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154 Cards in this Set
- Front
- Back
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What course do the ureters take?
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[Water under the bridge]
Ureters pass UNDER Uterine A. and UNDER ductus deferens |
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What are the fluid compartments of the body?
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[60-40-20 rule]
TBW = 40% nonwater, 60% TBW. TBW = 1/3 ECF, 2/3 ICF ECF = 1/4 plasma, 3/4 interstitial |
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How do you measure ECF volume?
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inulin
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How do you measure plasma volume?
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radiolabeled albumin
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How do you calculate renal clearance?
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Cx = Ux * V/Px
Cx = Clearance of X Ux = Urine Conc. of X Px = Plasma Conc. of X V = Urine flow rate |
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Cx < GFR?
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net tubular reabsorption of X
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Cx > GFR?
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net tubular secretion of X
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Cx = GFR?
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no net secretion or reabsorption of X
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Afferent arteriole?
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blood flow TO the glomerulus
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Efferent arteriole?
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blood flow OUT of the glomerulus
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GFR calculation
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Inulin is freely filtered and neither reabsorbed nor secreted so:
GFR = Cinulin ~ Ccreatinine |
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Glomerular filtration barrier
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1. Fenestrated capillary endothelium (size)
2. Fused basement membrane with heparan sulfate (negative charge) 3. Epithelial layer of podocyte fp's |
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What substance accounts for the glomerular filtration according to charge
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heparan sulfate on basement membrane
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Afferent arteriole?
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blood flow TO the glomerulus
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Efferent arteriole?
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blood flow OUT of the glomerulus
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GFR calculation
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Inulin is freely filtered and neither reabsorbed nor secreted so:
GFR = Cinulin ~ Ccreatinine |
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Glomerular filtration barrier
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1. Fenestrated capillary endothelium (size)
2. Fused basement membrane with heparan sulfate (negative charge) 3. Epithelial layer of podocyte fp's |
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What substance accounts for the glomerular filtration according to charge
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heparan sulfate on basement membrane
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How do you calculate Effective Renal Plasma Flow?
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ERPF = C[PAH] because PAH is both filtered & excreted -- all PAH entering kidney is excreted.
ERPF underestimates RPF by 10% |
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RBF?
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Renal Blood Flow = RPF/(1-Hct)
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FF?
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Filtration Fraction = GFR/RPF
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What dilates afferent arterioles?
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Prostaglandins (NSAIDs inhibit)
++RPF, ++GFR ... ==FF |
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What constricts efferent arterioles?
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Angiotensin II (ACE-I inhibits)
--RPF, ++GFR ... ++FF |
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What causes RPF & GFR to decrease?
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Afferent Arteriole constriction
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What causes --RPF, ++GFR & ++FF?
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Efferent arteriole constriction
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What causes --GFR & --FF?
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++plasma protein concentration or constriction of ureter
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What causes ++GFR & ++FF?
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--plasma protein concentration
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What does Afferent arteriole constriction do?
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--RPF, --GFR, ==FF
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What does Efferent arteriole constriction do?
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--RPF, ++GFR, ++FF
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What does ++plasma protein concentration do?
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==RPF, --GFR, --FF
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What does --plasma protein concentration do?
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==RPF, ++GFR, ++FF
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What does constriction of ureter do?
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==RPF, --GFR, --FF
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How do you calculate Free Water Clearance?
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C[H2O] = V/C[osm]
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What is significant about Glucose clearance?
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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.
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What is significant about Amino Acid Clearance?
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Reabsorption by at least 3 distinct carrier systems, with competitive inhibition within each group. Secondary active transport occurs in proximal tubule and is saturable.
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Early PCT physiology.
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"workhorse of nephron". Reabsorbs all of the glucose and aminoa acids and most of the bicarbonate, sodium & water. Secretes ammonia to buffer secreted H+.
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Thin decending loop fHenle physiology.
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passively reabsorbs water via medullary hypertonicity (impermeable to sodium).
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TALH physiology
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actively reabsorbs Na+, K+ & CL- via triple transporter and indirectly induces the reabsorption of Mg2+ and Ca2+. Impermeable to H2O
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Early DCT physiology
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actively reabsorbs Na+, Cl- together. Reabsorption of Ca2+ is under control of PTH.
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Collecting tubules physiology
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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.
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What are the relative concentrations of ions along the renal tubule?
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>1.0 = PAH, Inulin, Cl-
~1.0 = K+, Na+ <1.0 = Pi, HCO3- =0 = Amino Acids, Glucose |
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What is the mechanism of the Renin-Angiotensin system?
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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).
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What are the actions of Angiotensin II
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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. |
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What acts as a "check" on the Renin-Angiotensin system?
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ANP released from atria eg in heart failure.
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What makes up the JGA?
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Juxtaglomerular apparatus consists of JG cells (modified smooth muscle of afferent arteriole) and macula densa (Na+ sensor, part of DCT).
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What does the JG cells do?
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Juxtaglomerular cells secrete renin to increase angiotensin II and aldosterone levels in response to (+)BP, (-)Na+ in DCT and (+)Sympathetic tone.
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What are the endocrine functions of the kidney?
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(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. |
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What does NSAIDs do to renal function?
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NSAIDs can cause renal failure in high vasoconstrictive states by inhibiting renal production of prostaglandins which keep afferent arterioles vasodilated to maintain GFR.
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What does ANF do?
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Atrial Natriuretic Factor is secreted in response to [+]atrial pressure causing [+]GFR & [+]Na+ excretion
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What does PTH do?
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Parathyroid Hormone is secreted in response to [-]Ca2+. It causes [+]Ca2+ reabsorption in DCT, [-]Phosphate reabsorption in PCT, [+] vitamin D production
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What does Aldosterone do?
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Aldosterone is secreted in response to [-]blood volume (via ATII) and [+]plasma K+. Causes [+]Na+ reabsorption, [+]K+ secretion, [+]H+ secretion.
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What does AT II do?
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Angiotensin II causes efferent arteriole constrictionleading to [+]GFR and [+]Na+ and HCO3- reabsorption
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What does ADH/Vasopressin do?
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Secreted in response to [+]plasma osmolarity and [-]blood volume. Binds to receptors on principal cells, causing [+]# of water channels and [+]H2O reabsorption
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What physiological values are found in Metabolic Acidosis?
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Primary: [-]HCO3-
Compensatory: [-]pH, [-]PCO2 |
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What is the compensatory response to Metabolic Acidosis?
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HYPERVentilation
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What physiological values are found in Metabolic Alkalosis?
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Primary: [+]HCO3-
Compensatory: [+]pH, [+]PCO2 |
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What is the compensatory response to Metabolic Alkalosis
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HYPOVentilation
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What physiological values are found in Respiratory Acidosis?
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Primary [+]PCO2
Compensatory [-]pH, [+]HCO3- |
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What is the compensatory response to Respiratory Acidosis?
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Renal HCO3- reabsorption
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What is the compensatory response to Respiratory Alkalosis?
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Renal HCO3- secretion
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What physiological values are found in Respiratory Alkalosis?
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Primary [-]PCO2
Compensatory [+]pH, [-]HCO3- |
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What state is characterized by: low pH, PCO2 & HCO3-?
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Metabolic acidosis (HCO3 is primary)
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What state is characterized by: high pH, PCO2 & HCO3-?
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Metabolic alkalosis (HCO3 is primary)
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What state is characterized by: low pH but high PCO2 & HCO3-?
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Respiratory acidosis. (PCO2 is primary)
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What state is characterized by: high pH but low PCO2 & HCO3-?
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Respiratory alkalosis.(PCO2 is primary)
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How do you differentiate between metabolic & respiratory acidosis?
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If PCO2 > 40 mmHg then it is a Respiratory Acidosis
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How do you differentiate between metabolic & respiratory alkalosis?
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If PCO2 is lower than 40 mmHg than Respiratory Alkalosis.
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What are the causes of Respiratory acidosis?
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Hypoventilation due to:
[] Airway obstruction [] Acute lung disease [] Chronic lung disease [] Opioids, narcotics, sedatives [] Weakening of respiratory muscles. |
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How do you calculate anion gap?
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Na+ - (Cl- + HCO3-)
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What are the causes of metabolic acidosis with increased anion gap?
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MUD PILES:
[] Methanol [] Uremia [] Diabetic ketoacidosis [] Paraldehyde or Phenformin [] Iron tablets or INH [] Lactic Acidosis [] Ethylene glycol [] Salicylates |
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What causes metabolic acidosis with normal anion gap?
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Normal anion gap (8-12 mEq/L):
[]Diarrhea []Glue Sniffing []Renal tubular acidosis []Hyperchloremia |
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What are the causes of respiratory alkalosis?
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Hyperventilation & Aspirin Ingestion
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What are the causes of Metabolic alkalosis?
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[]Vomiting
[]Diuretic use []Antacide use []Hyperaldosteronism |
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What is the formula for compensation in metabolic acidosis?
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PCO2 = 1.5(HCO3-)+8 +/- 2
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What is the formula for compensation in metabolic alkalosis?
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PCO2 increases 0.7 mmHg for every 1 mEg/L increase in HCO3-
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What is the formula for compensation in respiratory acidosis?
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Acute: +1 mEq/L HCO3
Chronic: +3.5 mEq/L HCO3 For every +10 mmHg PCO2 |
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What is the formula for compensation in respiratory alkalosis?
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Acute: -2 mEq/L HCO3
Chronic: -5 mEq/L HCO3 For every -10 mmHg PCO2 |
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What is Potter's syndrome?
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[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. |
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What is Horshoe kidney?
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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.
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What do RBC casts in urine signify?
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[] glomerular inflammation (nephritic syndromes)
[] ischemia [] malignant hypertension |
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What do WBC casts in urine signify?
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[] tubulointerstitial disease
[] acute pyelonephritis [] glomerular disorder |
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What do granular casts in urine signify?
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Acute Tubular Necrosis (casts of the tubules themselves)
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What do Waxy casts in the urine signify?
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Advanced renal disease/CRF
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What do hyaline casts in the urine signify?
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nonspecific
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What does the presence of RBCs in the urine signify?
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Bladder cancer
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What does the presence of WBCs in the urine signify?
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Acute cystitis
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What are the findings associated with Nephritic syndrome?
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NephrItic = Inflammation
[] hematuria [] hypertension [] oliguria [] azotemia |
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What are the findings associated with Nephrotic syndrome?
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NephrOtic = prOteinuria
[] massive proteinuria >3.5 g/day [] hypoalbuminemia [] peripheral & periorbital edema [] hyperlipidemia |
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What diseases are associated with Nephritic syndrome?
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[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 |
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What diseases are associated with Nephrotic syndrome?
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[1] Membranous glomerulonephritis
[2] Minimal change disease [3] Focal segmental glomerular sclerosis [4] Diabetic nephropathy [5] SLE |
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What are the clinical findings in Acute poststreptococcal glomerulonephritis?
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LM: "lumpy-bumpy" w/ neutrophils
EM: subepithelial humps IF: granular pattern Resolves spontaneously |
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What are the clinical findings in RPGN?
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Crescent-moon shape in bowman's capsule
Worst diagnosis. |
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What are the clinical findings in Goodpasture's syndrome?
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Hemoptysis & Hematuria
IF: Linear pattern, anti-GBM antibodies |
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What are the clinical findings in Membranoproliferative glomerulonephritis
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"tram track"
EM: subendothelial humps |
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What are the clinical findings in IgA nephropathy?
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IF & EM: mesangial deposits of IgA. Mild, often postinfectious & periodic occurance.
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What are the clinical findings in Alport's syndrome?
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split basement membrane due to collagen IV mutation.
Nerve deafness & occular disorders |
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What are the clinical findings in Membranous glomerulonephritis?
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Most common cause of adult nephrotic syndrome.
LM: diffuse capillary & basement membrane thickening IF: granular EM: "spike & dome" |
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What are the clinical findings in Minimal Change Disease?
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Most common cause of childhood nephrotic syndrome.
LM: NORMAL! EM: Foot process effacement |
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What are the clinical findings in Focal Segmental Glomerular Sclerosis?
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Most common cause of nephroic syndrome in HIV & IV Drug abusers.
only part of the glomerulus is sclerosed in only some of the glomeruli. |
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What are the clinical findings in Diabetic nephropathy?
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"Golf balls" = Kimmerlstiel-Wilson lesions.
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What are the clinical findings in SLE?
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5 patterns of renal involvement. Wire-loop lesions.
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What renal disease presents with supepithelial humps?
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Acute poststreptococcal glomerulonephritis
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What renal disease presents with linear IF pattern?
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Goodpasture's Syndrome
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What renal disease presents with subendothelial humps & "tram tracks"?
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membranoproliferative glomerulonephritis
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What renal disease presents with IF mesangial deposits?
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IgA nephropathy
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What renal disease presents with spike and dome patterns?
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Membranous glomerulonephritis
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What renal disease presents with "golf ball" lesions?
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Diabetic nephropathy
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What are the different types of kidney stones?
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[]Calcium (most common)
[]Ammonium magnesium phosphate (2nd most common) []Uric acid = Radiolucent []Cysteine = Radiolucent |
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What causes calcium kidney stones?
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Most common type.
Calcium oxalate or calcium phosphate due to hypercalcemia (cancer, [+]PTH, [+]vitamin D) Tend to recur |
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What causes struvite kidney stones?
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Ammonium magnesium phosphate = 2nd most common kidney stone. Caused by infection w/ urease-positive bugs (Proteus, Staph, Klebsiella)
Can lead to staghorn calculi |
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What causes uric acid kidney stones?
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Hyperuricemia (e.g. gout)
Often seen as a result of disease with increased cell turnover, ie leukemia & myeloproliferative disorders. |
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What causes cystine kidney stones?
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secondary to cystinuria
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What are the clinical findings associated with a staghorn calculus?
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Ammonia smelling, high pH urine due to urease-positive bugs (Proteus, Staph, Klebsiella)
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What is the most common renal malignancy?
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Renal Cell Carcinoma
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What is Renal Cell Carcinoma?
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[] 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) |
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What is the clinical presentation of Renal Cell Carcinoma?
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[] Hematuria
{} palpable mass [] 2o polycythemia [] flank pain [] fever [] weight loss |
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What is the most common renal malignancy in children?
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Wilms' tumor
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What is the clinical presentation of Wilms' Tumor?
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[] early childhood (2-4 y/o)
[] Hemihypertrophy [] WAGR: Wilms, Aniridia, Genitourinary malformation & mental-motor Retardation [] WT1 tumor suppressor gene on chromosome 11 |
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What is the clinical presentation of Transitional Cell Carcinoma?
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[] Most common tumor of urinary tract.
[] Painless hematuria suggestive of bladder cancer. [] Pee SAC: Phenacetin, Smoking, Aniline dyes & Cyclophosphamide |
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[Aniridia & Hemihypertrophy]
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Wilms' Tumor
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[polygonal clear cells]
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Renal Cell Carcinoma
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[White cell casts in urine]
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Acute pyelonephritis
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What is the clinical presentaiton of Acute Pyelonephritis?
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Affects cortex w/ sparing of glomeruli. White cell casts in urine. Fever + CVA tenderness.
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What is the clinical presentation of Chronic Pyelonephritis?
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Coarse, asymmetric corticomedullary scarring + blunting of calices. Eosinophilia.
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What is the clinical presentation of diffuse cortical necrosis?
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Acute generalized infarction of cortices of both kidneys. Likely due to combination of vasospasm & DIC. Associated w/ obstetric catastrophes & septic shock.
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What is the clinical presentation of Acute Tubular Necrosis?
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Most common cause of acute renal failure. Reversible, but fatal if untreated. Associated with renal ischemia (shock), crush injury (myoglobulinuria) & toxins.
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What is associated with Renal papillary necrosis?
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[] Diabetes mellitus
[] Acute pyelonephritis [] Chronic phenacetin use |
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What is Acute Renal Failure?
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Abrupt decline in renal function with [+]creatinine & [+]BUN over several days.
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How do you differentiate between the three types of Acute Renal Failure?
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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 |
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What are the consequences of renal failure?
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[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 |
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What happens in Na+ imabalance?
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Too low: stupor, coma
Too High: delirium, coma |
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What happens in Cl- imabalance?
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Too low: secondary to metabolic alkalosis
Too high: secondary to non-anion gap acidosis |
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What happens in K+ imabalance?
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Too low: U waves, flattened T waves, arrhythmias
Too high: Peaked T waves, arrhythmias |
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What happens in Ca2+ imabalance?
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Too low: Tetany
Too high: Delirium, renal stones |
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What happens in Mg2+ imabalance?
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Too low: Neuromuscular irritability, arrhythmias
Too high: Delirium, cardiopulmonary arrest, [-]DTR |
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What happens in PO4 2- imabalance?
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Too low: Bone loss
Too high: metastatic calcification & renal stones |
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What diuretic acts on the PCT?
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Acetazolamide & Mannitol
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What diuretic acts on the Thin descending loop of Henle?
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Mannitol
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What diuretic acts on the Thick ascending loop of Henle?
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Furosemide
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What diuretic acts on the DCT?
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Furosemide, Thiazide & K+ sparing
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What diuretic acts on the Collecting Duct?
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Mannitol & ADH antagonists
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<Mannitol>
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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 |
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<Acetazolamide>
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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 |
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<Furosemide>
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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. |
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<Ethacrynic acid>
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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. |
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<Hydrochlorothiazide>
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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. |
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What are the Four K+-sparing diuretics?
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[K+ STAys]: Spironolactone, Triamterene, Amiloride, eplereone
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<Spironolactone>
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K+ sparing diuretic.
Competetive aldosterone receptor antagonist in Collecting tubule. Clinical use: Hyperaldosteronism, K+ depletion, CHF Toxicity: Hyperkalemia, endocrine effects (gynecomastia, antiandrogen effects) |
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What electrolyte changes are caused by diuretics?
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Urine NaCl: [+]All
Urine K+: [-]All except K+ sparing Urine Ca+: [+]Loop diuretics, [-]Thiazides |
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What changes to Blood pH are seen after diuretics administration?
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Acidosis: carbonic anhydrase inhibitor, K+ sparing diuretic
Alkalosis: Loop, Thiazides |
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<Captopril>
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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 |
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How do urine osmolality levels differ among different forms of acute renal failure?
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Prerenal: >500
Renal: <350 Postrenal: <350 |
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How do urine Na levels differ among different forms of acute renal failure?
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Prerenal: <10
Renal: >20 Postrenal: >40 |
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How do urine FeNa levels differ among different forms of acute renal failure?
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Prerenal: <1%
Renal: >2% Postrenal: >4% |
