increased resp rate
> CNS hyperactivity
> Hypoxia (penumonia, PE)
**Compensation HCO3:pCO2: acute 2:10, chronic 4:10

—METABOLIC—
- Decreased H
> Vomiting
> NG tube
- Increased HCO3
> Total volume loss (shock, diuretics)
> Mineralcorticoid excess (hyperaldosterone; Cushing’s)
> Over-reaction hypercapnia (COPD)
**Compensation pCO2 = 1.5 x HCO3 + 8

28
Q

Types of shock

A

Inadequate tissue perfusion → ischemia → necrosis → organ failure

HYPOVOLEMIC
- Decreased cardiac output, increased resistance, increased HR, cyanosis
- Blood loss: GI bleed, AAA rupture, trauma, post-partum
- Non-blood fluid loss: burns, vomit, diarrhea, bowel obstruction, DKA

CARDIOGENIC
- Decreased circulating volume → low BP → high HR → RAAS → ischemia → deacreased ATP & increased lactate → organ failure
- MI, myocarditis, aortic/mitral valve stenosis, arrhythmias

OBSTRUCTIVE
- Tension pneumothorax
- Pericardial tamponade
- Pulmonary embolism
- Proximal aortic dissection

DISTRIBUTIVE
- Septic shock
> inflammation, acute phase reactant proteins, endotoxins
decrease plasmin
- Anaphylactic
> Leukotrienes, histamines
- Neurogenic
> Acute spinal cord injury
> Regional anesthesias

29
Q

Normal saline vs Ringer’s lactate

A

Normal: high Cl content → hypercloremia if long time
Ringers: NaCl, CaCl, KCl; closer to body composition

30
Q

Pre-renal AKI

A

Blood supply to kidney decreased

BUN/cr > 20:1
Decreased GFR
High blood Na and water
FENa < 1%
Less urea, Na, water in urine

  • Decreased blood volume
    > CHF
    > Liver failure
    > Kidney injury
    > Pancreatitis
    > Shock
    > Diarrhea
    > Vomitting
    > Burns
  • Large vessel block
    > Renal artery stenosis
    > Afib
  • Small vessel block
    > Hepatorenal syndrome: liver failure → portal
    hypertension → vasodilators compensation → low BP
    > NSAIDs
    > Increased Ca (vasoconstriction)
    > ACEi/ARBs: dilate efferent
31
Q

Intrinsic AKI

A

Kidney cell damage

BUN/cr < 15:1
Decreased GFR
Low blood Na and water
FENa > 2%
High urea, Na, water in urine
Proteinuria, hematuria

  • Acute tubular necrosis
    > Ischemia: decreased blood flow, rhabdomyolysis, sepsis,
    HF
    > Toxins:
    - Meds: NSAIDs, aminoglyosides, vancomycin,
    antiviral acyclovir, IV contrast dye
    - Hemolysis: Hb and Fe
    - Cancer: uric acid metabolism waste product
    - Multiple myeloma: bets jones proteins
    - Ethylene glycol: antifreeze
    **Rise in Cr, oligouric → diuretic → recovery, hyperK,
    metabolic acidosis
  • Glomerulonephritis
    > Podocytes: SLE, membranous glom, diabetes
    > Basement membrane: anit-GMB Abs (Good Pastors_
    > Immune-complex mediated: post strep, endocarditis,
    Hep B, C, IgA nephropathy
  • Acute interstitial nephritis
    > Medications: B-lactams, PPIs, NSAIDs, sulfonamides
    > Sarcoidosis: granulomas deposited in tissues
    > Amyloidosis: B plaques deposited in tissues
    > Infection: systemic infection, direct renal infection
    > Lupus: auto-Abs
32
Q

Post-renal AKI

A

Obstruction

  • Ureter
    > Kidney stones
    > Intra-abdominal tumor
  • Bladder
    > BPH
    > Prostate cancer
    > Uterine prolapse
    > Hypoactive bladder
33
Q

Complications of AKI

A
  • Uremia:
    > platelet dysfunction → bleeding
    > pericarditis → pericardial effusion → tamponade
    > excess neuron firing → seizures, encephalopathy,
    asterixis
  • Acidosis:
    > Injured tubules → arrhythmias, hypotension
  • Drugs:
    > Less excretion
  • Electrolytes:
    > Less K excretion → hyperK → arrhythmias
    > Hyperphosphatemia
34
Q

Investigation of AKI

A

IS IT AKI?
- Creatinine elevated
- Decreased urine outpus

WHAT IS THE CUASE
- Pre-renal AKI
> WBC casts, bacteria, nitrates on urinalysis → sepsis
> Low Na and urea in urine & hypervolemic → CHF,
hepatorenal syndrome, nephrotic syndrome
> Low Na and urea in urine & hypovolemic → burns,
dehydrates, vomiting, diarrhea
- Intrinsic AKI
> WBC casts, bacteria, nitrates on urinalysis →
pyelonephritis
> WBC casts, eosinophils → AIN
> RBC casts, proteinuria, lipiduria → glomerulonephritis
> Muddy brown casts → acute tubular necrosis
> High Na and urea in urine
- Post-renal AKI
> Renal ultrasound, CT (+bladder scan) → hydronephrosis,
tumors/masses
- Other
> Hx CKD, small atrophic kidneys on imaging

35
Q

Indications for renal replacement therapy

A
  • Acidosis: can’t secrete H
  • Electrolytes: severe hyperK
  • Intoxication: high drug accumulation
  • Overload: severe volume overload
  • Uremia: encephalopathy, seizures
36
Q

Causes of CKD

A
  • HTN: hyperfiltration → cell necrosis →
    GLOMERULOSCLEROSIS → low GFR
  • Diabetic nephropathy: non-enzymatic glycation → inflammatory molecules → arteriosclerosis → higher pressure → GLOMERULOSCLEROSIS → low GFR
  • Glomerulonephritis: immune complexes on BM → infalmmation → hyperfiltration → high GFR → mesangial cells try to correct → TGF-B → GLOMERULOSCLEROSIS → low GFR
  • Polycystic kidney disease: cysts compress nearby vessles → low GFR → ischemia → necrosis → renin release → HTN → GLOMERULOSCLEROSIS
  • NSAIDs: PGI2 and PGE2 vasodilate afferent arterioles → high
    [NSAIDs] inhibit → vasoconstriction → low GFR
  • AKI: prolonged or frequent
37
Q

Diagnosing CKD

A
  • Kidney injury for 3+ months
    > GFR (normal 125 mL/min)
    - Stage 1: >90
    - Stage 2: 60-89
    - Stage 3a: 45-59
    - Stage 3b: 30-49
    - Stage 4: 15-29
    - Stage 5: <15
    > Creatinine
  • Albuminuria (urine albumin:cr)
    > Mild: <30
    > Moderate: 30-299
    > Severe: > 300
  • Renal ultrasound
    > Polycystic
    > Small, atrophied kidneys
    > Vascularity
  • Renal biopsy and serology
    > ANA (SLE), RF (RA), HIV, Hep
  • Additional tests
    > BMP: hyperK, hyperPHOS, hypoCa, hypo/hyperNa
    > CBC: anemia
    > ABG: metabolic acidosis
    > Lipid panel
    > PTH levels: hyperparathyroidism, hyperCa in severe CKD
38
Q

CKD complications

A
  • Electrolytes
    > HyperK: less filtration K → arrhythmias
    > Low vitD: kidney enzymes make vitD → low Ca absorb
    > HyperPHOS: less vitD → low Ca → low PO4 excretion
    > Na fluctuates
    - Retention of fluid → delusional hyponatremia
    - Worse GFR → cannot excrete Na → hyperNa
  • Water imbalance
    > Low GFR → water retention → volume overload →
    edema → pulmonary, peripheral, HTN
    > Damage to kidney → albuminuria → edema
  • Waste removal
    > Urea build up: Azotemia → encephalopathy, seizures,
    fatigue, nausea, vomiting, uremic
    pericarditis, uremic frost, platelet
    interference (can’t clot)
  • Hormone imbalance
    > Erythropoietin: kidney makes EPO
    > Renin: released with low GFR
    > PTH: low vitD → low Ca → PTH release → release bone
    Ca → renal osteodystrophy, osteitis cystica fibrosa
  • Metabolic acidosis: a-intercalated cells damaged
  • Albumin regulation: albuminuria → third spacing fluid →
    liver makes proteins → hyperlipidemia
  • Erectile dysfunction: HTN → atherosclerosis/ep damage →
    less blood flow
39
Q

CKD treatment

A
  • HTN: ACEi/ARBs (avoid ACEi in severe CKD)
  • Water retention: loop diuretics, Na/H2O restriction
  • Glomerulonephritis: steroids
  • HyperK: insulin, SABA, loop diuretic
  • HyperPHOS: sevelamer HCl
  • HypoCa: Ca, vitD
  • Anemia: synthetic EPO, IV iron
  • Low albumin: ACEi/ARBs
  • Hyperlipidemia: statinds
  • Platelet activity: DDAVP
40
Q

PKD

A

Polycystic Kidney Disease
- Cysts compress blood vessels → necrosis, low GFR → HTN
- Cysts compress collecting → urinary stasis → stones
- Flank pain, hematuria → eventual renal failure
- Ca influx → cell proliferation → water pumps activated

  • Autosomal Dominant PKD
    > Adult; inherited PKD1/PKD2 mutation then random
    > PKD1 more severe
    > Cysts can pop up on liver, seminal vessels, pancreas,
    vasculature
  • Autosomal Recessive PKD
    > Infant
    > Prenatal ultrasound
    > Congenital hepatic fibrosis: portal hypertension
    > Ascending cholangitis: block bile ducts → cholestasis
41
Q

Major functions of the kidney

A
  1. Waste excretion: nitrogenous (urea, Cr), urate, drugs, peptide hormones
  2. Electrolyte balance and osmoregulation: NaCl, K, H, HCO3, Ca, Mg, PO4
  3. Hormonal synthesis: EPO (cortex), vitD activation (PCT), renin (JGs)
  4. Blood pressure regulation: Na excretion, renin
  5. Glucose homeostasis: gluconeogenesis (lactate, pyruvate, AAs), clearance of insulin
42
Q

Glomerular basement membrane

A
  1. Mesengial cells: support capillaries, contractile (can alter GFR), can secrete chemo/cytos, minimize accumulation
  2. Capillary endothelial cells: fenestrated; interface with blood (target for antibodies and contact site for neutrophils/lymphocytes)
  3. Visceral epithelium/podocytes: interdigitated foot processes (slit diaphragm)
  4. Parietal epithelium: line interior of Bowman’s capsule, contain podocyte progenitor population
  5. Juxtaglomerular cells: smooth muscle lining afferent arteriole; renin
43
Q

Factors affecting GFR

A

Afferent arteriole
- Prostaglandins = dilation → increase GFR
- NSAIDs = constriction → decrease GFR

Efferent arteriole
- ACEi = dilation → decrease GFR
- Angiotensin II = constriction → increase GFR

44
Q

GFR autoregulation

A
  1. Myogenic mechanism: release vasoactive factor (prostaglandins, NO → increase GFR)
  2. Tubuloglomerular feedback: changes in Na delivery to macula densa lead to changes in afferent arteriole tone (increased Na delivery → afferent constriction → decrease GFR)
45
Q

RAAS System

A

Stimuli for renin release:
> Decrease stretch of afferent arteriole
> JG B-adrenergic receptor stimulation
> Low Na in fluid composition at macula densa in DCT

AII targets:
> Vasocontriction
> Increased vascular smooth muscle growth
> Increased aldosterone → Na retention
> Increased bicarbonate products

46
Q

Urinalysis Dipstick

A
  1. Specific gravity
    > Mass of equal volumes of urine/H20; 1.001-1.030
    > If <1.010 = dilute, >1.020 = concentrated
    > 1.010 = isosthenuria (same specific gravity as plasma)
  2. pH
    > 4.5-7.0
    > Persistent alklaline → RTA, UTI
  3. Glucose
    > Hyperglycemia, increased GFR, PCT dysfunction
    (Fanconi), SGLT2 inhibitors
  4. Protein
  5. Leukocyte esterase
    > Infection (UTI) or inflammation (AIN) along urinary tract
  6. Nitrites
    > UTI
  7. Ketones
    > Alcoholic/diabetic ketoacidosis
  8. Hemoglobin
    > Hemolysis (hemoglobinuria), rhabdomyolysis
    (myogolobinuria), true hematuria
47
Q

Urine microscopy (Cells, casts, crystals)

A

RBCs
> Dysmorphic = glomerular bleeding (glomerulonephritis)
> Isomorphic = bladder cancer

Leukocytes
> Inflammation
> Infection

Eosinophils
> AIN
> Atheroembolic disease (plaque from large arteries blocks
renal arteries)

Oval fat bodies (renal tubular cells filled with lipid)
> Nephrotic syndrome

Casts
> Hyaline = physiologic → concentrated, fever, exercise
> RBC = glomerular bleeding → proliferative GN, vasculitis
> WBC = pyelonephritis, interstitial nephritis
> Muddy brown = ATN, acute proliferative GN
> Fatty = Nephrotic syndrome

Crystals
> Uric acid = acidic urine, tumor lysis syndrome
> Calcium phosphate = alkaline urine
> Calcium oxalate = hyperoxaluria, ethylene glycol
poisoning, nephrolithiasis
> Sulfer = sulfa antibiotics

48
Q

Nephritic-Nephrotic Spectrum

A

NEPHROTIC
- Focal segmental glomerulosclerosis
- Membranous glomerulopathy
- Minimal change

INTERMEDIATE
- Membranoproliferative GN
- Focal proliferative GN
> IgA nephropathy (Berger’s; local inflammation)
> Idiopathic membranoproliferative GN
> Hep B, C
> SLE
> Cryoglobunemia (form of vasculitis; cryoglobins clump)

NEPHRITIC
- Diffuse proliferative GN
- Crescentic GN (chronic immune-mediated, glomerular
inflammation and injury)

49
Q

NSAIDs in nephrology

A
  • Decrease GFR by constricting the afferent arteriole
    > Sodium retention, water retention
    > Hypoaldosteronism
    - HyperK
    - HTN
    > Vasomotor AKI (renal ischemia)
    > Acute interstitial nephritis
    > Chronic interstitial nephritis
    > Acute tubular necrosis
50
Q

Presentation of end stage renal disease

A
  1. Volume overload
  2. Electrolyte imbalances
    > HyperK
    > HyperPO4
    > Hyper uric acid
    > HypoNa
    > HypoCa (low vitD)
    > HypoHCO3
  3. Uremic syndrome
    > Asterixis
    > SOB, pleuritic chest pain
    > weight loss, amennohrea
    > Anorexia, nausea, vomiting
    > Pruritus, pallow, jaundice
    > Palpable bladder, hematuria
    > Muscle weakness, cramps

Medical School (9 decks)

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