1What do the kidneys modulate?
endocrine function
blood pressure
solute and water transport
acid base balance
waste/toxin/metabolite excretion
2What is the functional unit of the kidney?
nephron
3What makes up the neprhon?
glomerulus
tubules
4What are the majority of nephrons?
cortical
5What are cortical nephrons responsible for?
filtration
6What are cortical nephrons surrounded by?
peritubular capillaries
7Where are cortical nephrons located?
mid to outer cortex of the kidney
8What is the other type of nephron?
juxtamedullary
9Where are the juxtamedullary nephrons located?
boundary of cortex and outer medulla
10What are the juxtamedullary nephrons surrounded by?
individual capillaries (vasa recta)
11What is the main function of the juxtamedullary nephrons?
create osmotic gradient for concentrating urine
12What are the 3 major factors involved in autoregulation of GFR?
myogenic reflex
tubuloglomerular feedback
angiotensin II
13What is the first line defense against fluctuations in renal flow? What does it act on?
myogenic reflex
afferent arteriole
14What is the tubulo-glomerular feedback?
changes the rate of filtration by constricting/dilating the afferent arteriole
15Where are the tight epithelia found?
collecting ducts
16Where are the leaky epithelia found?
proximal tubule
17What are the leaky epithelia good for?
bulk fluid reabsorption
18What are the tight epithelia good for?
more refined control or regulation
19Aldosterone boosts the activity of:
sodium/potassium channels
20What are the 2 types of dysfunction with renal disorders?
glomerular dysfunction
tubular dysfunction
21What is a hallmark finding of glomerular dysfunction?
albuminuria
22What can cause tubular dysfunction?
electrolyte disorders
disorders of concentration
23True/False CKD has elements of both tubular dysfunction and glomerular dysfunction?
true
24What are the nephritis syndromes?
glomerulonephritis
tubulointerstitial nephritis
acute allergic or immune interstitial nephritis
nephrotic syndrome
25What s/s should raise your suspicion for glomerulonephritis?
hypertension
edema
proteinuria
hematuria
cellular casts
26What are the post renal causes of AKI?
obstruction caused by stone and prostate hypertrophy
27What is the second most common cause of CKD?
hypertension
28C3 complement suggests
lupus
29What is a common cause of acute allergic and immune interstitial nephritis?
hx of new medication or recent change in medications
30What drugs are the common culprits of acute allergic and immune interstitial nephritis?
NSAIDs
ampicillin
31What are the clinical findings for acute allergic and immune interstitial nephritis?
fever
rash
eosinphilia (not present if caused by NSAID)
32What are the other common drugs causing AIN?
PPIs
sulfa drugs
thiazides
furosemide
rifampin
33What are the three clinical findings of nephrotic syndrome?
edema
hypoalbuminemia
proteinuria
34Nephrotic syndrome is often associated with ?
high LDL
low HDL
lipiduria
35What will you see on microscopic urinalysis with nephrotic syndrome?
oval fat bodies in urine
fatty casts
36What are the common presentations of a lower UTI?
frequency
urgency
dysuria
37What are the pre-renal causes of AKI?
decreased renal performance from drugs or hypotension
renal artery stenosis
heart failure
hemorrhage
38What are the intrinsic causes of AKI?
damage to the renal tubules by gram negative sepsis, toxins, myoglobinuria
glomerulonephritis
tubular necrosis
interstitial nephritis
39What are the post renal causes of AKI?
obstruction caused by stone and prostate hypertrophy
nephrolithiasis
BPH
neoplasm
40What are some things that can develop
sodium and water balance
potassium balance
elimination of nitrogenous waste
erythropoietin production
acid base balance
activation of vitamin D
phosphate elimination
41What is the most common cause of CKD?
diabetes
42How does diabetes cause CKD?
hyperglycemia causes an overproduction of reactive oxygen species which leads to a production of inflammatory cytokines and overproduction of growth factors
43What is the second most common cause of CKD?
hypertension
44How does hypertension cause CKD?
HTN leads to thickening of renal arterial wall which causes a narrowing of arterial lumen and decreased perfusion though the afferent arteriole this effects the RAAS system by activating and causing increased HR and BP (continous loop)
45Hypertension causes what specific to the glomerulas?
glomerular sclerosis
46What are the two types of polycystic kidney disease?
autosomal recessive
autosomal dominant
47Why type of polycystic kidney disease is more common?
autosomal dominant
48What is the typical age of diagnosis for autosomal dominant polycystic kidney disease?
30-40
49What is mutated with autosomal dominant polycystic kidney disease?
PKD1 and PKD2
50What imaging can you see autosomal dominant polycystic kidney disease on and how is it found?
CT, MRI, US
often seen incidentally
51How does autosomal dominant polycystic kidney disease progress?
cyst enlarges and compromises healthy renal tissue
52What is diagnostic for autosomal dominant PKD from ages 15-29?
more than 2 cysts (unilateral or bilateral)
53What is diagnostic for autosomal dominant PKD in patients ages 30-59?
2 cysts bilaterally
54What is diagnostic for autosomal dominant PKD in patients older than 60?
4 cysts bilaterally
55T/F a 70 year old patient with 4 cysts bilaterally but with no history of cysts prior would be diagnosed with PKD
false
if the patient does not have ANY cysts between the age of 30-59 they do not have PKD
56What are some ways to manage autosomal dominant PKD since there is no cure?
HTN/DM
low protein diet
eventually they will require renal replacement therapy
57What is the mutation for autosomal recessive PKD?
PKHD1
58When are patients with autosomal recessive PKD diagnosed?
in utero
59What are patients with autosomal recessive PKD born with?
ESRD
60reduced fetal urine production seen with autosomal recessive PKD causes?
pulmonary hypoplasia
61What is the dietary intake of sodium in comparison to excretion in patients with CKD?
dietary intake is greater than excretion
62Glomerular hyperfiltration leads to
increased pressure which causes glomerular sclerosis which decreases GFR and urinary output
63What should paients be counseled on with sodium and water balance?
restricting salt in their diet
64What does sodium and water balance cause?
increased extracellular volume which leads to hypertension which causes damage to the nephron leading to more extra cellular volume
65What is used to manage the edema/HTN?
diuretics
66When do thiazide diuretics start to have limited use in patients with CKD? What should be added?
stage 3-5
loop diuretics
67When managing the patients fluids what should you consider?
the patient with have extra renal fluid loss in the GI tract which leads to under perfusion causing a pre-renal injury leading to an acute on chronic renal failure
68What should you do to manage the extra renal fluid loss through the GI tract?
hold or adjust dose of diuretics
69What will you see in patients with CKD caused by potassium balance?
muscle weakness
EKG changes
fibrillation
70How does CKD cause hyperkalemia?
loss of nephrons causes decreased renin which leads to decreased aldosterone which causes dysfunction in the Na+/K pump leading to potassium retention
71How do you treat potassium balance?
potassium sparing diuretics/ACE inhibitors
72How does CKD cause acid base balance?
diminished capacity to excrete hydrogen iions
diminished capacity to generate bicarb
this lead to metabolic acidosis
73How does CKD lead to mineral balance and osteodystrophy?
decreased capacity of the nephron leads to decreased capacity to excreted phosphates which causes phosphate retention
phosphate retention causes synthesis of PTH which causes parathyroid gland hypertrophy/mass
Parathyroid enlargement causes decreased production of calcitriol and decreased levels of calcium which leads to parathyroid stimulation and secondary hyperparathyroidism ultimately causing skeletal demineralization
74What are the side effects of uremia?
hiccups and muscle cramps
75What else can uremia cause?
anorexia
vomiting
amenorrhea
impotence
decreased ibido
pruritus
76What is erythropoetin?
glycoprotein responsible for RBC production
77Where is erythropoietin made?
kidney
78How does CKD cause anemia?
nephron destruction leads to decreased production of erythropoietin which causes decrease stimulation of erythropoiesis causing decrease in RBC production
79What are the risk factors for CKD?
HTN
DM
autoimmune dz
advanced age over 60
prior AKI
family hx
small gestation age or birth weight
childhood obesity
african ancestry
80What is the normal peak GFR? How much does it decline?
120 mL/min
delines 1 mL/min per 1.73 m2 per year
81When are the CKD-EPI and MDRD no accurate?
pregnancy
acute rheumatic fever
comorbidities (sepsis)
82When is CKD-EPI more accurate?
if GFR estimate is greater than 60
83What do you worry about with cockcroft-gault equation?
risk of over-estimating renal function resulting in overdose on medications with renal clearance
84What is a normal albumin/cr ratio?
less than 30
85What is azotemia?
increased concentration of urea and other nitrogen products in the bloodstream
86What systemic changes does uremic syndrome cause?
vasculitis
vascular insufficiency
malnutrition
87What are the two renal replacement therapies?
peritoneal dialysis
hemodialysis
88What are the complications of peritoneal dialysis?
peritonitis (over 100 WBC in peritoneal fluid)
weight gain
residual uremia
89Which is the first access site for hemodialysis?
fistula
90What are the complications of hemodialysis?
hypotension
muscle cramps
allergic reaction to dialyzer
91Which donor do you get longer life expectancy for a kidney transplant?
living donor
92What causes syphilis?
treponemia pallidum (spirochete)
93How is treponema pallidum seen?
dark field microscopsy
94What are the s/s of primary syphillis?
chancre
regional lymphadenopathy
95What is the classic triad of an ulcer of syphilis?
non-tender
nonpurulent
indurated
96T/F you should use darkfield microscopy to examine oral lesions
false
97What are the 2 serologic tests for syphilis?
nontreponemal and treponemal
98T/F nontreponemal serologic tests are not specific for T. pallidum?
true
99What are the nontreponemal serological tests?
CDRL
RPR
TRUST
100When do nontreponemal serological tests become positive?
4-6 weeks after infections
101What are the disadvantages to nontreponemal seroligic tests?
insensitive in certain stages
false positive reactions may occur
102Which test is used to assess treatment response?
nontreponemal serologic tests
103What are the two types of treponemal serologic tests?
TP-PA (T. pallidum particle agglutination assay)
FTA-ABS (checks for antibodies to the bacteria that cause syphilis)
104False positive treponemal serologic tests can occur with what disorders?
SLE
malaria
other spirochetal infections
105What is the treatment for primary syphilis?
PCN G 2.4 millions unit IM
106What are some alternatives to PCN?
doxy 100 mg PO BID x 14 days
tetracycline 500 mg PO QID x 14 days
ceftriaxone 1g IM x 8-10 days
107What is a side effect of treatment of syphilis?
jarisch-herxheimer reaction
108T/F jarisch herxheimer reaction is a reaction to the penicillin?
false- its a reaction to the sudden killing of spirochetes after treatment and the release of toxins
109If a patient was recently exposed to syphilis within the last 3 months and seronegative should you treat them?
yes
110How often should patients treated with syphilis be monitored with serological nontreponemal titers?
every 3-6 months
111In primary and secondary syphilis titers should be expected to decrease..
fourfold by 12 month
112What should you do if a patient is reinfected or therapy failed?
HIV test
lumbar puncture
113When do the secondary lesions occur?
after the primary chancre appears
114How do the secondary lesions look?
nonpruritic
macular
papular
pustular
follicular
115Where are the lesions commonly found in secondary syphilis?
palms and soles
116What are the clinical manifestations of secondary syphilis?
rash
lymphadenopathy
malaise
mucous patches (lips, throat, mouth, genitalia and anus)
condylomata lata
alopecia
liver/kidney involvement
splenomegaly
117At which stage is there meningeal, hepatic, renal, bone and joint invasion?
secondary
118What is the treatment for secondary syphilis?
PCN G 18-24 million units IV daily every 3-4 hours or continuous infusion for 10-14 days
119What do you do if secondary syphilis has involvement with the CNS, ocular disease or neurological s/s?
lumbar puncture
if positive treat like neurosyphilis
120What is latent syphilis?
no lesions are clinically apparent
only evidence is positive serologic test
history of syphilis with inadequate tx
121What is early latent syphilis?
infection less than 1 year after primary infection
122What is late latent syphilis?
infection greater than one year
123How do you treat early latent syphilis? When would you not treat it this way?
PCN G 2.4 million units IM once
if CNS disease is present
124How do you treat late latent syphilis?
PCN G 2.4 million units IM every week for 3 weeks
125What should you do if there is CNS involvement with late latent syphilis?
LP
126What should you consider about titer decline with latent syphilis?
may not decline as rapidly
127What is tertiary late syphilis?
delayed hypersensitivity reaction of the tissue to the organism
128What are the common tissues or organs involved in tertiary (late syphilis)?
skin/mucous membranes
skeletal system
eyes
respiratory system
GI system
CVS system
Neuro system
129What are the clinical findings in tertiary (late) syphilis?
skin gummas
nodular gummas on mucous membranes
muscle pain severe at night
hoarseness
respiratory distress
wheezing
epigastric pain
regurg
belching
weight loss
CVS
130What is the treatment in tertiary (late) syphilis?
PCN G 2.4 million units IM every week for 3 weeks
131Will you get negative serologic tests despite treatment of tertiary syphilis?
no they will always be positive
132When can neurosyphilis occur?
at any stage of syphilis and decades after infection
133What are the clinical manifestations of early neurosyphilis?
acute syphilitic meningitis
meningovascular syphilis
ocular movements
134What is the treatment for neurosyphilis?
treatment with higher doses of PCN
135When are serological tests done?
every 3-6 months
136When do you do CSF examinations?
6 month intervals until CSF count is nl
137When is syphilis screened in pregnancy?
1st PN visit
28 weeks
delivery
138What is the only treatment option in pregnant patients?
penicillin
139When do infants show signs of congenital syphilis?
6-8 weeks of life
140What are common findings of congenital syphilis?
skin rash
condylomas
mucous membrane patches
nasal discharge
141What can happen if congenital syphilis goes untreated?
keratitis
hutchinson teeth
saddle nose
deafness
CNS involvement
142What are indications of probable treatment failure or reinfection?
persistent or recurring clinical s/s
substained 4-fold increase in titer
titer fails to show a 4-fold decrease w/ in 6-12 months
143What causes gonorrhea?
N. gonorrhoeae- gram negative dioplococcus
144Where does N. gonorrhoeae infection?
mucous membranes of the reproductive tract, mouth, throat, eyes and rectum
145What are the s/s of urethritis in a male infected with gonorrhea?
dysuria
urethral discarge
urethral pain
146What are the s/s of female urogenital infection of gonorrhea?
usually asymptomatic until it becomes PID
vaginal discharge
dysuria
urinary frequency
labial pain/swelling
147When else can gonorrhea become symptomatic?
during menses
148What are the s/s of rectal infection of gonorrhea?
discharge
anal itching
soreness
bleeding
painful bowel movements
asyptomatic
149What is the diagnostic test for gonorrhea?
nucleic acid amplification tests
females- endocervical or vaginal swab and first catch urine
males- first catch urine
150What are the complications of gonorrhea in females?
PID
151What are the complications of gonorrhea in men?
epididymitis
urethral strictures
infertility
152What is a disseminated disease in patients with gonorrhea?
purulent arthritis
153What is the triad for purulent arthitis?
rash
tenosynovitis
arthralgias
154How are uncomplicated gonococcal infections of the cervix, urethra and rectum treated?
ceftriaxone 250 mg IM
azithromycin 1 GM PO x 1
155What is the treatment for disseminated gonococcal infection?
ceftriaxone 1 GM IV daily
Azithromycin 1 GM PO x 1
for 48 hours after improvement begins then therapy is switched to cefixime 400 mg PO daily x 1 week
156What causes chancroid?
short gram negative bacillus H. ducreyi
157S/S of chancroid?
painful soft ulcer with a necrotic base
surrounding eythema
undermined edges
158How is chancroid diagnosed?
culturing a lesion
159What is the treatment for chancroid?
azithromycin 1 gm PO x 1
or
ceftriaxone 250 mg IM x 1
160S/S of women with chlamydia clinical findings?
asymptomatic
s/s of cervicitis and PID
161How do the s/s of gonococcal infections compare to chlamydia infections in women?
urethral/cervical discharge is less painful, less purulent and watery compared to gonococcal
162What are the clinical findings of chlamydia in men?
discharge
dysuria
epididymitis
163What are the s/s of rectal chlamydia?
rectal pain
discharge
bleeding
164What are the complications of chlamydia?
PID
infertility (men and women)
ectopic pregnancy
165What are the lab tests for chlamydia?
culture (vagina, penis, rectum or urine)
nucleic acid amplification test
166What is the treatmet for chlamydia?
axithromycin 1 gm PO x 1 (safe in pregnancy)
doxycycline 100 mg PO BID x 7 days
levofloxacin 500 mg PO QD x 7 days
167Who is recommended for chlamydia screenings?
pregnant women
sexually active women under 25
older women with risk factors for STDs
men with risk factors for STDs (HIV positive or MSM)
168What causes lymphogranuloma venereum (LGV)?
C. trachomatis
169What is a red flag for LGV?
recent travel to endemic area
170What is the treatment for LGV?
doxycycline 100 mg PO BID x 21 days
erythromycin 500 mg QID x 21 days
Azithromycin 1 gm PO qweek x 3