ACUTE HD THEORY CLASS FINAL ESSENTIAL
STUDY QUESTIONS AND ANSWERS
◉ EPO.
Answer: Synthesized by kidney, responsible for regulation of RBC
formation --> chronic kidney disease leads to anemia that can be
corrected by giving IV EPO
EPO produced in response to low alveolar pO2 (hypoxia)
Oxygen tension in peritubular fibroblasts regulates EPO production
When oxygen is high/normal fragmentation of HIF alpha (hypoxia
inducible factor) is promoted
In low oxygen environment, HIF alpha will bind with HIF beta to
create HIF1 -- the transcription factor required for production of
EPO
◉ Renin angiotensin system.
Answer: Renin secretion regulated by ANG II (inhibitory), potassium
(stimulatory), SNS (stimulatory) and perfusion pressure
,ACE1 -- produces ANG 1-7 which acts in opposite effect as ANGII -->
vasodilation, inhibition of cell growth, these effects largely mediated
through angiotensin receptor type II
ACE2 -- produces ANGII
AT1 -- receptor that mediates most f effects comonly attributed to
ANG II (increased cell growth, secretion of aldosterone)
Increased blockade at AT1 receptors (ARBS) lead to increased
effects at AT receptors
◉ Prostaglandins.
Answer: Synthesized from fatty acid precursors (arachidonic acid)
which are converted by cyclooxygenase to the cyclic endoperoxides
Renal prostaglandins act to locally regulate renal perfusion
PGE2 augments renal excretion of electrolytes, Na particularly
◉ Renal catabolism of hormones.
Answer: Proximal tubule is major site involved in degradation of
peptides via receptor mediated endocytosis
,◉ Clinical approach to kidney disease.
Answer: History and physical examination
Measurement of GFR
Measurement of urine protein excretion
Examination of urine dipstick and microscopy
Radiologic evaluation
Renal biopsy
◉ Hallmarks of kidney disease.
Answer: Abnormal GFR (serum creatinine)
Abnormal urine microscopy (protein and/or blood)
◉ Urine protein excretion.
Answer: Tamm-Horsfall protein -- produced by mTAL, comprised
matrix for urinary casts and inhibits crystallization in urine and
kidney stone formation
Low grade (below 3.5mg/d) -- may go undetected by dipstick, need
24 hour collection, may be seen in early kidney disease
, Transient -- often seen with CHF, infection or other stress related
illness, can occur in healthy individuals, not associated with
significant kidney disease, benign
Orthostatic -- only when upright, common in adolescents
Nephrotic syndrome -- synonymous w/ glomerular disease
◉ Hematuria.
Answer: Presence of >5 RBCs per high power field constitutes a
significant finding (otherwise likely myoglobinuria/hemoglobinuria)
RBCs in urine can arise from anywhere in the urinary tract -- most
due to UTIs or stones
Dysmorphic RBCs are typically from glomerulus --> misshapen due
to exposure to hypertonic and acidic conditions in nephron
RBCs origination from urinary pelvis, urueter, bladder, or urethra ar
eusually round and uniform in shape
◉ Urine dipstick.
Answer: pH -- basic with UTI, metabolic alkalosis, vegetarian diet;
acidic w high protein intake and metabolic acidosis
STUDY QUESTIONS AND ANSWERS
◉ EPO.
Answer: Synthesized by kidney, responsible for regulation of RBC
formation --> chronic kidney disease leads to anemia that can be
corrected by giving IV EPO
EPO produced in response to low alveolar pO2 (hypoxia)
Oxygen tension in peritubular fibroblasts regulates EPO production
When oxygen is high/normal fragmentation of HIF alpha (hypoxia
inducible factor) is promoted
In low oxygen environment, HIF alpha will bind with HIF beta to
create HIF1 -- the transcription factor required for production of
EPO
◉ Renin angiotensin system.
Answer: Renin secretion regulated by ANG II (inhibitory), potassium
(stimulatory), SNS (stimulatory) and perfusion pressure
,ACE1 -- produces ANG 1-7 which acts in opposite effect as ANGII -->
vasodilation, inhibition of cell growth, these effects largely mediated
through angiotensin receptor type II
ACE2 -- produces ANGII
AT1 -- receptor that mediates most f effects comonly attributed to
ANG II (increased cell growth, secretion of aldosterone)
Increased blockade at AT1 receptors (ARBS) lead to increased
effects at AT receptors
◉ Prostaglandins.
Answer: Synthesized from fatty acid precursors (arachidonic acid)
which are converted by cyclooxygenase to the cyclic endoperoxides
Renal prostaglandins act to locally regulate renal perfusion
PGE2 augments renal excretion of electrolytes, Na particularly
◉ Renal catabolism of hormones.
Answer: Proximal tubule is major site involved in degradation of
peptides via receptor mediated endocytosis
,◉ Clinical approach to kidney disease.
Answer: History and physical examination
Measurement of GFR
Measurement of urine protein excretion
Examination of urine dipstick and microscopy
Radiologic evaluation
Renal biopsy
◉ Hallmarks of kidney disease.
Answer: Abnormal GFR (serum creatinine)
Abnormal urine microscopy (protein and/or blood)
◉ Urine protein excretion.
Answer: Tamm-Horsfall protein -- produced by mTAL, comprised
matrix for urinary casts and inhibits crystallization in urine and
kidney stone formation
Low grade (below 3.5mg/d) -- may go undetected by dipstick, need
24 hour collection, may be seen in early kidney disease
, Transient -- often seen with CHF, infection or other stress related
illness, can occur in healthy individuals, not associated with
significant kidney disease, benign
Orthostatic -- only when upright, common in adolescents
Nephrotic syndrome -- synonymous w/ glomerular disease
◉ Hematuria.
Answer: Presence of >5 RBCs per high power field constitutes a
significant finding (otherwise likely myoglobinuria/hemoglobinuria)
RBCs in urine can arise from anywhere in the urinary tract -- most
due to UTIs or stones
Dysmorphic RBCs are typically from glomerulus --> misshapen due
to exposure to hypertonic and acidic conditions in nephron
RBCs origination from urinary pelvis, urueter, bladder, or urethra ar
eusually round and uniform in shape
◉ Urine dipstick.
Answer: pH -- basic with UTI, metabolic alkalosis, vegetarian diet;
acidic w high protein intake and metabolic acidosis
