High Yield Topics-Renal Flashcards by Geun Young Park

Normal values of pH, HCO3, and CO2 and their relationship

pH = 7.4
HCO3 = 24
CO2 = 40

pH = HCO3/CO2
pH = metabolic/respiratory

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Describe steps to determine primary deficit with compensatory MOA for acid/base problems

Determine acidosis or alkalosis to given pH, HCO3, and CO2
Matching = Primary deficit
What’s left = compensatory MOA

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Determine primary deficit with compensation for this example.

pH = 7.31 
HCO3 = 18
CO2 = 28

pH = 7.31 --> acidosis
HCO3 = 18 --> metabolic acidosis
CO2 = 28 --> respiratory alkalosis

Metabolic acidosis w/ compensatory respiratory alkalosis

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(Normal/Elevated) anion gap is due to loss of HCO3

Normal

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(Normal/Elevated) anion gap is due to the presence of extra external acid (HCO3 is used to buffer the aci)

Elevated

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Equation to determine compensation for metabolic acidosis

Winter’s formula:

Expected Pco2=1.5[HCO3-]+8 +/-2

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In normal anion gap metabolic acidosis, if expected Pco2 > actual Pco2, then there is too little Pco2.

You have a “concomitant” respiratory

alkalosis

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In normal metabolic acidosis, if expected Pco2 < actual Pco2, then there is too much Pco2.

You have a “concomitant” respiratory

acidosis

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Diarrhea, renal tubular acidosis, and saline infusion are common causes of what acid-base disturbance?

Normal anion gap metabolic acidosis

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Lactic acidosis, diabetic ketoacidosis, renal failure (uremia), and toxicities (methanol, ethylene glycol, salicylates) are common causes of what acid-base disturbance?

Elevated anion gap metabolic acidosis

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Equation to check anion gap

AG = Na+ - (Cl- + HCO3-)

AG = 8-12 –> Normal AG
AG > 12 –> ↑AG

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Glomerular disease caused by destruction of GBM negative charge and podocyte effacement (thinning) leading to protein leakage (proteinuria >3.5 g/day)

Nephrotic syndrome

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Which nephrotic syndrome is described by the following:

Common in children after recent infection/immunization; Corticosteroids for tx

Minimal change disease

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Normal histology on “LM” and podocyte effacement & fusion on EM are findings of

Minimal change disease

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Which nephrotic syndrome is described by the following:

Common in AA and hispanics; caused by idiopathic, viral infections (HIV/Hepatitis), heroin abuse, or other conditions (sickle cell, obesity)

Focal Segmental Glomerulosclerosis

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Segmental sclerosis and hyalinosis, podocyte effacement & fusion is Histology/LM/EM findings of

Focal Segmental Glomerulosclerosis

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Which nephrotic syndrome is described by the following:

Primary cause is by auto-antibodies against “phospholipase A2” receptors on GBM

Membranous nephropathy

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Which nephrotic syndrome is described by the following:

Secondary cause is by Drugs (NSAIDs, penicillamine), SLE, Cancer, and viral infections (Hepatitis)

Membranous nephropathy

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Capillary loop thickening and GBM thickening on LM; granular IF; subepithelial deposits of immune complexes (“spike and dome” appearance) on EM are findings of

Membranous nephropathy

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Which nephrotic syndrome is described by the following:

Amyloid deposits in mesangium (early) –> endothelium (late)

Amyloidosis

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+ Congo red and apple green birefringence is Histology/LM/EM findings of

Amyloidosis

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What organ is the most commonly involved organ of Amyloidosis?

Kidney

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Which nephrotic syndrome is described by the following:

Most common cause ESRD in the US; caused by diabetes

Diabetic glomerulonephropathy

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Mesangial expansion and “nodular” glomerulosclerosis (Kimmenstiel-Wilson nodules) is Histology/LM/EM findings of

Diabetic glomerulonephropathy

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Glomerular disease caused by "inflammation" (lymphocytes are involved); present with hematuria, dysmorphic RBCs, RBC casts, and WBC casts in urine

Nephritic syndrome

Which nephritic syndrome is described by the following: "2-4 weeks" after group A strep infection of pharyngitis or skin rash (impetigo); caused by type III (immune complex deposition) hypersensitivity; presents with periorbital edema, hypertension, and cola-colored urine

Poststreptococcal glomerulonephritis

granular (IgG, IgM, c3) IF in mesangium and GBM; subendothelial and subepithelial (GBM) immune complex deposition on LM are findings of

Poststreptococcal glomerulonephritis

Which nephritic syndrome is described by the following: Caused by SLE

Diffuse proliferative glomerulonephiritis

"wire looping" (neutrophilic infiltration) of capillaries; granular IF; subendothelial immune complex deposition on EM is Histology/LM/EM findings of

Diffuse proliferative glomerulonephiritis

Which nephritic syndrome is described by the following: Caused by hepatitis infection or idiopathic; subendothelial immune-complex deposition; granular IF

Type I Membranoproliferative glomerulonephiritis

Which nephritic syndrome is described by the following: Caused by C3 nephritic factor (IgG autoantibody that overactivates complement activation); immune-complex deposition intramembranously; "tram-tracking" or GBM splitting on H&E or PAS stains

Type II Membranoproliferative glomerulonephiritis | aka. dense deposit disease

What kidney diseases are considered both nephrotic and nephritic syndromes?

Diffuse proliferative glomerulonephiritis & Membranoproliferative glomerulonephiritis

Which nephritic syndrome is described by the following: rapidly deteriorating renal function; includes several diseases that show this pattern

Rapidly progressive glomerulonephiritis

Which nephritic syndrome is described by the following: RPGN that shows "LINEAR" IF due to antibodies against type IV collagen on GBM and alveolar BM --> hematuria & hemoptysis

Goodpasture syndrome

Which nephritic syndrome is described by the following: RPGN that is pauci-immune (no Ig/c3 deposition); negative IF but + C-ANCA

Granulomatosis with polyangiitis (aka. WeCner’s syndrome)

Which nephritic syndrome is described by the following: RPGN that is pauci-immune (no Ig/c3 deposition); negative IF but + P-ANCA (2)

Microscopic polyangiitis OR Eosinophilic Granulomatosis with polyangiitis (aka. Churg-Strauss)

PSGN and DPGN can rapidly deteriorate renal function leading to

Rapidly progressive glomerulonephiritis

Unique LM finding of RPGN

Crescent (fibrin) formation in glomerulus * crescent is made of fibrin + proliferation of cells (macrophages, fibroblasts, etc.)

Which nephritic syndrome is described by the following: Occurs a few days (2-5) after URI or GI tract infection --> IgA immune complex deposition in mesangium; "mesangial" proliferation and granular IgA immune complex on IF

IgA nephropathy | aka. Berger Disease

Vasculitis associated with IgA nephropathy; cause non-blanching palpable purpura

IgA vasculitis | aka. Henoch Schonlein Purpura

Which nephritic syndrome is described by the following: Caused by mutation in type IV collagen --> thinning and splitting of GBM; present with triad (eye problem, hearing loss, and kidney problem)

Alport syndrome *STUDY AID: Albert can't pee, can't see, can't hear a bee

"basket weave" with thinning and splitting of GBM is Histology/LM/EM findings of

Alport syndrome

What is the complement level finding in nephritic syndrome?

C3 will be low due to activation of complement by immune complex --> deposition --> low serum C3 level

You will see WBC casts in urine only in what glomerular disease?

Nephritic syndrome

What kidney-related disorder can present with UNILATERAL flank tenderness, colicky pain radiating to groin, and hematuria?

Kidney stones

the most common reason for Ca (Ca oxalate and Ca PO4) kidney stones in adults; caused by ↑ GI absorption, ↑ mobilization of Ca from bone, or ↓ renal tubular Ca reabsorption

Hypercalciuria

Serum Ca+2 level in hypercalciuria is

normocalcemic * due to regulation of plasma Ca levels by vitamin D and PTH

Explain how hypocitraturia can increase formation of Ca-oxalate nephrolithiasis?

When citrate level is normal in urine, Ca+2 binds with citrate and forms a soluble calculi. When citrate level in urine decreases or Ca+2 excretion increases, calcium will bind to oxalate (or phosphate) and form an insoluble calculi

↑ urinary concs of Ca2+, oxalate, and uric acid promote

salt crystallisation

↑ urinary citrate conc and high fluid intake prevent

calculi formation

Tx for calcium (oxalate or phosphate) renal calculi

thiazides (increase reabsorption of Ca+2), low Na+ diet, citrate (if hypocitraturia), and increased fluid intake

Shape of calcium oxalate crystals in urine

envelope or dumbbell

Shape of calcium phosphate crystals in urine

wedge-shaped prism

Type of renal stones that is caused by UTI with urease + bugs that hydrolyze urea to ammonia (increase urine pH)

Ammonium Magnesium Phosphate (aka. struvite)

Large renal stones that take on the shape of the renal calyces; very big!

Staghorn calculi

Staghorn calculi is made of

struvite (MgNH4PO4)

What kidney stones precipitate at low pH?

Everything else except phosphate stones

What kidney stones precipitate with increased pH due to alkalinized urine?

Phosphate stones

UTI-causing urease+ bugs

staph. saprophyticus Klebsiella Proteus mirabilis

Shape of struvite (MgNH4PO4) crystals in urine

coffin lid

Type of renal stones that is caused by hyperuricemia (gout), low urine pH (loss of HCO3- due to diarrhea), and low urine volume (dehydration)

Uric acid

Either overproduction of uric acid or under excretion of uric acid can lead to

hyperuricemia --> gout

Shape of struvite uric acid crystals in urine

Rhomboid (soft diamond shaped) or rosettes

Tx for uric acid stones

allopurinol (gout tx)

Type of renal stones that is caused by a hereditary disorder in which cystine-reabsorbing PCT transporter loses function --> cystinuria; the transporter can't also reabsorb COLA (cystine, ornithine, arginine, and lysine) --> recurrent nephrolithiasis

Cystine stone

Shape of Cystine stone in urine

hexagonal (six-sided) crystals * STUDY AID: Cystine sounds like "SIX"tine

what test can be used to detect excess cystine in the urine?

Na+ Cyanide Nitroprusside Test

Mannitol site of action as diuretic

PCT

Acetazolamide (carbonic anhydrase inhibitor) site of action as diuretic

PCT

Loop diuretics (furosemide) site of action as diuretic

Thick ascending limb of loop of henle

Thiazide diuretics site of action as diuretic

DCT

K+ sparing diuretics (spironolactone, eplerenone) site of action as diuretic

DCT

Most common renal malignancy of children (ages 2-4); presents with large, palpable, unilateral flank mass + hematuria + "HTN"; tumor does NOT cross the MIDLINE; part of WAGR complex and Beckwith-Wiedemann syndrome

Nephroblastoma (aka. Wilms tumor)

Mutation of Nephroblastoma (aka. Wilms tumor)

- WAGR: mutation of tumor suppressor gene WT1 | - Beckwith-wiedemann: mutation of tumor suppressor gene WT2

Symptoms in WAGR complex

Wilms tumor Aniridia (no iris) Genitourinary malformation Retardation (mental)

Symptoms in Beckwith-Wiedemann syndrome

Wilms tumor macroglossia omphalocele * STUDY AID: BeckWith-Wiedemann B: Big Tongue W: Wilms Tumor W: (abdominal) Wall Defect

Most common adrenal medulla malignancy of children (ages <4); arises from neural crest cells; presents with abdominal distension, a firm, irregular mass that crosses MIDLINE (not unilateral as in Wilms tumor); NO "HTN"

Neuroblastoma *think about it as a pheochromocytoma in children w/o HTN

What is a paraneoplastic syndrome associated with neuroblastoma?

Opsoclonus-Myoclonus *dancing eyes-dancing feet

Urine findings in neuroblastoma

Homovanillic acid (HVA) & vanillylmandelic acid (VMA) *they are catecholamine metabolites

Mutation of neuroblastoma

N-myc oncogene

Histologic finding in Neuroblastoma

Homer-wright rosettes (neuroblasts surrounding a central lumen)

ADH reabsorbs water in what part of nephron?

collecting duct

ADH also reabsorbs urea in "collecting duct" to establish

medullary osmotic gradient (for water reabsorption)

Autosomal dominant polycystic kidney disease is caused by what two genetic mutations that result in the development of multiple cysts in the kidney because of structural abnormalities of the renal tubules?

- PKD1 on Chromosome 16 (85% of cases) - PKD2 on Chromosome 4 (15% of cases) * PKD1/2 genes make protein POLYCYSTIN

ADPKD is associated with what aneurysmal vascular disease?

Berry aneurysm (rupture can cause subarrachnoid hemorrahge) * STUDY AID: bubbles in kidneys, bubbles in the head & liver

Cysts caused by ADPKD compress adjacent normal renal parenchyma and cause

Chronic HTN/ CKD

A mutation in _____ gene results in autosomal "recessive" polycystic kidney disease

PKHD1 on Chromosome 6 * PKHD1 gene makes protein FIBROCYSTIN

Adrenal cortex is derived from what embryologic origin layer?

Mesoderm

Adrenal medulla (Chromaffin cells) is derived from what embryologic origin layer?

Neural crest cells

The most common cause (organism) of urinary tract infection (UTI) in both healthy adults and elderly patients

E. Coli

costovertebral angle tenderness and flank/back pain radiating to groin indicates

renal stones

Steps to Solving Every High Altitude ABG Problems

1. At high altitude --> ↓ pO2 --> Hyperventilation 2. Hyperventilation --> ↓ pCO2 3. ↑ pH --> ↓ HCO3-

Steps to Solving Every Acid-Base Disorder Problems

1. Determine primary deficit with compensatory MOA 2. If the primary deficit is metabolic acidosis, then check anion gap using AG formula 3. If the primary deficit is metabolic acidosis, then also calculate expected PCO2 using Winter's Formula 3. Determine any concomitant respiratory alkalosis/acidosis

Hypoventilation caused by: - Airway obstruction - Opioids, sedatives - Chronic lung disease are common causes of what acid-base disturbance?

Respiratory Acidosis

Hyperventilation caused by: - Hypoxemia/high altitude - Anxiety/Panic Disorder - PE/Dyspnea - Salicylates (in EARLY toxicity phase) are common causes of what acid-base disturbance?

Respiratory Alkalosis

H+ Loss caused by: - Vomiting - Hyperaldosteronism are common causes of what acid-base disturbance?

Metabolic Alkalosis

HCO3- Excess caused by: - Antacid Use - Loop/Thiazide Diuretics (Hypovolemia-induced ↑ RAAS --> ↑ aldosterone --> ↑ H+ excretion @ CD --> ↑ Na+/HCO3- reabsorption @ PCT) are common causes of what acid-base disturbance?

Metabolic Alkalosis

Increased Serum External Acid caused by: - Hyperchloremia - Addison Disease - Renal Tubular Acidosis - Diarrhea - Acetazolamide - Spironolactone - Saline Infusion are common causes of what acid-base disturbance?

NORMAL Anion Gap Metabolic Acidosis * STUDY AID: HARDASS

Increased Serum External Acid caused by: - Methanol - Uremia - Diabetic Ketoacidosis - Propylene glycol - Iron tablets/Isoniazid - Lactic Acidosis - Ethylene glycol (antifreeze) - Salicylates (in LATE toxicity phase) are common causes of what acid-base disturbance?

High Anion Gap Metabolic Acidosis * STUDY AID: MUDPILES

What initially causes respiratory alkalosis and then later (several hours) presents with elevated anion gap metabolic acidosis, leading to a mixed acid-base disorder?

Salicylate (ASA) Toxicity/Poisoning

Nephrotic syndrome is defined by what five signs and symptoms?

* Proteinuria: > 3.5 grams per day * Hypoalbuminemia * Peripheral/periorbital edema * Hyperlipidemia * Fatty Casts * Frothy Urine

Other than albumin, what else can be lost in the urine of those with nephrotic syndrome?

Antithrombin III Immunoglobulin * they are all made of protein!

Due to the loss of antithrombin III, _____________ can occur in nephrotic syndrome.

renal vein thrombosis * STUDY AID: Sketchy Path (the guy getting stabbed in his flank with the polymerized fibrin sticks)

What is the most likely diagnosis in a patient presenting with nephrotic syndrome (proteinuria) with chronic inflammatory diseases (ex. Crohn disease)?

Amyloidosis

What indicates the need to start ACE inhibitors in diabetic patients?

Albuminuria with BP >130/80 * ACE inhibitors prevents the progression of albuminuria

The most important parameter for early detection of renal condition in diabetic patients

URINARY albumin

In order to increase the reduced oncotic pressure caused by hypoalbuminemia, what synthesis process in the liver is increased in nephrotic syndrome?

Hepatic lipoprotein synthesis

Nephritic syndrome is defined by what seven signs and symptoms?

* Hematuria (dark/"cola-colored" urine) * Peripheral/periorbital edema * Hypertension * Decreased urine output (oliguria) * "WBC" Casts * RBC Casts * Dysmorphic RBCs (acanthocytes) * May also see mild proteinuria (<3.5 g/day)

What are two renal examples of type II HSR?

- Goodpasture Syndrome | - Membranous Nephropathy

The only type of kidney stone that forms radioLUCENT stones

Uric Acid stones

Gout (Hyperuricemia leading to uric acid accumulation in joints) can be exacerbated by consumption of

Alcohol

What clinical presentations are associated with ADPKD?

* > 30 years of age with renal insufficiency * Hematuria * Hypertension * Recurrent UTIs * Flank pain * Family Hx

What is the diagnostic ultrasound findings of ADPKD?

Bilateral (usually) enlarged kidneys with multiple parenchymal anechoic masses of varying size

What clinical presentations of ARPKD help distinguish it from ADPKD?

ARPKD manifests in INFANCY

N-Myc gene mutation, which can cause neuroblastoma is due to (loss of fx/gain of fx).

Gain of fx * All Myc (C-myc, L-myc, N-myc) genes are ONCOGENES!

Other extra-renal manifestations of ADPKD include

- Cerebral saccular/berry aneurysms - Mitral Valve Prolapse - Hepatic Cysts

What should be measured in metabolic alkalosis to determine diagnosis?

Urine chloride concentration

Etiologies (2) of metabolic alkalosis associated with a NORMAL urinary chloride concentration is called a chloride-responsive metabolic alkalosis because it corrects with administration of fluid with NaCl.

- Vomiting - Loop diuretic use * Caused by fluid loss

Etiologies (2) of metabolic alkalosis associated with an ELEVATED urinary chloride concentration

- Hyperaldosteronism | - Antacids

Metabolic alkalosis with NORMAL urinary chloride concentration is chloride (resistant/responsive)

Responsive * they can be corrected with administration of fluid with NaCl

Metabolic alkalosis with ELEVATED urinary chloride concentration is chloride (resistant/responsive)

Resistant * they cannot be corrected with administration of fluid with NaCl

High Yield Topics-Renal Flashcards

(121 cards)