Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/154

Click to flip

154 Cards in this Set

  • Front
  • Back
What course do the ureters take?
[Water under the bridge]
Ureters pass UNDER Uterine A. and UNDER ductus deferens
What are the fluid compartments of the body?
[60-40-20 rule]
TBW = 40% nonwater, 60% TBW.
TBW = 1/3 ECF, 2/3 ICF
ECF = 1/4 plasma, 3/4 interstitial
How do you measure ECF volume?
inulin
How do you measure plasma volume?
radiolabeled albumin
How do you calculate renal clearance?
Cx = Ux * V/Px

Cx = Clearance of X
Ux = Urine Conc. of X
Px = Plasma Conc. of X
V = Urine flow rate
Cx < GFR?
net tubular reabsorption of X
Cx > GFR?
net tubular secretion of X
Cx = GFR?
no net secretion or reabsorption of X
Afferent arteriole?
blood flow TO the glomerulus
Efferent arteriole?
blood flow OUT of the glomerulus
GFR calculation
Inulin is freely filtered and neither reabsorbed nor secreted so:

GFR = Cinulin ~ Ccreatinine
Glomerular filtration barrier
1. Fenestrated capillary endothelium (size)
2. Fused basement membrane with heparan sulfate (negative charge)
3. Epithelial layer of podocyte fp's
What substance accounts for the glomerular filtration according to charge
heparan sulfate on basement membrane
Afferent arteriole?
blood flow TO the glomerulus
Efferent arteriole?
blood flow OUT of the glomerulus
GFR calculation
Inulin is freely filtered and neither reabsorbed nor secreted so:

GFR = Cinulin ~ Ccreatinine
Glomerular filtration barrier
1. Fenestrated capillary endothelium (size)
2. Fused basement membrane with heparan sulfate (negative charge)
3. Epithelial layer of podocyte fp's
What substance accounts for the glomerular filtration according to charge
heparan sulfate on basement membrane
How do you calculate Effective Renal Plasma Flow?
ERPF = C[PAH] because PAH is both filtered & excreted -- all PAH entering kidney is excreted.
ERPF underestimates RPF by 10%
RBF?
Renal Blood Flow = RPF/(1-Hct)
FF?
Filtration Fraction = GFR/RPF
What dilates afferent arterioles?
Prostaglandins (NSAIDs inhibit)

++RPF, ++GFR ... ==FF
What constricts efferent arterioles?
Angiotensin II (ACE-I inhibits)

--RPF, ++GFR ... ++FF
What causes RPF & GFR to decrease?
Afferent Arteriole constriction
What causes --RPF, ++GFR & ++FF?
Efferent arteriole constriction
What causes --GFR & --FF?
++plasma protein concentration or constriction of ureter
What causes ++GFR & ++FF?
--plasma protein concentration
What does Afferent arteriole constriction do?
--RPF, --GFR, ==FF
What does Efferent arteriole constriction do?
--RPF, ++GFR, ++FF
What does ++plasma protein concentration do?
==RPF, --GFR, --FF
What does --plasma protein concentration do?
==RPF, ++GFR, ++FF
What does constriction of ureter do?
==RPF, --GFR, --FF
How do you calculate Free Water Clearance?
C[H2O] = V/C[osm]
What is significant about Glucose clearance?
Glucose at normal levels is completely reabsorbed in proximal tubule. At plasma glucose of 200 mg/dL, glucosuria begins. At 350 mg/dL, transport mechanism is saturated.
What is significant about Amino Acid Clearance?
Reabsorption by at least 3 distinct carrier systems, with competitive inhibition within each group. Secondary active transport occurs in proximal tubule and is saturable.
Early PCT physiology.
"workhorse of nephron". Reabsorbs all of the glucose and aminoa acids and most of the bicarbonate, sodium & water. Secretes ammonia to buffer secreted H+.
Thin decending loop fHenle physiology.
passively reabsorbs water via medullary hypertonicity (impermeable to sodium).
TALH physiology
actively reabsorbs Na+, K+ & CL- via triple transporter and indirectly induces the reabsorption of Mg2+ and Ca2+. Impermeable to H2O
Early DCT physiology
actively reabsorbs Na+, Cl- together. Reabsorption of Ca2+ is under control of PTH.
Collecting tubules physiology
Reabsorb Na+ in exchange for secreting K+ or H+ (regulated by aldosterone). Reabsorption of water is regulated by ADH (vasopressin). Osmolarity of medulla can reach 1200 mOsm.
What are the relative concentrations of ions along the renal tubule?
>1.0 = PAH, Inulin, Cl-
~1.0 = K+, Na+
<1.0 = Pi, HCO3-
=0 = Amino Acids, Glucose
What is the mechanism of the Renin-Angiotensin system?
Renin is released by the JGA of the kidneys upon sensing decreased BP and cleaves angiotensinogen to angiotensin I (decapeptide). Angiotensin I is then cleaved by ACE, primarily in the lung capillaries, to Angiotensin II (octopeptide).
What are the actions of Angiotensin II
Overall, increases Intravascular Volume and BP via:

(1) Potent VASOCONSTRICTION (especially Efferent Arterioles).
(2) Release of ALDOSTERONE from adrenal cortex.
(3) Release of ADH from posterior pituitary
(4) Stimulate hypotalamus to increase thirst.
What acts as a "check" on the Renin-Angiotensin system?
ANP released from atria eg in heart failure.
What makes up the JGA?
Juxtaglomerular apparatus consists of JG cells (modified smooth muscle of afferent arteriole) and macula densa (Na+ sensor, part of DCT).
What does the JG cells do?
Juxtaglomerular cells secrete renin to increase angiotensin II and aldosterone levels in response to (+)BP, (-)Na+ in DCT and (+)Sympathetic tone.
What are the endocrine functions of the kidney?
(1)Endothelial cells of peritubular capillaries secrete ERYTHROPOIETIN in response to hypoxia.
(2)Conversion of 25-OH vitamin D to 1,25-(OH)2 vitamin D by 1ALPHAHYDROXYLASE, which is activated by PTH
(3)JG cells secrete RENIN in response to [-]Renal Arterial Pressure and [+]Renal Sympathetic Discharge via Beta-1 receptors
(4)Secretion of prostaglandins that vasodilate afferent arterioles to [+]GFR.
What does NSAIDs do to renal function?
NSAIDs can cause renal failure in high vasoconstrictive states by inhibiting renal production of prostaglandins which keep afferent arterioles vasodilated to maintain GFR.
What does ANF do?
Atrial Natriuretic Factor is secreted in response to [+]atrial pressure causing [+]GFR & [+]Na+ excretion
What does PTH do?
Parathyroid Hormone is secreted in response to [-]Ca2+. It causes [+]Ca2+ reabsorption in DCT, [-]Phosphate reabsorption in PCT, [+] vitamin D production
What does Aldosterone do?
Aldosterone is secreted in response to [-]blood volume (via ATII) and [+]plasma K+. Causes [+]Na+ reabsorption, [+]K+ secretion, [+]H+ secretion.
What does AT II do?
Angiotensin II causes efferent arteriole constrictionleading to [+]GFR and [+]Na+ and HCO3- reabsorption
What does ADH/Vasopressin do?
Secreted in response to [+]plasma osmolarity and [-]blood volume. Binds to receptors on principal cells, causing [+]# of water channels and [+]H2O reabsorption
What physiological values are found in Metabolic Acidosis?
Primary: [-]HCO3-
Compensatory: [-]pH, [-]PCO2
What is the compensatory response to Metabolic Acidosis?
HYPERVentilation
What physiological values are found in Metabolic Alkalosis?
Primary: [+]HCO3-
Compensatory: [+]pH, [+]PCO2
What is the compensatory response to Metabolic Alkalosis
HYPOVentilation
What physiological values are found in Respiratory Acidosis?
Primary [+]PCO2
Compensatory [-]pH, [+]HCO3-
What is the compensatory response to Respiratory Acidosis?
Renal HCO3- reabsorption
What is the compensatory response to Respiratory Alkalosis?
Renal HCO3- secretion
What physiological values are found in Respiratory Alkalosis?
Primary [-]PCO2
Compensatory [+]pH, [-]HCO3-
What state is characterized by: low pH, PCO2 & HCO3-?
Metabolic acidosis (HCO3 is primary)
What state is characterized by: high pH, PCO2 & HCO3-?
Metabolic alkalosis (HCO3 is primary)
What state is characterized by: low pH but high PCO2 & HCO3-?
Respiratory acidosis. (PCO2 is primary)
What state is characterized by: high pH but low PCO2 & HCO3-?
Respiratory alkalosis.(PCO2 is primary)
How do you differentiate between metabolic & respiratory acidosis?
If PCO2 > 40 mmHg then it is a Respiratory Acidosis
How do you differentiate between metabolic & respiratory alkalosis?
If PCO2 is lower than 40 mmHg than Respiratory Alkalosis.
What are the causes of Respiratory acidosis?
Hypoventilation due to:
[] Airway obstruction
[] Acute lung disease
[] Chronic lung disease
[] Opioids, narcotics, sedatives
[] Weakening of respiratory muscles.
How do you calculate anion gap?
Na+ - (Cl- + HCO3-)
What are the causes of metabolic acidosis with increased anion gap?
MUD PILES:
[] Methanol
[] Uremia
[] Diabetic ketoacidosis
[] Paraldehyde or Phenformin
[] Iron tablets or INH
[] Lactic Acidosis
[] Ethylene glycol
[] Salicylates
What causes metabolic acidosis with normal anion gap?
Normal anion gap (8-12 mEq/L):
[]Diarrhea
[]Glue Sniffing
[]Renal tubular acidosis
[]Hyperchloremia
What are the causes of respiratory alkalosis?
Hyperventilation & Aspirin Ingestion
What are the causes of Metabolic alkalosis?
[]Vomiting
[]Diuretic use
[]Antacide use
[]Hyperaldosteronism
What is the formula for compensation in metabolic acidosis?
PCO2 = 1.5(HCO3-)+8 +/- 2
What is the formula for compensation in metabolic alkalosis?
PCO2 increases 0.7 mmHg for every 1 mEg/L increase in HCO3-
What is the formula for compensation in respiratory acidosis?
Acute: +1 mEq/L HCO3
Chronic: +3.5 mEq/L HCO3
For every +10 mmHg PCO2
What is the formula for compensation in respiratory alkalosis?
Acute: -2 mEq/L HCO3
Chronic: -5 mEq/L HCO3
For every -10 mmHg PCO2
What is Potter's syndrome?
[Babies with Potter's can't "Pee" in utero.]
Bilateral renal agenesis -> oligohydramnios -> limb deformities, facial deformities, pulmonary hypoplasia. Caused by malformation of ureteric bud.
What is Horshoe kidney?
Inferior poles of both kidneys fuse. As they ascend from pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in abdomen.
What do RBC casts in urine signify?
[] glomerular inflammation (nephritic syndromes)
[] ischemia
[] malignant hypertension
What do WBC casts in urine signify?
[] tubulointerstitial disease
[] acute pyelonephritis
[] glomerular disorder
What do granular casts in urine signify?
Acute Tubular Necrosis (casts of the tubules themselves)
What do Waxy casts in the urine signify?
Advanced renal disease/CRF
What do hyaline casts in the urine signify?
nonspecific
What does the presence of RBCs in the urine signify?
Bladder cancer
What does the presence of WBCs in the urine signify?
Acute cystitis
What are the findings associated with Nephritic syndrome?
NephrItic = Inflammation
[] hematuria
[] hypertension
[] oliguria
[] azotemia
What are the findings associated with Nephrotic syndrome?
NephrOtic = prOteinuria
[] massive proteinuria >3.5 g/day
[] hypoalbuminemia
[] peripheral & periorbital edema
[] hyperlipidemia
What diseases are associated with Nephritic syndrome?
[1] Acute poststreptococcal glomerulonephritis
[2] RPGN (crescentic)
[3] Gloodpasture's syndrome (type II hypersensitivity)
[4] Membranoproliferative glomerulonephritis
[5] IgA nephropathy (Berger's disease)
[6] Alport's syndrome
What diseases are associated with Nephrotic syndrome?
[1] Membranous glomerulonephritis
[2] Minimal change disease
[3] Focal segmental glomerular sclerosis
[4] Diabetic nephropathy
[5] SLE
What are the clinical findings in Acute poststreptococcal glomerulonephritis?
LM: "lumpy-bumpy" w/ neutrophils
EM: subepithelial humps
IF: granular pattern

Resolves spontaneously
What are the clinical findings in RPGN?
Crescent-moon shape in bowman's capsule

Worst diagnosis.
What are the clinical findings in Goodpasture's syndrome?
Hemoptysis & Hematuria
IF: Linear pattern, anti-GBM antibodies
What are the clinical findings in Membranoproliferative glomerulonephritis
"tram track"
EM: subendothelial humps
What are the clinical findings in IgA nephropathy?
IF & EM: mesangial deposits of IgA. Mild, often postinfectious & periodic occurance.
What are the clinical findings in Alport's syndrome?
split basement membrane due to collagen IV mutation.
Nerve deafness & occular disorders
What are the clinical findings in Membranous glomerulonephritis?
Most common cause of adult nephrotic syndrome.

LM: diffuse capillary & basement membrane thickening
IF: granular
EM: "spike & dome"
What are the clinical findings in Minimal Change Disease?
Most common cause of childhood nephrotic syndrome.

LM: NORMAL!
EM: Foot process effacement
What are the clinical findings in Focal Segmental Glomerular Sclerosis?
Most common cause of nephroic syndrome in HIV & IV Drug abusers.

only part of the glomerulus is sclerosed in only some of the glomeruli.
What are the clinical findings in Diabetic nephropathy?
"Golf balls" = Kimmerlstiel-Wilson lesions.
What are the clinical findings in SLE?
5 patterns of renal involvement. Wire-loop lesions.
What renal disease presents with supepithelial humps?
Acute poststreptococcal glomerulonephritis
What renal disease presents with linear IF pattern?
Goodpasture's Syndrome
What renal disease presents with subendothelial humps & "tram tracks"?
membranoproliferative glomerulonephritis
What renal disease presents with IF mesangial deposits?
IgA nephropathy
What renal disease presents with spike and dome patterns?
Membranous glomerulonephritis
What renal disease presents with "golf ball" lesions?
Diabetic nephropathy
What are the different types of kidney stones?
[]Calcium (most common)
[]Ammonium magnesium phosphate (2nd most common)
[]Uric acid = Radiolucent
[]Cysteine = Radiolucent
What causes calcium kidney stones?
Most common type.
Calcium oxalate or calcium phosphate due to hypercalcemia (cancer, [+]PTH, [+]vitamin D)
Tend to recur
What causes struvite kidney stones?
Ammonium magnesium phosphate = 2nd most common kidney stone. Caused by infection w/ urease-positive bugs (Proteus, Staph, Klebsiella)
Can lead to staghorn calculi
What causes uric acid kidney stones?
Hyperuricemia (e.g. gout)
Often seen as a result of disease with increased cell turnover, ie leukemia & myeloproliferative disorders.
What causes cystine kidney stones?
secondary to cystinuria
What are the clinical findings associated with a staghorn calculus?
Ammonia smelling, high pH urine due to urease-positive bugs (Proteus, Staph, Klebsiella)
What is the most common renal malignancy?
Renal Cell Carcinoma
What is Renal Cell Carcinoma?
[] Most common renal malignancy.
[] Men aged 50-70.
[] ++ w/ smoking & obesity
[] Associated w/ von Hippel-Lindau
[] Originates in renal tubule cells --> polygonal clear cells.
[] Invades IVC & spreads hematogenously
{} Paraneoplastic (EPO, ACTH, PTHrP, prolactin)
What is the clinical presentation of Renal Cell Carcinoma?
[] Hematuria
{} palpable mass
[] 2o polycythemia
[] flank pain
[] fever
[] weight loss
What is the most common renal malignancy in children?
Wilms' tumor
What is the clinical presentation of Wilms' Tumor?
[] early childhood (2-4 y/o)
[] Hemihypertrophy
[] WAGR: Wilms, Aniridia, Genitourinary malformation & mental-motor Retardation
[] WT1 tumor suppressor gene on chromosome 11
What is the clinical presentation of Transitional Cell Carcinoma?
[] Most common tumor of urinary tract.
[] Painless hematuria suggestive of bladder cancer.
[] Pee SAC: Phenacetin, Smoking, Aniline dyes & Cyclophosphamide
[Aniridia & Hemihypertrophy]
Wilms' Tumor
[polygonal clear cells]
Renal Cell Carcinoma
[White cell casts in urine]
Acute pyelonephritis
What is the clinical presentaiton of Acute Pyelonephritis?
Affects cortex w/ sparing of glomeruli. White cell casts in urine. Fever + CVA tenderness.
What is the clinical presentation of Chronic Pyelonephritis?
Coarse, asymmetric corticomedullary scarring + blunting of calices. Eosinophilia.
What is the clinical presentation of diffuse cortical necrosis?
Acute generalized infarction of cortices of both kidneys. Likely due to combination of vasospasm & DIC. Associated w/ obstetric catastrophes & septic shock.
What is the clinical presentation of Acute Tubular Necrosis?
Most common cause of acute renal failure. Reversible, but fatal if untreated. Associated with renal ischemia (shock), crush injury (myoglobulinuria) & toxins.
What is associated with Renal papillary necrosis?
[] Diabetes mellitus
[] Acute pyelonephritis
[] Chronic phenacetin use
What is Acute Renal Failure?
Abrupt decline in renal function with [+]creatinine & [+]BUN over several days.
How do you differentiate between the three types of Acute Renal Failure?
BUN/Cr ratio:
>20: Prerenal Azotemia due to [-]RBF
>15: Postrenal due to bilateral outflow obstruction
<15: Renal due to Acute Tubular necrosis or ischemia/toxins
What are the consequences of renal failure?
[Any Red Herring Makes U Cry Crazy Hell]
[1] Anemia via [-]erythropoietin
[2] Renal osteodystrophy via [-] vitamin D
[3] Hyperkalemia ~ arrhythmias
[4] Metabolic acidosis via [-]acid secretion & [-]HCO3 generation
[5] Uremic encephalopathy
[6] CHF & Pulmonary edema via NA/H2O excess
[7] Chronic pyelonephritis
[8] Hypertension
What happens in Na+ imabalance?
Too low: stupor, coma
Too High: delirium, coma
What happens in Cl- imabalance?
Too low: secondary to metabolic alkalosis
Too high: secondary to non-anion gap acidosis
What happens in K+ imabalance?
Too low: U waves, flattened T waves, arrhythmias
Too high: Peaked T waves, arrhythmias
What happens in Ca2+ imabalance?
Too low: Tetany
Too high: Delirium, renal stones
What happens in Mg2+ imabalance?
Too low: Neuromuscular irritability, arrhythmias
Too high: Delirium, cardiopulmonary arrest, [-]DTR
What happens in PO4 2- imabalance?
Too low: Bone loss
Too high: metastatic calcification & renal stones
What diuretic acts on the PCT?
Acetazolamide & Mannitol
What diuretic acts on the Thin descending loop of Henle?
Mannitol
What diuretic acts on the Thick ascending loop of Henle?
Furosemide
What diuretic acts on the DCT?
Furosemide, Thiazide & K+ sparing
What diuretic acts on the Collecting Duct?
Mannitol & ADH antagonists
<Mannitol>
Osmotic diuretic: Increases urine flow by increasing tubular fluid osmolarity
Site: PCT
Clinical use: Shock, drug overdose, lower intracranial/intraocular pressure
Toxicity: Pulmonary edema, dehydration. Contraindicated in annuria, CHF
<Acetazolamide>
Carbonic Anhydrase inhibitor. Causes NaHCO3 diuresis and reduction of HCO3-.
Site: PCT
Clinical use: Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
Toxicity: ACIDazolamide causes ACIDosis -- Hyperchloremic metabolic acidosis, nephropathy, NH3 toxicity, sulfa allergy
<Furosemide>
Sulfonamide loop diuretic. Inhibits Triple Transporter of TALH. Abolishes hypertonicity of medulla, preventing concentration of urine. Excretes Calcium.
Site: TALH
Clinical use: Edematous states, Hypertension, Hypercalcemia
Toxicity: [OH DANG]: Ototoxicity, Hypokalemia, Dehydration, Allergy, Nephritis, Gout.
<Ethacrynic acid>
Same action as Furosemide, but not a sulfonamide.
Clinical: Diuresis in pts allergic to sulfa drugs.
Toxicity: Similar to furosemide. Can be used in hyperuricemia.
<Hydrochlorothiazide>
Thiazide diuretic. Inhibits NaCl reabsorption in DCT, reducing diluting capacity of nephron. Lowers Calcium excretion.
Site: DCT
Clinical Use: Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
Toxicity: Sulfa allergy, Hypokalemic metabolic alkalosis, hyponatremia, [HyperGLUC] hyperGlycemia, hyperLipidemia, hyperUricemia, & hyperCalcemia.
What are the Four K+-sparing diuretics?
[K+ STAys]: Spironolactone, Triamterene, Amiloride, eplereone
<Spironolactone>
K+ sparing diuretic.
Competetive aldosterone receptor antagonist in Collecting tubule.
Clinical use: Hyperaldosteronism, K+ depletion, CHF
Toxicity: Hyperkalemia, endocrine effects (gynecomastia, antiandrogen effects)
What electrolyte changes are caused by diuretics?
Urine NaCl: [+]All
Urine K+: [-]All except K+ sparing
Urine Ca+: [+]Loop diuretics, [-]Thiazides
What changes to Blood pH are seen after diuretics administration?
Acidosis: carbonic anhydrase inhibitor, K+ sparing diuretic
Alkalosis: Loop, Thiazides
<Captopril>
ACE Inhibitor:
[-]AT II
[+]bradykinin a vasodilator
[+]Renin due to loss of feedback
Clinical use: Hypertension, CHF, diabetic renal disease
Toxicity: [CAPTOPRIL]
Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower angiotensin II & hyperkalemia
How do urine osmolality levels differ among different forms of acute renal failure?
Prerenal: >500
Renal: <350
Postrenal: <350
How do urine Na levels differ among different forms of acute renal failure?
Prerenal: <10
Renal: >20
Postrenal: >40
How do urine FeNa levels differ among different forms of acute renal failure?
Prerenal: <1%
Renal: >2%
Postrenal: >4%