Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPR > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

arteries from the start to the end of kidneys (6)

A
  1. renal arteries
  2. interlobar arteries
  3. arcuate arteries at corticomedullary junction
  4. interlobular arteries
  5. afferent arterioles branch to supply glomerulus in cortex
  6. efferent arterioles form peritubular vascualr beds and vasa recta drain glomerulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where is epo made?

A

epithelial cells of peritubular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

nephron includes which structures (4)

A
  1. bowman capsule
  2. PCT
  3. loop of henle
  4. DCT

collecting tubule and duct are not part of nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is a renal corpuscle

A

bowman + glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the renal medullary structures (3)

A
  1. lower part of collecting duct
  2. loops of henle
  3. vasa recta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

histological characteristics of proximal convoluted tubules (4)

A
  1. lots of mitochondria - acidophilic
  2. apical microvillous brush border
  3. cuboidal “puzzle piece” epithelium with junctional complexes
  4. basal striations infoldings - increasing surface area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the area cribosa?

A

the apex of the renal pyramid where the collecting ducts drain urine through papillary ducts into the minor calyx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what lines the visceral and parietal layers of bowman’s capsule

A

visceral = podocytes (with pedicels)

parietal = SS epithelium (continuous with PCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

blood-urine barrier (4)

A
  1. podocytes of visceral bowman
  2. diaphragms betwee foot processes of podocytes
  3. podocyte BM + cap BM = GBM
  4. fenestrated capillary endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

low, medium and high MW proteins through blood-urine barrier

A

low can pass directly through

intermediate are blocked by slit diaphragms

high are blocked by endothelial BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does a mutation in neprhin cause

A

neprhin is a protein that links the podocytes together via the slit diaphragm. mutations in neprhin will cause CONGENITAL NEPHROTIC SYNDROME- massive proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

components of the juxtaglomerular apparatus (3) and where they’re located

A
  1. juxtaglomerular cells (modified SM in wall of afferent arteriole that secrete renin)
  2. macula densa in the wall of the DCT
  3. extraglomerular mesangial cells (AKA lacis cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do macula densa cells look like and what do they contain

A

columnar, compared to cuboidal DCT cells

chemoreceptors - monitor chemical contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are JG cells and what do they do

A

intracellular granules of renin

the JG cells are modfified SM cells with mechanoreceptors that release renin when BP falls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

(extra)glomerular mesangial cells - location and function

A

hold capilaries together in glomerulus

outside pole, make direct contact between JG and MD cells with gap junctions - coordinate activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ureter histological characteristics - muscle (2) and epithelium (1)

A
  1. upper part by kidney = inner long and outer circular
  2. lower = inner long, middle circ, outer long
  3. has stratified transitional epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

urinary bladder histological characteristics (4)

A

1- poorly defined SM layers
2- luminal transitional epithelium
3- upper part covered by serosa, rest covered by adventitia
4- empty = many layers of round, full = few layers of flat (contain fusiform vesicles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

female urethra characteristics (2)

A

3-5cm long

  1. transitional epithelium near bladder
  2. stratefied squanous unkeratinized epithelium in vestibule of vagina (maybe some stratefied columnar in the middle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

male urethra characteristics (5)

A

10-15 cm long
1. intramural urethra surrounding neck, just below bladder and above prostate, very short
2. prostatic urethra -
transitional near bladder and through prostate gland
3. membranous urehtra with stratefied columnar epitehlium (thinnest part of urethra)
4. spongy/penile urethra with pseudostratefied columnar
5. stratified squamous unkeratinized in fossa navicularis at tip of penis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

renal stone characteristics (3)

A
  1. 75% are calcium salts (oxalate and phosphate)
  2. more in men than women, around 20-30 years
  3. 10% incidence over lifetime
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

renal stone PAIN characteristics (2)

A
  1. presents with sudden onset of intense, unilateral, colicky pain with hematuria and vomiting
  2. painfel with ureteral peristalsis causes movement of stone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

anatomical landmarks for kidneys

A
  • SUPERIOR POLE deep to the 11th (left) and 12th (right) ribs and opposite the T12 (left) to L1 (right) vertebrae
  • HILUM is at L1 (left) and L2 (right)
  • superior border is diaphragm
  • inferior border is quadratus lumborum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

areas of normal ureteric constriction (3)

A
  1. renal pelvis - uretopelvic junction
  2. pelvic brim
  3. entrance into bladder - uretovesicle junction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ureteric calculi pain location

A

pain along T11 to L2 nerve fibers (loin to groin pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

during surgery, where can you damage the ureter

A
  1. crossing the pelvic brim

2. passing under the uterine vessels “water under the bridge”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

muscles in bladder/urethra

A
  1. detrusor smooth muscle in bladder
  2. internal urethral spinchter - smooth muscle just under neck of bladder
  3. external urethral sphincter - skeletal muscle located in perineum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

isothenuria

A

specific gravity of 1.010 approximates plasma (less is dilute, more is concentrated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

normal urine pH range

A

4.5 - 6.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what kinds of proteins does the dipstick pick up

A

negatively charged proteins, like albumin, but not at low levels

will also not catch immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the most common protein in normal proteinuria

A

Tamm-Horsfall protein made in the thick ascending limb of the loop of Henle

up to 150mg is normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the kinds of pathologic proteinuria (3)

A

1- Glomerular proteinuria (albumin)

2- tubular proteinuria (low MW proteins)

3- overflow proteinuria (Ig, light chains)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what do you see in urine with nephritic syndrome (3)

A
  1. proteinuria 1-3 grams
  2. hematuria (dysmorphic red cells)
  3. casts (cellular)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what do you see systemically with nephritic syndrome (4)

A
  1. hyptertension
  2. renal insufficiency
  3. edema
  4. decreased urine output (oliguria)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what do you see in urine for nephrotic syndrome (2)

A
  1. more than 3.5 grams of protein/day

2. lipiduria and oval fat bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what do you see systemically with nephrotic syndrome (3)

A
  1. edema (anasarca)
  2. hypoalbuminemia
  3. hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

origin of kidneys

A

intermediate mesoderm - from the urogenital ridge

but the lining is endodermally derived - from cloaca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

neural control of voiding

A
  1. sympathetic = “storing” T10-L2 relax bladder body and contract bladder base and urethra
  2. parasympathetic = “pee” S2-S4 contract bladder and relax urethra
  3. somatic - pudendal contracts external sphincter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

control over detrusor muscle and receptors

A

sympathetic inhibition - B3 adrenergic receptors

parasympathetic stimulation - muscarinic M2/M3 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

control over bladder neck and receptors

A

sympathetic stimulation - alpha1 adrenergic

parasympathetic inhibition - no meds to target these receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

examples of conditions in (+) bladder (4)

A

cause too much peeing

  1. poor bladder wall compliance (amyloid, radation)
  2. overactive bladder
  3. inflammatory conditions (UTI, IBD)
  4. Drugs (caffeine, diuretics etc.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

examples of conditions in (-) bladder (3)

A

cause too little peeing

  1. diabetes
  2. drugs (anesthesia)
  3. bladder diverticulum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

examples of conditions in (+) outlet (4)

A

cause too little peeing

  1. BPH
  2. urethral stricture
  3. DSD/pseudo DSD
  4. Drugs (adrenergics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

examples of conditions in (-) outlet (4)

A

cause too much peeing

  1. prolapse
  2. urethral hypermobility
  3. surgery - prostatectomy
  4. radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

medical treatments for (+) outlet conditions (2)

A
  1. alpha-blocker tamsulosin (symp antagonist)
  2. 5 alpha reductase inhibitor finasteride (blocks conversion of testosterone to dihydrotestosterone -
    shrinks prostate growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

medical treatments for (+) bladder conditions (3)

A
  1. adrenergic agonist (sympathetic agonist)
  2. anticholinergic agonist (parasympathetic antagonist)
  3. botox
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

remnants of mesonephros (2)

A
  • male excurrent ducts

- uroteric bud = outbranch from mesonephric duct (forms ureters and collecting ducts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

rudiements of definative kidney

A
  1. uroteric bud (ureter and collecting ducts)

2. metanephric blastema (renal corpuscle, PCT, loop fo Henle, DCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

potter syndrome

A

bilateral renal agenisis causes oligohydramnios - small for date, reduced amnionic fluid.

babies have wrinkled skin, creases below eyes, ear defects, limb defects (limited space)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

horseshoe kidney

A

fusion of caudal poles before ascent - gets stuck at level of inferior mesentetric artery (hindgut blood supply)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

development of urniary bladder

A

septum in cloaca separates bladder from rectal precursor. urogenital sinus has tip that projects into umbillicus called allantois - most of the time becomes urachus and degenerates, but things can not degenerate properly (have fistula, cyst, or sinus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

bladder exstrophy

A

urachus is open, can get everted bladder and hemi genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

cystic renal dysplasia cause and clinical presentation

A

disordered development of kidney maybe due to obstruction of ureter,

clinically similar to agenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

adult polycystic kidney disease cause

A
  • hereditary AD mutation in PKD1 gene on chrom 16 or PKD2 gene on chrom 4 (altered Ca flux or cilia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

childhood polycystic kidney disease cause

A

AR inheritence of mutation of PKHD1 gene on chrom 6p21-23 which encodes fibrocystin, which is essential for collecting duct and biliary differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

childhood polycystic kidney disease clinical

A

most commonly presents with neonatal renal failure. may be similar to renal agnesis but with enlarged and palpable kidneys

sometimes hepatic fibrosis with minimal kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

childhood polycystic kidney disease gross and histo presentation

A

enlarged, only involves collecting ducts - outer surface is smooth. only involves medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

adult polycystic kidney disease gross and histo presentation

A

grossly, cysts everywhere

histo, fibrosis, flattened tubules, inflammatory infiltrate, hypertensive hyaline tubules, sometimes hemosiderin laden macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

adult polycystic kidney disease clinical presentation

A

clinical presentation in older patients - hematuria, hypertension, ab pain, renal infection, berry aneurysms, mitral valve prolapse, hepatic cysts, colonic diverticula

patients can survive for a while - low incidence high prevalence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

cystic renal dysplasia gross and histo findings

A

grossly large and multicystic

micro have primative glomerular structures and cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

medullary sponge kidney cause and clinical

A

unknown pathogenesis, causes multiple cystic dilation of collecting ducts

asymtomatic usually, discovered in adults incidentally or due to complications such as infection hematuria and kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

variants of nephronophthisis

A
  1. sporadic, non-familial
  2. familial juvenile (most common) adult medullary cystic disease
  3. renal-retinal dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

genetic causes of nephronophthisis

A

most common - familial juvenile - AR mutation of NPHP1-11, JBTS2, JBTS3, JBTS9, JBTS11

or AD mutation of MCKD1 and MCKD2 in adult medullary cystic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

nephronophthisis gross and histo presentation

A

kidneys normal or small in size

cysts along corticomedullary junction

involve distal tubules with tubular basement membrane with fibrosis, inflammation and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

simple cortical cyst cause and findings

A

incidental findings, asymptomatic, 1-5cm cysts with flattened or cuboidal epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

dialysis associated cystic disease findings

A

multiple corticomedullary cysts, fibrosis, oxylate crystals, increased risk for renal cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

tubular reabsorption

A

transfer of substances OUT of tubular lumen INTO peritubular capillaries (for goodies like AAs and glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

tubular secretion

A

transfer of substances FROM peritubular capillaries INTO tubular lumen (for metabolic products)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

excretion rate equation

A

excretion rate = filtration rate - reabsorption rate + secretion rate

ER = FR - RR + SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

ohm’s law

A

Q = deltaP / R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

driving pressure in the kidney (delta P) and glomerulus

A

kidney deltaP = renal artery P - renal vein P

glomerulus deltaP = afferentP - efferentP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what area of kidney is the most perfused

A

the cortex ~95% of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what cells regulate the surface area of the glomerulus

A

intraglomerular mesangial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is the interstitium around the vasa recta like

A

hyperosmolar (need gradient for water reabsorption)

in the peritubular capillaries its about equal to plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

cortical nephrons - characteristics and purpose (4)

A
  • 80-85% of tubules
  • short LoHs with little/no thin ascending
  • purpose is secretion and reabsorption
  • no vasa recta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

juxtamedullary nephrons - characteristics and purpose (4)

A
  • 15-20% of tubules
  • very long LoHs
  • have vasa recta
  • purpose is to generate very concentrated urine - generates osmotic gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

which passes through the glomerulus easier, positively charged, negatively charged, or neutral particles?

A

best is positive, then neutral, then negative

- larger molecuels that are postiively charged go through much much easier than negative (proteins, like albumin or Ig)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what causes this difference in charge preference in glomerular filtration?

A

fenestrae, BM and slits have negative charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what physiological changes happen in diabetic nephropathy

A

thickekning of BM and mesangial matrix, reducing ability of molecules to get into filtrate, reducing GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

starling equation/ glomerular filtration rate equation

A

Jv = Lp x A ((net hydrostatic out) - (net oncotic in))

Jv = fluid moving across capillary
Lp = permeability
A = surface area

rest is net filtration force AKA ultra filtration pressure = what kidney regulates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what happens to pressure over the length of the glomerulus

A

net hydrostatic pressure stays the same

increasing concentration of protein within capillary, so cap oncotic pressure increases (but this value stays below the net hydrostatic pressure to keep flow unidirectional)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is the main starling force that determines ultrafiltration?

A

Pgc = hydrostatic pressure in the glomerular capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

renal plasma flow equation

A

= renal blood flow x (1-hematocrit)
= 1200 mL x 50%
= 600mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

how much of the plasma that gets into the kidney gets filtered through the glomerulus

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

so what’s an estimate of GFR

A

0.2 x renal plasma flow
= 0.2 x 600
= 120mL/min
normal is 120-140

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

how do mesangial cells affect GFR

A

can affect surface area A - if they contract, they reduce surface area and decrease GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

how do you change hydrostatic glomerular cap pressure?

A

target:

  1. renal arterial BP
  2. afferent arteriolar resistance
  3. efferent arteriolar resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is glomerular pressure in relation to systemic pressure under normal conditions

A

half. because you have two arterioles (afferent and efferent) at the same resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what happens to GFR if you constrict afferent arteriole

A

decrease Pgc, decrease GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

how can you constrict afferent arterioles

A

with adrenergic agonists - increased sympathetic activity and increased circulating catecholamiines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what happens to GFR if you constrict efferent arterioles

A

increase upstream Pgc and increase GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

how can you constrict efferent arterioles

A

low levels of Ang2 (because at high levels, afferent would also be constricted)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

when do you have myogenic response

A

during an acute change in BP - responds in 1-2 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is the myogenic response

A

High BP:
afferent senses the stretch due to increased systemic BP and clamps down in response

Low BP:
afferent will dilate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

how does the juxtaglomerular apparatus regulate GFR in response to high BP (2)

A

juxtaglomerular apparatus includes macula densa and juxtaglomerular ccells

  1. macula densa are specialized epithelial cells that senses sodium chloride and releases ATP -> adenosine -> constriction of afferent, reducing Pgc
  2. juxtaglomerular cells are specialized SM that have renin granules. release is inhibited by the adenosine released by macula densa during HTN, leading to decreased ang2, which causes dilation of efferent arterioles, reducing Pgc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

when do you have how does the juxtaglomerular apparatus regulation of GFR

A

during long term changes in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

how does the juxtaglomerular apparatus regulate GFR in response to low BP (2)

A
  1. decreased NaCl causes macula densa to release NO and prostaglandins to dilate the afferent arterioles to increase Pgc
  2. prostaglandins cause juxtaglomerular cells to release renin granules which results in high Ang 2, which constricts efferent arterioles to increase Pgc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what mechanisms does the kidney use to regulate GFR and why does it do it

A
  1. myogenic (afferent constriction/dilation short term)
  2. juxtaglomerular apparatus

to maintain normal GFR for kidney function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what mechanisms does the body (Extra-renal) use to regulate GFR and what does it do it

A
  1. neural
  2. hormonal

to maintain normal volume and perfusion throughout the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what are the neuronal extra-renal responses on GFR to big drop in BP (i.e. in hemorrhage) (2)

A
  1. baroreceptors increase symp activity which stimulate B1 receptors on juxtaglomerular cells which increase renin release (at high Ang2, afferent is constricted too) and also
  2. stimulation of alpha 1 receptors in afferent arteriole to promote constriction

causes reduced kidney perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is the hormonal extra-renal response to GFR in response to high BP (6)

A
  1. stretch in ventricle causes release of brain naturetic peptide, stretch in atria causes release of atrial naturetic peptide
    natiuretic peptides dilate afferent arteriole cells
  2. ANP and BNP also relax mesangial cells, increasing surface area, causing increased GFR, resulting in greater excretion of sodium and water
  3. ANP and BNP constrict efferent arterioles
  4. increased blood flow in vasa recta - to was away osmotic gradient - allowing for dilute urine and decreased fluid retention
  5. decreased sodium reabsorption in DCT and cortical collecting ducts via phosphorylation of sodium channels
  6. inhibit renin and aldosterone secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

theoretically, how do you get 100% clearance

A

free filtration (20%) + 100% secretion (rest of the 80%)

clearance/excretion is MORE than GFR - clearance is equal to RPF (renal plasma flow) like with PAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

theoretically how do you get 0% clearance

A

filtration (20%) - reabsorption (same 20%)

clearance/excretion is LESS than GFR - basically 0 clearance, like with GLUCOSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

when does GFR = clearance/excretion?

A

when there is just filtration

like with inulin or ~creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

clearance equation

A

Cx = mass in the urine / plasma concentration

Cx = Ux x V / Px

Ux = conc in the urine
V = urine flow rate
Px = conc in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

excretion equation

A

= V x Ux

= urine flow rate x urine conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how to measure GFR by measuring substances in urine

A

inulin = substance that is freely filtered and NOT reabsorbed, secreted or metabolized = JUST filtered

creatinine from muscle, freely filtered and slightly secreted but also overestimated, so equals out. so clearance = GFR

= mass of creatinine/ plasma creatinine

= (Ucreat x flow rate)/ Pcreat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what’s the theoretical relationship between GFR and plasma creatinine

A

inverse –> theoretically if GFR falls to 25% of normal, Pcr should increase 4x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

whats the minimum normal value for GFR

A

60

that’s 50% of normal (120)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

filtered load equation

A

for a free filtered substance

FL = GFR x Px

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

fractional excretion equation

A

= amount excreted/amount filtered
= mass in urine/ filtered load
= Ux x V/Px x GFR

= 100 x Una/Sna x Scr/Ucr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

primary causes of nephrotic syndrome (3)

A
  1. minimal change glomerulopathy
  2. membranous glomerulopathy
  3. focal segmental glomerulosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

primary causes of nephritic syndrome (3)

A
  1. proliferative glomerulonephritis
  2. acute diffuse proliferative glomerulonephritis
  3. crescentic glomerulonephritis (worst, can become rapidly progressive glomerulonephritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what’s the most common nephrotic syndrome in kids

A

minimal change disease (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what would you do for someone with minimal change disease

A

predisone - have to give steroids to immunosuppress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what do you see on histo (2) and TEM (1) for minimal change disease (3)

A

almost normal at low power:
1- no increased cellularity
2- no interstitial inflammation
3- on TEM you see effacement of podocytes - fusion, continuous lining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

african americans are more likely to have what kind of nephrotic syndrome

A

FSGS - focal segmental glomerulosclerosis because of APO mutation that protects against african sleeping sickness - trypanosomiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what histo changes do you see in FSGS (3)

A

1- some (not all) glomerular collapse, shrinking in bowmans space (higher power see only PART of the glomeruli are affected) i.e. focal segmental
2- dilation of tubules with casts
3- sclerosis of capillary in some parts and adhesion to bowman’s capsule in those parts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what do you see on IF in FSGS

A

IF is non-specific positive only in areas of sclerosis - no immune complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

which is more favorable, minimal change, membranous nephropathy or FSGS

A

minimal is best -
responds better to steroids and tend not to progress.

membranous is in the middle - 1/3 progress, 1/3 remission, 1/3 stable

FSGS the worst - progression is more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what are other associated conditions with FSGS (4)

A
  1. HIV (sit and replicate inside podocytes)
  2. sickle cell (hyperfiltration and secondary form of FSGS)
  3. morbid obesity (hyperfiltration and sclerosis of glomer cap bed)
  4. pamidronate (bisphosphonate for osteoperosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what do you see in histology for membranous nephropathy (4)

A
  1. diffuse involvement
  2. cap walls are thickened - BM thick
  3. no increase in cellularity
  4. no inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what do you see on GMS stain for membranous nephropathy

A

diffuse thickening of BM with “spikes” of GMS pos BM surrounding pale sites of epimembranous subethithelial deposit (indicating immune complex deposition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what do you see on IF for membranous nephropathy

A

diffuse granular deposit along whole BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what do you see on histology for diabetic nephropathy (5)

A
  1. nodular slcerosis in mesangium and afferent and efferent
  2. arterial hyalinzation
  3. lymphocytic infiltrate
  4. diffuse thickening of BM without immune deposition
  5. iscemic necrosis of papillae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

do you give predinsone for diabetic nephropathy?

A

no because it raises blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what do you see in histology (2) and EM (1) for post-infectious glomerulonephritis

A
  1. diffuse global increase in cellularity within glomeruli (polys)
  2. proliferation of cell types (epithelial and mesangial)
  3. TEM humps on subepithelial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what do you see on IF for post-infectious glomeruloneprhtis

A

global chunky “starry sky” appearance caused by complex deposits at the subeptithelial aspect of BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what is C3 level for post infectious glomerulonephritis

A

low - because of immune complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what do you see in histo for lupus nephritis (5) and EM (1)

A
  1. diffuse involvement of glomeruli
  2. some have focal sclerosis, some are totally scarred over
  3. thickened capillary walls
  4. slight increase in mesangial cells, no infiltrate
  5. large subendothelial deposits on GMS and PAS- immune complex deposition
  6. effacement of podocytes on EM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

what do you see on IF for lupus nephritis

A

“full house” staining (IgG, IgM, IgA, C3, C1q) in capillary loops and mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

what do you see on histology for goodpasture’s symdrome (3)

A
  1. diffuse glomerular involvement, some completely sclerosed
  2. increased cellularity beneath bowman’s capsule (macrophages and epithelial cells) in crescent shape with fibrinoid necrosis
  3. RBCs in urinary space and tubules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what do you see on IF for goodpasture’s syndrome

A

linear staining of BM positive for IgG and C3 - not granular (no immune complex depositions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what are clinical clues for goodpasture’s syndrome

A

both renal and pulm involvement with rapidly progressing glomerulonephritis (can have crescents)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what serologic test would be helpful in diagnosis for goodpasture

A

Anti-GBM titer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what do you see on histology for microscopic polyangiitis (2)

A
  1. vascular space with destruction of wall by inflammatory cells - vasculitis - seen in both renal and skin biopsy
  2. focal segmenting glomerulonephritis with crescents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what do you see on renal IF and skin for microscopic polyangiitis

A

nothing in renal, skin has C3, IgM and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

clinical clue with microscopic polyangiitis

A

purpura - skin involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what serology test would you ask for if you suspect microscopic polyangiitis

A

antineutrophil cytoplasmic antibody (ANCA) titer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what do you give for goodpastures and ANCA vasculitis

A

combination of steroids and cyclophospholides or ritoximab or plasmophoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

paracellular pathway

A

movement across tubular epithelium across TIGHT JUNCTIONS depending on electrochemical gradient and permeability properties of the TJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

transcellular route

A

includes trans-apical, trans-basal and trans-lateral

depending on electrochemical driving force and active energy transport with channels and transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

difference between simple and facilitated diffusion

A

simple is through the membrane itself, facilitated is using carriers BOTH are WITH the electrochemical gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

difference between primary and secondary active transport

A

BOTH require energy and are AGAINST the electrochemical gradient.

primary uses an ATPase

secondary uses the downhill movement of one substance to provide energy required to move the other substance against the gradient (cotransport/symport = 2 molecules go in the same direction, countertransport/antiport = opposite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

endocytosis vs transcytosis

A

endo is outside into the cell, trans is outside all the way through to the other side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

how does sodium get from tubular lumen to capillary

A

there’s a high sodium concentration in the tubular lumen and lower concentration in the tubular epithelial cell, so the sodium passively diffuses into the cell.

then, the sodium gets pumped into the interstitium via a sodium potassium ATPase that pumps 3 molecultes of sodium out for ever 2 molecules of potassium in.

then the sodium will get into the BV via oncotic pressure, which also pulls other solutes via solvent drag (2/3rd get reabsorbed this way in proximal tubule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what is solvent drag

A

movement of solutes with water that’s moved by osmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

how do glucose and amino acides get from tubular lumen into BV

A

transcellular via sodium/glucose cotransport/symport (sodium linked glucose tranpsorters - or AA transporters) in apical membrane, and then gets into interstitium passively along gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what happens if you have too high a concentration in the tubular lumen

A

the transporters are saturable, so there’s a limit and you’ll get glucose and AAs in urine

glucoseria via diabetes mellitus, for example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what is type A renal glucosuria?

A

there is defect that causes a reduced affinity of SGLT2 (the sodium/glucose transporter) so you get less reabsorption of glucose and you get benign mild-severe glucoseria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what happens to organic anions and cations? what is used?

A 
want them to be secreted.
secretion happens via 3 protein types in proximal tubule:
1. organic cation transporters 
2. organic anion transporters 
3. multidrug resistance proteins (p-
 glycoprotein --> cyp3a4 associated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

how do we get rid of cations?

A

OCT sits on basolateral surface, which gets cation into cell, export of cation into tubular lumen is driven by exchange of protons with cation at apical surface via acid gradient (which is maintained by sodium/proton exchanger)

THUS this is all maintained by SODIUM/POTASSIUM ATPase so that intracellular sodium remains low, so that protons can pump out for exchange of sodium in with its gradient, creating acid gradient to bring proton back in in exchange for cation out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

how do we get rid of anions?

A

have OAT on basolateral surface. OAT brings anion into cell via the establishment of a gradient with sodium and alpha KG transporters. MDR (p-glycoprotein) allows anion to go into tubular lumen via ATPase. this is also driven by SODIUM/POTASSIUM ATPase, but also MDR ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

is creatinine an anion or a cation

A

cation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what are anions are secreted in proximal tubule (7)

A

endogenous:
1- oxylate
2- urate

exogenous:
3,4,5,6- FACE diuretics (furosemide, acetazolamide, chlorothiazide, ethacrynate)
7- PAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

PAH characteristics

A

freely filtered AND avidly secreted - can get complete clearance of this molecule –> this can tell us what RENAL PLASMA FLOW is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

how do you calculate for renal blood flow from renal plasma flow

A

RBF = RPF / (1-Hct)

since plasma is only a part of total blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

what happens to clearance of glucose and PAH as you keep increasing plasma concentration

A

eventually, they both reach around GFR - PAH can’t be fully secreted and glucose can’t be fully reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what happens to clearance of glucose and PAH as you keep increasing the flow through the tubular lumen

A

same thing with increased concentration - eventually both get clearance that’s equal to GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

how do smaller peptides get into tubular epithelium

A

peptidases on the tubular surface break them down and abosrb AAs via AA/Na+ cotransporters, then get dumped into interstitial space and back into circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

how do larger peptides get into tubular epithelium

A

two options:

  1. intact - can be trancytosed
  2. if not recognized as intact, can get endocytosed, degraded and get then get into interstitial space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what happens to ions in thin descending loop of Henle

A

nothing, thin descending loop is impermeable to ions. only thing that’s permeable is water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what happens to sodium ions in the thick ascending loop of Henle

A

about 25% of sodium is reabsorbed via the sodium/potassium/2 chloride cotransporter

furosemide inhibits this cotransporter - strong effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what happens to sodium ions in distal convoluded tubule

A

4% of sodium is reabsorbed via sodium/chloride cotransporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

what happens to sodium ions in collecting duct

A

3% of sodium reabsorbed via luminal membrane aldosterone-sensitive sodium channel (ENaC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what are the main sodium transporters in proximal tubular epithelium (4)

A

basolaterally =
1- sodium/potassium ATPase

apically =
2- cotransproters (AA, glucose, phosphate)
3- countertransport (protons)

4-some paracellularly with chloride and water in solvent drag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

what are the main sodium transporters in the thick ascending loop of Henle

A

apically =
1. sodium/potassium/2 choride contransporter (inhibited by LOOP DIURETICS - furosemide) which creates backleak of potssium, driving paracellular flow into interstitium

  1. paracellular: flow of cations (Na+ K+ Ca++) out of tubular lumen into interstitium because of gradient set up by potassium leak channels (more positive in lumen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

is thick ascending limb permeable or impermeable to water?

A

impermeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

is thin descending loop of Henle permeable or impermeable to water?

A

permeable ONLY to water, nothing else

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

is early distal convoluted tubule permeable or impermeable to water?

A

impermeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

how does sodium get transported in the early distal convoluted tubule

A

via sodium/chloride cotransporter (inhibited by THIAZIDE diuretics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

is the late distal convoluted tubule/ collecting duct permeable or impermeable to water?

A

it’s variable - under control of ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

how does sodium get transported in the late distal convoluted tubule/ collecting duct?

A
  1. luminal epithelial sodium ENaC channels
  2. basolateral sodium potassium ATPase

BOTH are stimulated by aldosterone (increased expression and activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what does increased sodium fractional excretion value tell you

A

that there’s an intrinsic renal problem - less sodium reabsorption, more sodium excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what happens with chloride reabsorption in proximal convoluted tubule (what percentage and how)

A

60% reabosrbed paracellulary predominately via solvent drag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

what happens with chloride reabsorption in thick ascending limb (what percentage and how)

A

30% reabsorbed via sodium/potassium/2 chloride cotransporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

what happens with chloride reabsorption in early distal convoluted tubule (what percentage and how)

A

7% via transcellular Na+/Cl- cotransport

177
Q

what happens with chloride reabsorption in late distal convoluted tubule/collecting duct (what percentage and how)

A

3% via transcellular countertransport with bicarb with beta-intercalated cells

178
Q

fanconi’s syndrome

A

generalized dysfunction in PCT cotransporters

this impairs kidney function and production of vitamin D - get bone disease

179
Q

hyperkalemia causes what to resting membrane potential

A

depolarization

180
Q

hypokalemia causes what to resting membrane potential

A

hyperpolarization

181
Q

relationship between potassium and acid-base balance

A

too much acid in plasma triggers potassium proton antiporter - get potassium leaving cell, have risk for becoming hyperkalemic acidosis

too little acid causes increase movement of potassium into cell and you get hypokalemic alkalosis (also often see hypochlorinic)

182
Q

relationship between insulin and potassium

A

insulin and epinephrine stimulate sodium/potassium ATPase, so you can help patient with hyperkalemia by administering insulin

183
Q

how much and how is potassium transported in PCT

A

67% via paracellular solvent drag

184
Q

how much and how is potassium transported in thick ascending limb

A

20% via na+/K+/ 2Cl-

and ROMK2 backleak channel

185
Q

how much and how is potassium transported in distal convoluted tubule and collecting duct?

A

variable (10-50%) depending on what your potassium load is.

if you’re hyperkalemic, secretion will occur via PRINCIPAL cells in an aldosterone-sensitive fasion, also affected by luminal sodium levels (distal sodium delivery = potassium wasting)

if you’re hypokalemic, reabsorption will happen via apical H+/K+ ATPase in alpha-intercalated cells (only activated in low intracellular potassium)

186
Q

Bartter and Bartter-like Syndrome

A
  • defects in ROMK2 and NA+/K+/2Cl- channels lead to electrolyte disturbances, bone disorders, growth and cognitive disorders
187
Q

inorganic phosphate and Ca2+ together are soluble or insoluble?

A

insoluble - they make bone

188
Q

phosphate transport in proximal convoluted tubule - how much and how?

A

variable - 30-80% via sodium/phosphate cotransporters - can regulated by parathyroid hormone (in response to low calcium, PTH decreases phosphate levels to prevent formation of crystals in blood)

189
Q

phosphate transport in proximal straight tubule - how much and how?

A

varaible, ~ 5% paracellular solvent drag AND transporters that can be expressed when you need to recover phosphate

190
Q

phosphate transport in distal convoluted tubule - how much and how?

A

variable 10-15% paracellular solvent drag AND transporters that can be expressed when you need to recover phosphate

191
Q

how and how much calcium is transported in PCT?

A

70% via paracellular solvent drag

192
Q

how and how much calcium is transported in the thick ascending limb?

A

20% driven by potassium positive charge and paracellular flow

193
Q

how and how much calcium is transported in the distal convoluted tubule

A

9% via luminal calcium channels under the control of PTH - upregulated by PTH

194
Q

chronic kidney disease and vitamin d

A

kidney is where vitamin D is activated, so you get loss of bone and low plasma calcium and high PTH – severe bone defects

195
Q

where do you get most of your magnesium reabsorption

A

in the thick ascending limb (50-60%) paracellularly due to positive lumen charge with potassium backflow

reaborption in low in PCT (20-30%) because it doesn’t work as well with solvent drag

196
Q

what happens to urea in PCT

A

50% via passive reabsorption paracellularly through tight juctions (NO TRANSPORTERS IN PCT)

197
Q

what happens to urea in the loop of Henle

A

that same 50% is secreted via urea transporters

198
Q

what happens to urea in collecting duct

A

50% reabsorbed again via urea transporters

199
Q

in a general sense, are the ascending tubules permeable or impermeable to water?

A

impermeable. the descending tubules (PCT, DLH, CD) are impermeable

200
Q

what regulates the acquaporin vessicle docking?

A

ADH - ADH stimulates apical membrane channels to increase water reabsorption in the COLLECTING DUCT

in nephrogenic diabetes, there’s an ADH receptor defect, so you don’t get water reabsorbtion

201
Q

what is lithium associated nephropathy

A

lithium looks like sodium, accumlates in collecting duct via the ENaC channels which in turn downregulates ADH regulated aquaporins

202
Q

iondine-rich contrast induced neprhopathy

A

contrast is cytotoxic to PCT

203
Q

calcineurin inhibitor nephrotoxicity

A

get tubular resistance to aldosterone and resulting hyperkalemia

204
Q

heavy metal (Pb, Cd) nephropathy

A

PCT dysfunction leading to hyperuricemia, gout and HTN

205
Q

aldosterone has an effect on what channels? (3)

A

K channels,
ENaC
Na+/K+ ATPase

206
Q

what’s the gradient from cortical side to papillary side

A

300 mOsm/L

1200 mOsm/L

207
Q

in “Active transport” region of medulla (upper portion with thick ascending) which area has highest and lowest sodium concentration

A

interstitium is higher than both thick descending and thin ascending

208
Q

in “passive transport” region of medulla (lower portion with thin ascending) which area has highest and lowest sodium concentration

A

thin ascending > interstitium > thin descending

209
Q

what is the net flow in the descending vasa recta

A

sodium in

210
Q

what is the net flow in the ascending vasa recta

A

water in

211
Q

what is the [NaCl] difference at any level through the vasa recta and interstitum

A

ascending > interstitium > descending

212
Q

What transporters does ADH control (3)

A

urea transporters
Na/K/2Cl
aquaporins

213
Q

regulators of ADH release (3)

A
  1. plasma osmolality (major) - increased plasma osmolality increased ADH release (very sensitive, causes small changes)
  2. blood volume, sensed by stretch receptors, less sensitive but more potent
  3. systemic arterial BP - sensed by stretch receptors, less sensitive but more potent
214
Q

free water clearance

A

positive if urine has lower concentration than plasma (low ADH)

negative if urine has higher concentration than plasma (high ADH)

215
Q

central diabetes insipidus, cause and treatment

A

caused by too little ADH release from posterior pituitary (caused by brain trauma, infection or neoplasms), treated by exogenous ADH

216
Q

nephrogenic diabete insipidus cause and treatment

A

caused by lack of response of kidney collecting duct cells to ADH (may be caused by lithium) cannot be treated by exogenous ADH

217
Q

Syndrome of inappropriate ADH secretion (SIADH) cause and treatment

A

elevated plasma ADH relative to plasma osmolarity and have very concentrated water(can accumulate excess water if not restrained) - caused by brain infections, neoplasms, anti-tumor drugs and lung cancer

218
Q

what does the active form of vitamin D do systemically (3)

A

gets activated by PTH in the proximal tubules in response to low plasma calcium levels

  1. increases gut Calcium uptake
  2. decreases calcium loss in kidney
  3. decreased bone reabsorption
219
Q

chronic low vitamin D would cause what effect on phosphate levels

A

because your vitamin D is low, your parathyroid hormone is high which leads to increased plasma levels of calcium and phosphate. in order to avoid crystals being formed in the blood, phosphate reabsorption is decreased

220
Q

which diuretics are potassium wasting? (3)

A

those that work early in the nephron delivering high sodium load to distal nephron

Loop diuretics AKA Na/K/2Cl blockers (TALH):

  1. furosemide
  2. ethacrynic acid

Thiazide diuretics AKA Na/Cl blockers (DCT):
1. hydrochlorothiazide

221
Q

which diuretics are potassium sparing? (3)

A

those that act at collecting duct (late)

inhibitors of ENaC (CD):
1. amiloride

aldosterone antagonists (CD):

  1. spironolactone
  2. eplerenone
222
Q

what are examples of diseases that lead to “edematous states” (4)

A
  1. CHF
  2. pulm edema
  3. nephrotic syndrome
  4. hepatic cirrhosis
223
Q

what are the reflex compensatory mechanisms when first starting a diuretic

A
  • sensed as low blood pressure,
    1. actvates symp activity
    2. RAAS pathway
    3. increased ADH
    4. decreased ANP

results in diuretic “braking” - establishing a new set point

224
Q

what’s an example of an osmotic diuretic? where does it work

A

mannitol - througout but starts in PCT

225
Q

what’s an example of a carbonic anhydrase inhibitor and where does it work?

A

in PCT - acetazolamide

226
Q

what’s an example of ADH antagonist and where does it work

A

tolvaptan - CD

227
Q

What does carbonic anhydrase do? what happens if you inhibit it (2)

A

converts bicarb and CO2 into water

  1. less resorbtion of bicarb anion, which leads to less sodium leaving because you are pumping less protons into the lumen via Na/H antiporter. this INCREASED LUMINAL SODIUM is sensed by the MACULA DENSA which releases ATP, increasing adensoine, leading to afferent arteriolar contraction, decreased renin, increased efferent relaxation (reduces GFR because it senses high Na as high blood pressure) – DIURETIC BRAKING
  2. also, at the collecting duct, you have high bicarb, increasing negative charge of lumen, causing K+ loss and Cl retention (HYPOKALEMIC, HYPERCHLORINIC)
228
Q

uses for acetazolamide (3)

A
  1. metabolic alkalosis (to correct the alkalosis caused by other loops/thiazides, decreasing bicarb in plasma)
  2. decrease intraocular pressure topically
  3. acute mountain sickness (in anticipation of resp alkalosis)
229
Q

adverse effects of acetazolamide (2)

A
  1. renal stones (calcium salts are less soluble at alkaline urine pH)
  2. cross-hypersensitivity with other sulfonamides
230
Q

what are loop diuretics the best for?

A

reducing blood volume

231
Q

loop diuretic effect on ions

A

inhibiting the resporption of potassium into the cell (inhibits the Na/K/Cl transporter). thus you have less backleak back into the lumen. this decreases the reabsorption of calcium and magnesium which used this backleak channel for a charge gradient for paracellular transport. thus, causes HYPOCALCEMIA and HYPOMAGNESEMIA

232
Q

what are the overall effects of loop diuretics (3)

A
  1. get increased luminal Na, Cl and K due to inhibition of the rock channel (also leads to hypocalcemia and hypomagnesemia because no more potassium back leak)
  2. the macula densa uses the Na/K/2Cl to sense sodium and chloride, so loop diuretics inhibit their ability to sense the increases in sodium and chloride in the DCT. thinks you’re not filtering enough, so works to INCREASE GFR through prostaglandins and NO, increasing renin release and increased aldosterone – diuretic braking
  3. also get potassium WASTING and ALKALOSIS downstream in the collecting duct because of negative charge from chloride.
233
Q

what happens when you first take furosemide?

A

in large doses, abolishes osmotic gradient, and thus you get very dilute urine - high diuresis

but once compesnatory mechanisms kick in (renin, increased RBF) you reesablish baseline and improve osmotic gradient

234
Q

what is first line approach for patient with hypertension and congestive heart failure

A

furosemide

235
Q

adverse effects of loop diuretics (5)

A
  1. low ion levels (K, H, Mg, Cl etc.)
  2. cardiac arrhythmias (toursades)
  3. hypotension due to hypovolemia (esp in elderly)
  4. ototoxicity
  5. hyperuricemia (gout)
236
Q

what do thiazide diuretics cause? (3)

A
  1. thiazides inhibit the Na/Cl symporter in the DCT - resulting in higher Na and Cl levels in the urine
  2. this sodium gradient drives a basolateral sodium calcium exchanger, causing more resorbtion of calcium (HYPERCALCEMIA)
  3. increased sodium delivery to collecting duct, leading to potassium wasting and proton secretion (HYPOKALEMIA, ALKALOSIS)
237
Q

what do you use in conjunction with thiazide diuretics?

A

ACE inhibitors to combat hypokalemia

238
Q

uses for loop diuretics (2)

A
  1. edema

2. hypertension (with heart failure esp)

239
Q

uses for thiazides (4)

A
  1. hypertension - first choice for simple essential HTN
  2. CHF (reduces morbitidy)
  3. Hypercalcinuria - prevent renal stones
  4. nephrogenic diabetes insipidus
240
Q

adverse effects for thiazides (4)

A
  1. electrolyte imbalance (HYPOKALEMIA, HYPERCALCEMIA, HYPERURICEMIA)
  2. hypotension
  3. hyperglycemia in patients with diabetes
  4. hyperlipidemia
241
Q

ENaC blocker effects (2)

A
  1. amiloride inhibits sodium ENaC channels, indepedent of aldosterone
  2. get decreased excretion of K and H (HYPERKALEMIA, ACIDOSIS)
242
Q

uses for ENaC blockers (1)

A
  1. in conjunction with thiazides or loops to spare potassium
243
Q

adverse effects for ENaC blockers

A
  1. hyperkalemia (esp in renal disease)
244
Q

does amiloride decrease morbidity?

A

yes, for elderly patients in conjunction with HCTX

245
Q

effect of aldosterone inhibitors (3)

A

most effective when aldosterone is high

  1. inhibits potassium channel (less potassium secretion - HYPERKALEMIA)
  2. inhibits ENac expression (less sodium reabsorption)
  3. inhibits Na/K ATPase
246
Q

adverse effects of aldosterone antagonists

A
  1. hyperkalemia

2. gynecomastia esp spironolactone (and menstural irregularities in women)

247
Q

do aldosterone antagonists decrease mortality?

A

yes, in heart failure patients when given in combo with loop or thiazide

248
Q

osmotic diuretic effects (3)

A

(mannitol)
1. freely filtered, increasing osmomtic suction to keep water in the lumen - remain in the tubule the whole way. thus, they work at sites where water is permeable (tDLH for example)

  1. increase plasma osmolality, increasing RBF, due to increased vascular volume
  2. increased magnesium excretion for unkonwn reason
249
Q

therapeutic use for mannitol (1)

A

reduce intracranial or intraoccular pressure before and after sx

250
Q

adverse effects for mannitol (1)

A

hyperkalemia, shrinks cells, increasing intracellular [K], causing passive diffusion out

251
Q

vasopression antagonists effect (1)

A

(tolvaptan)

block ADH signalling, block production and docking of aquaporins in CD

252
Q

use for vasopressin antagonists (1)

A

SIADH

253
Q

can you add a loop to a thiazide?

A

yes, you get synergism for sodium excretion, however, be careful because you can get severe postural hypotension

254
Q

what is effective vascular volume?

A

part of the ECF that is in the vascular space AND effectively perfusing the tissues

determined by ECF fluid volume, CO and vascular tone. related to BP

255
Q

ECF volume is related to sodium or water?

A

sodium

256
Q

TBF Osmolality is related to sodium or water?

A

water

257
Q

where are the osmoreceptors

A

hypothalmus

258
Q

what are the clinical signs of volume depletion (5)

A
  1. orthostatic decrease in PB and increase in pulse rate
  2. decreased pulse volume
  3. loss of axillary sweating
  4. decreased skin turgor
  5. dry mucous membranes
259
Q

what are clinical signs of volume expansion (6)

A
  1. edema
  2. pulm crackles
  3. ascites
  4. JVP distension
  5. hepatojugular reflex
  6. hypertension
260
Q

volume depleted state causes what physiological effects? (3)

A
  1. increased symp activity (leads to Na reabsorption in kidneys)
  2. RAAS (leads to Na reabsorption via Ang2 and aldosterone)
  3. ADH (water retention)
261
Q

where does Ang2 work in the kidney

A

PCT to reabsorb Na

262
Q

what 3 things go into osmolarity and what is the equation?

A

2Na + BUN/2.8 + Glucose/18

263
Q

acute tubular necrosis presents with

A

muddy brown casts - injured tubules. most common in hospital setting

264
Q

prerenal azetemia is most common in what setting (hospital, outside etc.) and what are some causes (3)

A

outside the hospital

  • hypovolemia
  • heart failure
  • cirrhosis
265
Q

definition and classifications of AKI (3)

A

fast deterioration of ability to excrete nitrogenous waste products

  1. prerenal
  2. acute parenchymal renal disease (vascular, glomerulo, interstitial or tubular)
  3. postrenal - obstruction
266
Q

Stage 1 AKIN classification requirements

A

greater than 1.3 serum creat or less than 0.5 urine output

267
Q

pigmented casts are indicative of

A

acute tubular necrosis

268
Q

if urine osmolarity and specific gravity are the same as plasma, what does that indicate?

A

acute tubular necrosis, or some intrinsic renal disease

269
Q

common drugs that cause prerenal syndrome (2)

A

NSAIDs

ACE inhibitors/ ARBs

270
Q

causes of ATN (3)

A
  • ischemia
  • toxin
  • sepsis
271
Q

phases of ATN (3)

A
  1. initiation
  2. maintenance
  3. recovery (noto all fully recover)
272
Q

definition of oliguria

A

less than 400mL over 24 hours - indicates a bad prognosis

273
Q

definition of polyuria

A

over 3000mL over 24

can be from diabetes insipidus

274
Q

what does BUN/creat ratio over 20 indicate

A

dehydration, hypovolemia, prerenal issue

275
Q

what causes SIADH (4)

A
  1. hypothalmic increase in ADH production (CNS issue, drugs, pulmonary disease, post op and nausea)
  2. increased ectopic production of ADH (oat cell, bronchogenic)
  3. potentiation of ADH effect (drugs)
  4. exogenous administration
276
Q

what causes euvolemic hypernatremia (2)

A

BOTH always have to be coupled with low water intake

  1. nephrogenic diabetes insipidus (no RESPONSE to ADH)
  2. neurogenic diabetes insipidus (no ADH)
277
Q

what are some acquired causes of nephrogenic DI? (3)

A
  1. severe hypercalcemia
  2. severe hypokalemia
  3. lithium
278
Q

free water deficit equation

A

= [serum Na+ measured - 1] / [serum Na+ desired] x weight(kg) x 0.6

279
Q

desmopressin

A

synthetic form of ADH - is antidiuretic but has no vasopressor activity

280
Q

what’s the range of urine osmolality?

A

50-1200 mOsm/kg

281
Q

at what change in EBV does ADH start ramping up

A

6-8% change in EBV

282
Q

what do you fix first, volulme or water

A

volume AKA salt

283
Q

3 phases of ATN

A
  1. initiation phase - cloudy swelling
  2. oliguric phase - back diffusion and obstructed dilated tubules
  3. diuretic phase (regenerated) - inability to concentrate urine as GFR increases
284
Q

in what part of the kidney (medulla or cortex) do you see acute tubulointerstitial nephritis

A

medulla

glomeruli are normal

285
Q

bacterial organisms you would expect in ascending pyelonephritis

A

gram neg:

E coli, staph saprophyticus, klebsiella, proteus pseudomonas

286
Q

bacterial organisms you would expect in hematogenous pyelonephritis

A

staph aureaus, salmonella, pseudomonas

more likely to see abcesses

287
Q

what is thyroidization and what is it indicative of

A

when you have dilated tubules filled with proteinaceous materials and pink hyaline casts - indicative of chronic renal damage

288
Q

what congenital defect is associated with acute pyelonephritis?

A

vesicoureteral reflux (retrograde flow or urine)

289
Q

what do you see with acute interstitial nephritis? in urine, histo, clinical and gross (4)

A
  • renal failure 1-2 weeks after exposure to drugs (sometimes with fever, skin rash and eosinophilia)
  • WBC casts in urine
  • enlarged edematous kidneys
  • diffuse or patchy infiltrate that spares glomeruli
290
Q

what is acute insterstiital nephrintis caused by? (2)

A

sometimes due to systemic infection, mostly due to drug-induced hypersensitivity reaction (antibiotics, NSAIDS, diuretics, allopurinol etc.)

291
Q

when do you decide to give someone predisone with nephritis?

A

if the creatinine doesn’t improve after 3-7 days after stopping offending agents, and after you do biopsy

292
Q

when do you see cast nephropathy?

A

multiple myeloma

293
Q

how do light chains cause acute kidney injury? (2)

A

direct tubular toxicity and intratubular cast formation

294
Q

what are risk factors for myeloma cast formation and acute kidney injury? (3)

A
  1. hypercalcemia
  2. volume depletion
  3. IV contrast
295
Q

where do light chains cause problems in the kidney?

A

light chains are freely filtered, absorbed by endocytosis in PCT usually, but with a monoclonal gammopathy they overwhelm the PCT and end up getting to the DCT and casts form, causing backflow causing increased GFR or rupture of tubule into interstitial and nephritis

296
Q

what is the treatment for adult polycistic kidney disease?

A

blood pressure control

tolvaptan(?) bad side effects

297
Q

when do you see muddy brown casts?

A

acute tubular necrosis

298
Q

what is the urine sodium concetration in prerenal

A

less than 20

299
Q

SV, HR, SVR, CVP/wedge for hypovolemic shock

A

SV: low
HR: high
SVR: high
CVP/wedge: low

300
Q

SV, HR, SVR, CVP/wedge for cardiogenic shock

A

SV: low
HR: high
SVR: high
CVP/wedge: high

301
Q

SV, HR, SVR, CVP/wedge for obstructive shock

A

SV: low
HR: high
SVR: high
CVP/wedge: low/high (depending on where the obstruction is)

302
Q

SV, HR, SVR, CVP/wedge for neurogenic distributive shock

A

SV: low
HR: low
SVR: low
CVP/wedge: low

303
Q

SV, HR, SVR, CVP/wedge for anaphylactic distributive shock

A

SV: high
HR: high
SVR: low
CVP/wedge: low

304
Q

SV, HR, SVR, CVP/wedge for septic distributive shock

A

SV: depends on if infection is in heart too
HR: high
SVR: low
CVP/wedge: low

305
Q

does hypernatremia cause hypokalemia

A

no

306
Q

does hypomagnesemia contribute to hypokalemia

A

yes

307
Q

3 overall categories of causes of hypokalemia

A
  1. transcellular shifts
  2. GI losses
  3. increases in urinary potassium excretion
308
Q

does metabolic alkalosis lead to hypokalemia

A

yes

309
Q

4 things that cause potassium shifts into the cell and lead to hypokalemia

A

most stimulate sodium/potassium ATPase

  1. insulin
  2. B2 agonists
  3. alpha antagonists
  4. metabolic alkalosis
310
Q

6 things that cause potassium shifts out of cell and lead to hyperkalemia

A
  1. hyperglycemia
  2. B2 antagonists
  3. alpha agonists
  4. metabolic acidosis
  5. increases in osmolality (solute drag with water)
  6. exercise
311
Q

does vomiting lead to hypo or hyperkalemia

A

hypo - vomitting leads to an increase in plasma bicarbonate (because you’re losing H+ ions in gastric fluid), which leads to bicarb wasting –> increased distal Na delivery
ALSO volume depletion causes aldosterone increase –> enhanced potassium secretion from distal nephron

312
Q

does hypomagnesemia cause hyper or hypokalemia

A

hypo - magnesium acts as plug on ROMK backleak channel

313
Q

which genetic defect is similar to giving someone furosemide?

A

Bartter’s syndrome (thick ascending limb transporter defects)

314
Q

which genetic defect is similar to giving someone a thiazide?

A

Gitelman’s syndrome (Na-Cl co transproter in DCT)

315
Q

how can you tell the difference in urine labs between Gitelman’s and Bartter’s?

A

G has hypOcalciuria (because knocking out NaCl co transporter stimulates calcium reabsorbtion)

B and hypERcalciuria (stimulates calcium wasting into urine)

316
Q

when do you see U waves on EKG

A

Hypokalemia

317
Q

what does a ratio of >20 of aldosterone/renin mean

A

primary hyperaldosteronism

318
Q

what test would you do to diagnose primary hyperaldosteronism

A

CT abdomen and adrenal vein sampling - look for unilateral adrenal adenoma in CT and look for lateralization of cortisol and aldosterone from one side over the other (both being high would be bilateral adrenal hyperplasia)

319
Q

do thiazides produce hypo or hyperkalemia

A

hypokalemia

320
Q

do beta blockers cause hypo or hyperkalemia

A

hyperkalemia

321
Q

3 overall categories of causes of hyperkalemia

A
  1. impaired cell entry
  2. increased cell release (rhabdo, hemolysis)
  3. reduce urinary potassium excretion
322
Q

does renal failure cause hypo or hyperkalemia

A

hyper - limited number of nephrons to get rid of potassium

urine output declines, thus distal sodium and water delivery declines

323
Q

what do you see on EKG for hyperkalemia (4)

A
  1. K of 6-7: peaked T waves around
  2. K of 7-8: increased PR interval
  3. K of 8-9: lose the P wave, widened QRS
  4. > 9 sine wave pattern
324
Q

what do you give someone with hyperkalemia (4)

A
  1. calcium (stabilize cardiac membrane)
  2. D50/insulin (stimulate sodium/potassium ATPase)
  3. sodium bicarb (shift into cell via buffering - don’t give on dialysis)
  4. kayexalate (cation exchanger - enhances K excretion in the gut in exchange for sodium)
325
Q

what syndrome is associated with familial renal cell carcinoma?

A

Von Hipple Lindau

326
Q

what is the most common subtype of renal cell carcinoma?

A

clear cell renal cell carcinoma

327
Q

what is the most common grading system for renal cell carcinoma?

A

Fuhrman- 4 tiered based on:

  1. nuclear size
  2. pleomorphism
  3. nucleolar size

staging using TMN
(tumor size and invasion, nodal, metastesis)

328
Q

what is the most significant risk factor for pladder urothelial carcinoma

A

tobacco

329
Q

what diagnostic technique do you use to evaluate bladder tumors

A

CT urogram with contrast or cytoscopy

330
Q

what are the most common bladder cancers

A

epithelial transitional

331
Q

shistosoma causes what

A

squamous bladder cancer

332
Q

what is it, if you see fat in a kidney tumor

A

indicates angiomyolipoma - benign tumor

333
Q

what is the von hippel lindau mutation

A

AD mutation of gene on 3p25 (upregulate angiogenesis veg-f gene)
retinal tumors, pheo an kidney clear cell = multifocal and recurent

334
Q

what is tuberous sclerosis mutation and presentation (3)

A

AD mutation on chromosome 9 (hamartin) or 16 (tuberin)

triad:
metnal retardation,
adenoma sebaceum
seizures

335
Q

how to treat kidney tumors

A

surgery - chemo and radiation are not effective

336
Q

what does clear cell carcinoma look like grossly (3)

A
  1. gold yellow - due to glycogen and fat particles
  2. areas of necrosis and hemorrage
  3. clear demarcations
337
Q

what does clear cell carcinoma look like on histology

A

nests of cells with chickenwire capillary network and clear cells

338
Q

collecting duct carcinoma findings

A
  1. highly aggressive
  2. malignmant cells form glands
  3. prominent fibrotic stroma
339
Q

if you have a kid with abdominal mass and aniridia (messed up iris) what do you think

A

wilms tumor

340
Q

what does a wilms tumor look like grossly

A

white grey well circumsribed

341
Q

pathologic characteristics of of wilms tumor

A

primative looking triphasic:

  1. blastemal
  2. epithelial
  3. stroma
342
Q

what is WAGR syndrome? genetics?

A
  1. Wilms
  2. Aniridia
  3. Genital anomalies
  4. mental Retardation

associated with germline deletion of 11p13 WT1 gene

343
Q

two kinds of bladder tumor architecure

A
  1. papillary (most common) cauliflower like finger-like projections (low or high grade)
  2. flat
344
Q

treatment for non-muscle invasive tumors (3)

A
  1. resection
  2. BCG (TB vaccine)
  3. mitomycin (chemo)

recurrence is common

345
Q

treatment for muscle invasive (2)

A
  1. remove bladder,

2. neoadjuvent chemo

346
Q

what foods have a lot of oxalate in them

A

spinach, dark chocolate, tea

347
Q

what is struvite made from

A

magnesium-ammonium-phosphate

348
Q

do phosphates for in alkaline or acidic urine

A

alkaline

349
Q

what stone cannot be seen on xray

A

uric acid

350
Q

what causes uric acid stones

A

leukemia, lymphoma and chemo

351
Q

someone who has stones for a long time and is young, what do you think

A

cysteinuria (can’t reabsorb “cola” - cystein ornithine, lysine, arginine)

352
Q

5 categorical causes of secondary htn

A
  1. renal (renal parenchymal, obstruction)
  2. renovascular (renovasc htn, athero, aortic coarctation)
  3. endocrine (pheo, aldoste, cushing, thyroid, parathyroid)
  4. OSA (obstructive sleep apnea)
  5. Drugs (NSAIDs, birth control, steroids, sympathomimetics, cyclosporines, EPO, cocaine, alcohol)
353
Q

whats the gold standard for evaluating renovascular secondary HTN

A

renal angiogram

354
Q

what issue is seen with fibromuscular disease

A

renovascular hypertension in young women

355
Q

why does nephritic syndrome cause secondary htn

A

increased sodium retention

356
Q

apparent mineralocorticoid excess cause

A

glycyrrhizic is an inhibitor of 11 B HSD2 enzyme which converts active cortisol to cortisone

357
Q

pheochromocytoma cause, presentation and test

A

tumors arise from chromaffin cells of neural crest

present with
headache, weight loss, sweating, palpiitations, pallor, orthostatic hypotension

plasma free metanephrines and catecholamines in plasma, MIBG for extrarenal

358
Q

definition of htn emergency vs urgency

A 
emergency = signs of ACUTE end organ damage
urgency = NOT acute end organ damage
359
Q

cushing syndrome cause and findings

A

sustained glucocorticoid excess from ACTH production from pituitary adenoma or lung cancer or adrenal adenoma

see insulin resistance, muscle wasting, purple striae

360
Q

azathioprine mechanism

A

CYTOTOXIC ANTIMETABOLITE inhibit clonal expansion of lymphocyte population by inhibiting DNA replication

liver cleaves azathioprine to 6-MP, which is converted by lymphocytes to 6-thio-GTP and 6-thio-dGTP via purine salvage pathway –> GTP gets incorporated into RNA, dGTP gets incorporated into DNA, inhibiting lymphocyte function and proliferation

361
Q

azathioprine use (2)

A
  1. high doses prevent organ rejection

2. low doses treat autoimmune disorders like rheum arthritis

362
Q

azathioprine adverse effects (4)

A

older version. is toxic to all rapidly dividing cells:

  1. GI tox and
  2. bone marrow suppression
  3. potentiated adverse with methotrexate
  4. potentiated adverse with ACE inhibitor
363
Q

cotisol/glucocorticoid mechanism (2)

A

inhibit the transcription of pro-inflammatory cytokines

  1. bind to receptor, dimerization, binds to promotor region GRE have trancriptional repression of TNF-alpha, IL-1,2,4, and 6.
  2. also inhibit mobilization of arachydonic acid and prostaglandin transcription
364
Q

cortisol/glucocorticoid use (2)

A
  1. to prevent tissue allograft rejection

2. blocks first-dose cytokine storm cause by Muromonab-CD3 in transplant recipients

365
Q

cortisol/glucocorticoid adverse effects (6)

A
  1. growth suppression
  2. osteopenia
  3. infection
  4. inhibited wound healing
  5. hypertension
  6. hyperglycemia (esp when combined with calcineurin inhibitors)
366
Q

cyclosporine mechanism

A

CALCINEURIN INHIBITOR - inhibit clonal expansion and activation by inhibiting intracellular lymphocyte signalling

inhibit IL-2 production by binding to cyclophilin which then binds and inhibits calcineurin – can’t dephosphorylate NFAT to induce IL-2 expression

367
Q

cyclosporine use (2)

A
  1. prevent transplant rejection (dosing requires monitoring signs of rejection = low cyclosporine, or tox = high cyclosporine)
  2. autoimmune disorders
368
Q

cyclosporine adverse effects (4)

A
  1. metabolized by Cyp3A (inhibitors like CC blockers, HIV protease inhibitors, allopurinol cause increased cyclosporine levels, inducers like phenytoin, rifampin, phenobarbital lead to decreased cyclosporine levels)
  2. renal dysfunction/ nephrotoxicity (dose limiting)
  3. hypertension
  4. diabetogenic when used with glucocorticoids
369
Q

mycophenolate mofetil mechanism

A

CYTOTOXIC ANTIMETABOLITE inhibit clonal expansion of lymphocyte population by inhibiting DNA replication - more selective in suppressing immune cells over azathriopirne

hydrolized to active mycophenolic acid in liver, which inhibits enzyme (inositil monophosphate dehydrogenase type 2 IMPDH) in denovo purine pathway, inhibiting DNA syth

370
Q

mycophenolate mofetil use

A
  1. prophylaxis for organ transplant rejection

2. autoimmune disorders

371
Q

mycophenolate mofetil adverse effects (3)

A
  1. fewer tox (less GI or bone marrow suppression) because it’s selective for B and T lymphocytes, but still present
  2. decrease dosage of mycophenolate when using tacrolimus
  3. congenital abnormailties - pregnancy loss
372
Q

tacrolimus mechanism

A

CYCLOSPORINE INHIBITOR - inhibit clonal expansion and activation by inhibiting intracellular lymphocyte signalling

inhibit IL-2 production by binding to FKBP-12 which then binds and inhibits calcineurin – can’t dephosphorylate NFAT to induce IL-2 expression

373
Q

tacrolimus use (1)

A
  1. prevent trasnplant rejection by decreasing IL-2 production
374
Q

tacrolimus adverse effects (5)

A
  1. renal dysfunction/nephro
  2. hypertension
  3. diabetogenic esp when used with glucocorticoids
  4. neurotoxic - tremors, headaches, seizures
  5. metabolized by Cyp3A (inhibitors like CC blockers, HIV protease inhibitors, allopurinol cause increased tacrolimus levels, inducers like phenytoin, rifampin, phenobarbital lead to decreased tacrolimus levels)
375
Q

sirolimus mechanism

A

AKA rapamycin
mTOR inhibitor - prevents T-cell activation and proliferation by inhibiting protein synthesis

binds to FKBP-12 which then binds to mTOR which regularly progresses from G1-S phases – so you can’t activate and proliferate T cells

376
Q

sirolimus use

A
  1. prevent trasnplant rejection

2. targeted therapeutic agent for certain solid tumors

377
Q

sirolimus adverse effects (5)

A
  1. metabolized by Cyp3A (inhibitors like CC blockers, HIV protease inhibitors, allopurinol cause increased sirolimus levels, inducers like phenytoin, rifampin, phenobarbital lead to decreased sirolimus levels)
  2. dose dependent hylerlipidemia
  3. dose dependent hypertension
  4. myelosuppression
  5. lymphocoele around renal transplantation
378
Q

how does 6-MP get metabolized/inactivated? (2)

A
  1. xanthine oxidase (which is decreased by gout drug allipurinol)
  2. TPMT - polymorphic gene - WT works properly, inactive allele doesn’t
379
Q

what’s the most common induction agent for kidney transplant immunosuppression

A

thymoglobuin

380
Q

what’s the most common maintenenece agent for kidney transplant immunosuppression

A

tacrolimus

381
Q

thymoglobulin mechanism, use and side effects

A

rabid derived polyclonal antibody which depletes lymphocytes

used as induction agent and in severe acute rejections

side effects: fever, arhtralgias, aseptic menngitis, marrow suppression, CMV, EBV infections

382
Q

common infections in solid organ transplant patients at <1mo, 1-6mo and >6mo

A

<1mo = common infections like mRSA

1-6mo = viral infections like CMV

> 6mo = less common infections like aspergillus and mucor

383
Q

top 3 reasons people get lung trasnplants

A

COPD, CF, IPF

384
Q

ABSOLUTE contraindications for lung transplants (8)

A
  1. cancer in the last 2 years (excluding BCC and SCC)
  2. dysfunction of another system (heart, liver, kidney)
  3. chronic infection (hep C, HIV)
  4. chest wall/spinal deformity
  5. non-adherence
  6. psych condition
  7. no social support
  8. substance abuse within 6 months
385
Q

lung allocation score goals (3)

A
  1. reduce mortality among patients on waiting list
  2. urgency-based prioritization
  3. deemphasize the role of waiting time and geography
386
Q

what are the types of lung transplants (3)

A
  1. bilateral (best for suppurative diseases like CF and bronchiectasis)
  2. single lung transplant
  3. heart-lung transplant (if you have eisenmenger with uncorrectable cardiac anomaly)
387
Q

what do you see with primary graft dysfunction, what do you do

A

within first 72 hours, reperfusion injury - alveolar damage and hypoxemia - most patients recover, but monitor

388
Q

what do you see with acute rejection, what do you do

A

within first 3 months
see inflammatory infiltration, decline in FEV and FVC
give steroids

389
Q

what do you see with chronic rejection, what do you do

A

within first 5 years
bronchiolitis obliterans. irreversible decline in FEV1, don’t do well, no treatment - major cause of mortality and morbidity

390
Q

post-transplant lymphoproliferative disorder cause, clinical, treatment

A

B cell lymphoma that’s EBV related

see CXR nodular density within first year after transplant

treat by REDUCING immune suppression

391
Q

mortality is better or worse for lung vs kidney trasnplant

A

worst for lung

392
Q

amygdala and aging

A

amygdala enhance positive emotional memory and allow older adults to disengage from experiences of regret - dependent on exercise, social interaction and environmental enrichment

393
Q

frailty components (5)

A
  1. reduced 2. walking speed
  2. longer time to perform ADL
  3. weight loss (more than 10% in the last 6 months)
  4. muscle wasting
394
Q

cardiac aging and cardiac output factors (3)

A
  1. left ventricular stiffness (decreases preload and ejection fraction)
  2. decreased aortic compliance (increased afterload, decreased ejection fraction)
  3. altered calcium (decreases myocardial contraction and HR, decreased ejection fraction) and decreased CO
395
Q

normal renal aging (4)

A
  1. sclerosis
  2. atrophy
  3. loss of glomeruli and total mass
  4. reduction of functional reserve
396
Q

what do you need to do as a physician for decreasing changes of renal failure in older adults (2)

A
  1. encourage fluids to avoid infection - beware of decreased fluid intake
  2. be careful what you prescribe
397
Q

pulmonary homeostenosis and aging (6)

A
  1. FEV1 declines
  2. decreased vital capacity
  3. enlargment of alveolar ducts due to loss of elastic tissue
  4. calcified constrochondral cartilage - less chest expansion
  5. abdominal muscles used in respiration - only effective while standing
  6. coughs less vigorous
  7. cilia is less effective
398
Q

what do K antigens do

A

make bacteria more virulent in urinary tract

399
Q

what do fimbrae do

A

make bacgeria more adherent to vaginal/uroepithelial cells (T type, type 1)

400
Q

what is aerobactin

A

iron scavenging protein in bacteria

401
Q

where is antibody response in urinary tract?

A

upper tract - pre-existing, but not protective

402
Q

epidermidis vs saprophyticus patients

A

sapro is more female, more young, more common, more symptomatic, more outpatient, rarely relapse and are often antibacterial sensitive

403
Q

candiduria

A

endoegnous flora

can be associated with cystitis -associated with DM and foley

can get hematogenous

if symptomatic treat with fluconazole (some are resistant to fluconazole though - cruzii and fibrata)

404
Q

what is the definition of chronic kidney disease (2)

A

kidney damage for >3 months with structural/functional abnormalities with/without decreased GFR

OR

GFR <60mL/min per 1.73m for >3mo with or without kidney damage

405
Q

populations at risk for CKD (2)

A

older age

african americans 4x more likely (have APOL-1 and MYH-9 loci)

406
Q

cystatin c

A

to measure AKD and somewhat CKD

407
Q

CKD staging - axes

A

A1-3 = albuminuria categoies (<30 to >300)

G1-G5 = GFR (>90 to <15)

408
Q

how may people >20 years have CKD

A

20 million

409
Q

how to get patients to inhibit RAAS to reduce GFR (3)

A
  1. low protein dient
  2. ACE/ARB
  3. aldosterone antagonist
410
Q

how to reduce proteinuria (2)

A
  1. ACE/ARB

2. statin

411
Q

what medicines should you avoid in chronic kidney disease

A
  1. metformin (causes lactic acidosis)
  2. IV contrast
  3. NSAIDs
  4. herbal medications
  5. aminoglycoside antibiotics (-mycins)
412
Q

calcium, phosphate and magnesium in CKD

A

hypocalcemia
hyperphosphatemia
hypermagnesemia

413
Q

two broad categories of health disparities

A

health (differences in morbidity and mortality across all disease categories)

and

health care (access, utilization, quality and outcomes)

414
Q

disparity = difference?

A

disparities are differences that should not happen -that would not occur through normal physiology

415
Q

RTA type 1

A

most severe phenotype = defect in distal tubule, impaired proton excretion, urine pH >5.3 (no room for nephron to kick out protons)

416
Q

RTA type 2

A

less severe phenotype = defect in proximal tubule, HCO3 wasting, variable pH depnding on level of HCO3 wasting

417
Q

RTA type 4

A

issue with aldosterone deficiency or resistance

418
Q

anion gap metabolic acidosis

A

C- citrate
U- uremia
T- toluene
E- ethanol

D- diabetic ketoacidosis
I- iron
M- methanol
P- paraldehyde
L- lactate
E- ethylene glycol
S- salicylate

ALL are ingestions except:

  • uremia
  • ketoacidosis
  • lactic acidosis
419
Q

what equation to use to see if there’s more than one metabolic distrubance

A

delta gap = change in AG/change in bicarb

every time anion gap goes up by1, your bicarb should go down by 1 –> normal delta gap is between 1 and 2

> 2 coexisting metabolic alkalosis (bicarb is higher than it should be)

<1 coexisting non-gap metabolic acidosis - diarrhea and lactic acidosis for example (bicarb is lower than it should be)

420
Q

how to tell if metabolic acidosis is due to diarrhea or renal tubular acidosis

A

urine AG = urine (Na + K) - Cl

if diarrhea and kidenyes are functioning, urine AG should be negative

if RTA, urine AG is positive - can’t get rid of enough Cl in urine

421
Q

anion gap equation

A

= Na - (Cl + bicarb)

422
Q

how can you tell if there’s appropriate compensation for a metabolic acidosis?

A

pCO2 = 1.5 (bicarb) + 8 +/- 2

(winter’s formula)

too high much means you also have a respiratory acidosis

423
Q

how can you tell if there’s appropriate compensation for a metabolic alkalosis?

A

pCO2 = 0.7 + (change in bicarb) + 40

424
Q

for acute respiratory acidosis, what happens to bicarb when CO2 changes

A

every change in CO2 by 10 causes a change in bicarb by 1

425
Q

metabolic alkalosis is usually seen with what chlorine and potassium levels

A

hypochloremia and hypokalemia

426
Q

what things generate a metabolic alkalosis (3 categories, 10 total)

A

GI proton losses:

  1. vomitting
  2. nasogastric suction
  3. villous adenoma
  4. congenital chloridorrhea

Renal proton losses:

  1. diuretics (loop and thiazide)
  2. transport defects
  3. mineralocorticoid excess
  4. posthypercapnia

addition of bicarb:

  1. hypercalcemia
  2. blood transfusion
427
Q

what things maintain a metabolic alkalosis (4)

A
  1. hypovolemia
  2. hypochloremia
  3. hypokalemia
  4. mineralocortiocoid excess
428
Q

normal compensation for metabolic alkalosis

A

respiratory acidosis - hypoventilation

429
Q

what ion do you look for in urine in metabolic alkalosis

A

Cl

if urine Cl is low, give them Cl (sodium chloride or potassium chloride if hypokalemic)
(they’re usually volume depleted)

if urine Cl is high, probably volume exapnded so you have to treat underlying issue

430
Q

if urine clhoride is low in metabolic alkalosis and blood pressure is HIGH what do you do next

A

look at RENIN

if renin is high, and cortisol is high: 
- cushings
if cortisol is low:
- renal artery stensosi
- malignant htn
, renin secreting tumor
- accellerated htn

if renin is low, could be

  1. primary aldosteronism
  2. licorice abuse,
  3. liddle’s syndrome
431
Q

if urin chloride is low in metabolic alkalosis and blood pressure is LOW or NORMAL, what do you think

A
  1. bartter’s syndrome
  2. gitelman’s syndrome
  3. diuretic use
432
Q

if urien chloride is low with metabolic alkalsosi, what could it be

A
  1. gastric fluid loss (vommitting)
  2. non-reabsorbable anion delivery
  3. post diuretic use
  4. post hypercapnea
  5. villous adenoma
  6. congenital chloridorrhea
433
Q

what does pregnancy cause (acid-base)

A

chronic respiratory alkalosis

434
Q

the two ways you can lose bicarbonate

A
  • big tubule (diarrhea = same number of unmeasured anions, higher Cl)
  • small tubule (tubular disfunction RTA2, normal anion gap)
435
Q

mechanisms of developing metabolic acidosis

A
  1. acid overload (increased acid production or addition - HCl or NH4Cl)
  2. decreased acid excretion (renal failure or RTA1)
  3. loss of bicarb ions (diarrhea or RTA2)
436
Q

causes of normal anion gap metabolic acidosis

A

renal issues:

  1. proximal RTA
  2. distal RTA
  3. hyperkalemic distal RTA
  4. early renal failure

GI issues:

  1. diarrhea
  2. small bowel losses
  3. ureteral diversions
  4. anion exchange resins
  5. ingestion of CaCl2

acid infusion:

  1. HCl
  2. Ariginine HCl
  3. Lysine HCl
437
Q

what is the relationship between insulin and potassium secretion?

A

insulin deficiency causes loss of potassium

438
Q

effectiveness vs efficacy

A 
efficacy = in study
effectiveness = in real world

CPR (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions