Renal and Repro-Final things I should know Flashcards
(607 cards)
1
Q
mesonephros
A
function as interim kidney for first trimester, later contributes to male genital system.
2
Q
metanephros
A
permanent, first appears in fifth week of gestation, nephrogenetisis continues through 32-36 weeks
3
Q
what is the uteric bud derived from
A
the caudal end to the mesonephric duct
4
Q
what does the uteric bud give rise to
A
it gives rise to the ureters, pelvises, calyces, collecting ducts, fully canalized by tenth week.
5
Q
what does the metanephric mesenchyme give rise to
A
it is where the uteric bud interacts with the tissue and the interaction induces differentiation and formation of glomerulus through to distal convaluted tubeless.
6
Q
what is the uteropelvic junction and what happens to it
A
last to canalize and most common site obstruction with hydronphrosis- this is usually seen by the second trimester on ultrasound and if not, it is seen at birth with a large kidney and an enlarge kidney
7
Q
vesicoureteral reflux
A
incomplete closure lead to dilation and chronic non-obstructive hydronehrosis and increased risk of infection
8
Q
what poles of the kidneys fuse on horseshoe kidney
A
it is inferior poles that are fused.
9
Q
what does the horseshoe kidney get stuck on
A
IMA
10
Q
what are horseshoe kidneys associated with
A
hydronephrosis, renal stones, infection, chromosomal aneuploidy and sometimes cancer
11
Q
unilateral renal agenesis
A
uteric bud fails to develp and induce differentiation of metanephrtic mesenchyme so complete absence of kidney and ureter
12
Q
multicystic dysplasic kidney
A
uretic bud fails to induce differentiation of metanephric mesenchyme so nonfunctional kidney consisting of cysts and connective tissue.
13
Q
duplex collecting system
A
bifurcation of uremic bud before it endter the metaphors, which creates a bifid ureter so vesicoureteral reflux and ureteral obstruction so increased risk of UTI
14
Q
congenital solitary functioning kidney
A
condition of being born with only one functioning kidney. Asymptomatic with compensatory hypertrophy of contralateral kidney. anomalies in the contralateral kidney are common
15
Q
fetal hydronephrosis
A
renal pelvis is highly compliant so if there is an abstraction it can cause hydronephrosis at the kick or narrowing of the proximal ureter at the uteropelvic junction. Can see it on ultrasound of a palpable mass and enlarged kidney in a child
16
Q
which kidney is taken for transplant and why
A
the left is taken because of the longer renal vein
17
Q
what is the renal blood flow
A
it is renal artery- segmental artery- interlobular artery- arcuate artery-interlobular arteries- afferent arterile–glomerulus- efferent arteriole- vasa recta-peritubular capillaries-venous outflow
18
Q
what is the arriving after to the glomerulus and which is the one leaving
A
it is afferent and efferent
19
Q
what does the ureter pass under
A
the uterine artery or under the vas deferens
20
Q
what can damage the ureters
A
ligation of uterine or ovarian vessels can damage it causes obstruction or leak
21
Q
pain and fever after a hysterectomy- what went wrong
A
one ureter is damaged and leading leading to fever and pain, but can still make urine because the other side is fine
22
Q
what can plasma volume be measured by
A
it can be measured by radiolabelled albumin
23
Q
extracellular volume can be measured by what
A
mannitol and inulin
24
Q
what is the percent water per body weight
A
- 60% of total body water
- 40% is the ICF
- 20% is the ECF
25
what is the normal body mass
70Kg
26
what is the glomerular filtration barrier composed of
it is fenestrated capillary endothelium, fused basement membrane that has heparin sulfate which is a negative charge and size barrier, and epithelial layer of podocytes for negative charge
27
when the charge barrier lost and what happens if it is lost
it is lost in nephrotic syndrome and it causes albuminuria, hyporpoteinemia, generalized edema, and hyperlipidemia
28
what is the formula for renal clearance
it is UV/P= volume of plasma from which the substance is completely cleared per unit time.
U is urine concentration of the substance
V is flow rate
29
what can be used to calculate clearance
inulin because its filtered and not reabsorbed or secreted
30
what is the GFR formula
UV/P
31
what is normal GFR
100
32
what is the substance used for estimating GFR
it is creatinine clearance is an approximate measure of GFR and it slightly overestimates GFR because creatinine is moderately secreted at the tubules
33
what does incremental reductions in GFR define
chronic kidney disease
34
what estimates RPF
PAH clearance is used because between filtration and secretion there is 100% excretion of all PAH that enters the kidneys
35
what is the formula for RPF
UV/P
36
what is the formula of RBF
RPF/(1-hct)
37
Cx
net tubular reabsroption
38
Cx>GFR
net tubular secretion
39
Cx=GFR
no net secretion or reabsorption
40
what is normal FF
20%
41
what is the formal of FF
GFR/RPF
42
what represents the P part of the net filtration pressure
hydrostatic and glomerular
43
what is the pi part of the net filtration pressure
oncotic pressure and bowman space
44
what happens to GFR, RPF, and FF with afferent arteriole constriction- also what drug causes this
decreased GFR, decreased RPF, and no change in FF- NSAIDs
45
what happens to GFR, RPF, and FF with efferent arteriole constriction- what can cause this
Increased GFR, decreased RPF, increased FF- and this is from ATII
46
what happens to GFR, RPF, and FF with increased plasma protein concentration
decreased GFR, no change in RPF and decreased FF
47
what happens to GFR, RPF, and FF with decreased plasma protein concentration
increased GFR, no change to RPF, and increased FF
48
what happens to GFR, RPF, and FF with constriction of the ureter
decreased GFR and decreased FF
49
what happens to GFR, RPF, and FF with dehydration
decreased GFR, decreased RPF, and increased FF
50
what happens to GFR, RPF, and FF with dilation of the efferent arteriole and what causes this
decreased GFR, increased RPF, decreased FF this is from ace inhibitors
51
how do you calculate the reabsortion
filtered-excreted
52
how do you calculate secretion
excreted-filtered
53
what is the FENa formula
Na excreted/Na filtered
54
where is glucose usually reabsorbed and by what receptor
it is usually from the PCT by the Na/hlucose cotransporter
55
where does glucosuria begin and when is it saturated
it starts at 200 and 375 is saturated
56
normal pregnancy does what to glucose clearance
it decreases the ability of the PCT to reabsorb glucose and amino acids- glycosuria and aminoaciduria
57
what is the splay region of glucose clearance from
its the region of substance clearance between threshold and Tm due to heterogeneity of the nephrons
58
what does the PCT reabsorb
all glucose, amino acids
most of the HCo3, Na, Cl, Po4, K, and H2O and uric acid
it generaties and decreased Nh3 to buffer H
59
where does PTH work in the kidney and what does it do
it works on the PCT and it inhibits the Na/Po4 cotranport so that Po4 is exctered
60
what does ATII do at the PCT
it increased Na and H2O and Hcro reabsorption leading to contraction alkalosis
61
what does the thin descending loop of here do
passively reabsobs H20 via medullary hypertonicity and its impermeable to Na making this the concentrating segment
62
what does the TAL do
it reabsorbed Na K and Cl by actively pumping it out. Mg and Ca pass though the lumen to create K backleak. It is impermeable to H20 and helps creates the gradient for the thin limb
63
Early DCT function
reabsorbed the Na and Cl and it makes urine fully dilute.
64
what does PTH do at the DCT
it increases the Ca/Na exchanges to increase Ca reabsorption
65
Collectung tubule function
it reabsorbed Na in exchange for K and H
66
what does aldosterone do at the CT
it increases protein synthesis and in the principal cells it increases K secretion. and in the intercalated cells, it increaes the activity of the hoco3/cl exchanger
67
what does ADH do at the CT
it acts at the V2 receptor and inserts aquaporins into the apical side
68
what blocks the V2 receptors
Lithium
69
Fanconi syndrome- what is it doing
generalized reabsorptive defect in the Pct, and it is associated with increased excretion of nearly all AA, glucose, Hco3 and Po4. May result in associated metabolic acidosis
70
what are the causes of Fanconi
Wilson, tyrosinemia, glycogen storage disorder, ischemia, multiple myeloma, nephrotoxns
71
what drugs can cause FAnconi
ifosfamide, cisplatin, tenofovir, expried tetrcytlines, lead poisoning
72
Bartter syndrome
reabsorptive defect in TAL AR effects Na/k/2Cl transporter. It presents like chronic loop diuretics. results in hypokalemia, and metabolisc alkalocsis with high calcium in the pee
73
Gitleman
defect of NAcli in the DCT like thiazide diuretics use. AR. it is low K and low Mg, and metabolic alkalosis, and hypocalciuria
74
Liddle Syndrome
gain of function mutation so increased NA reabsorption in the CT and presents ike hyperaldosteronism so increased HTN, hypokalemia, metabolic alkalosis ;pw serum aldosterone- treat with amiloride
75
syndrome of apparent mineralocorticoid excess (SAME)
deficiency of 11ba hydroxysteroid dehydrogenase- so increased mineralocorticoids. increased minrealocoticoid receptor acitvity- HTN, decreased K, metabolic alkalosis, low serum aldosteron
76
what can you get acquired SAME from
glycyrrhetinic acid which is present in licorice
77
what is the order of the solute secreted and reabsorbed lines on the graph
from secreted to reabsorbed: PAH, creating, inulin, urea, Cl, K, Na, osmolarity, HCO3, Amino acids, glucose
78
what activates the RAAS
decreased BP, decreased NA, increased sympathetic tone
79
what blocks renin release
beta cell blocker
80
what blocks renin binding
aliskrenin
81
what blocks ACE
prils- increased bradykinin by blocking ACE
82
what blocks angiotensin II binding
arbs and these end in artans
83
what does angiotensin II do to vascular smooth muscle
it causes vasoconstriction and increased BP
84
what does angiotensin II do to glomerulus
it is constricts efferent arteriole to increase FF to preserve renal function in low-volume states
85
what does angiotensin II do to adrenal gland
aldosterone which increases the Na channel and Na/Kpump insertion in principal cells and enhances K and H excerpt nub the way of principal cels. And alpha intercalated cells H+-ATPAses
86
what does angiotensin II do to the posterior pituitary
it increases aquaporin insertion into the CT in the principal cells. Increased H2O reabsorption
87
what does angiotensin II do to PCT
it increases the NA/H activity which increases Na, HCO3 reabsorption, and contraction alkalosis
88
what does angiotensin II do to hypothalamus
stimulates thirst
89
where does renin come from and what does it do
it is secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic deischarge- beta effect
90
where does ATII work and what does it affect
affects baroreceptors function and limit reflex bradycardia which would normally accompany its present effects, helps maintain blood volume and blood pressure
91
where does ANP and BNP work and what does it affect
released from atria and ventricles and it is in response to increased volume and may ac as a check on RASS system. it relaxes vascular smooth muscle through increased GFR and decreased renin. It dilates the afferent arterial and constricts the efferent to promote naturesis
92
where does ADH work and what does it affect
it regulates osmolarity and responsible for low volume states
93
where does aldosterone work and what does it affect
aldosteone regulates the ECF and NA content and responds to low blood volume states
94
where are the JG cells and what does it sense
they are on the afferent arteriole. It senses changes in decreased BP and increased sympathetic tone
95
where is the macula dense and what does it sense
it is in the DCT and it is from decreased NaCl delivery and increased renin release and efferent arteriole constricts and increased GFR
96
what happens with beta blockers
it is decrease in BP from inhibition of B1 receptors in the JGA cells by decreasing renin release
97
erythropoein
released by interstitial cells in the peritubular capillary bed to hypoxia. stimulates RBC proliferation in bone marrow. Erythropetin often supplement in chronic kidney disease
98
caciferol
PCT cells convert 25-OH to 1,25 ocnverserion by 1-alpha-hydroxylase
99
prostaglandins
paracine secretion vasodilates the afferent arterioles to increase RBF
100
what do NSAIDs do
it blocks renal protective prostaglandin synthesis. It is constriction of afferent arteriole and decrease GFR and this may result in acute renal failure and low blood flow states
101
low dopamine
dilates interlobular arteries, afferent arterioles, efferent arterioles to increase RBF little or no change in GFR
102
high dopamine
acts as a vasoconstrictor
103
where is dopamine secreted in the kidney
it is secreted from the PCT cells to increase naturesis
104
where does ANP work
on the afferent arteriole
105
where does PTH work in the serum
causes Ca reabsorption from DCT, and decreased PO4 from the PCT, and 1,25 Oh production is increased
106
what causes shift of K out of the cell
digitalis, hyperosmolarity, lysis of cells, acidosis, beta blockers, high blood sugar like DKA (need to be careful with correction of DKA from creating kalemia)
107
what shifts K into the cell
hypo-osmolarity, alkalossi, beta adrenergic agonist, insulin
108
low sodium concentration symptoms
nausea, maliase, stupor, coma, seizures
109
high sodium concentration symptoms
irritability, stupor, coma
110
low potassium concentration symptoms
u waves, flat T waves, arrhythmias, muscle cramps, spasm, weakness
111
high potassium concentration symptoms
wide QRS, peaked T waves, arrhythmia, muscle weakness
112
low Ca concentration symptoms
tetany, seizures, QT prolongation, twitching, and spasm
113
high Ca concentration symptoms
stones, bones, groans, increased urinary frequency, psychiatric overtones, anxiety, altered mental status
114
low Mg concentration symptoms
tetany, torsades de pointes, hypokalemia
115
high Mg concentration symptoms
decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
116
low phosphate concentration symptoms
bone loss, osteomalacia, rickets in kids
117
high phosphate concentration symptoms
renal stones, metastatic calcifications, hypocalcemia
118
what happens to the renin, aldoterone and urinary ca levels in Bartters syndrom
increased renin, aldosterone and urinary Ca
119
what happens to renin, aldosterone, Mg, and urinary Ca in Gitelman syndrome
increased renin, increased aldosterone, decreased Mg, and decreased urinary Ca
120
what happens to BP, renin, aldosterone in Liddle syndrome
increased BP, decreased renin, and decreased aldosterone
121
what happens to BP, renin, aldosterone in SIADH
increased BP, decreased renin, decreased aldosterone
122
what happens to BP, renin, and aldosterone during primary hyperaldosterone
BP is increased, renin is decreased, aldosterone increased
123
what happens to Bp, renin, aldosterone in a renin secreting tumor
Bp increased, renin increased and aldosterone increased
124
what are the pH, Pco2, and HCO3 levels in metabolic acidosis
decreased pH, decreased Pco2, decreased Hco3
125
what are the pH, Pco2, and HCO3 levels in metabolic alkalosis
increased pH, increased PCo2, increased HCO3
126
what are the pH, Pco2, and HCO3 levels in respiratory acidosis
decreased pH, increased PCO2, and increased HCO3
127
what are the pH, Pco2, and HCO3 levels in respiratory alkalosis
increased pH, decreased PCo2, and decreased HCo3
128
what is the henderson hassebech used for acid-base physiolgoy
Ph=hCO3/PaCO2
129
what causes respiratory accesses and how they breath
hypoventilation- airway obstruction, acute lung disease, chronic lung disease like COPD, opioids, sedatives, weak respiratory muscles
130
what are the causes of AGMA
methanol, uremia, DKA, propylene glycol, iron tablets, isoniazid, lactic acidosis, ethylene glycol, late salycilic acid
131
what are the causes of normal anion gap metabolic acidosis
hyperalimentation, addison disease, rental tubular acidosis, diarrhea, acetazolamide, spirolactone, saline infusion
132
what causes respiratory alkalosis and what is the breathing pattern
hyperventialtion- hysteria, hypoxemia and high altitude, early salicylate, tumor, pulmonary embolism
133
what causes metabolic alkalosis
loop diuretics, committing, antacids, hyperaldosteronism
134
what is the Cl level in the urine for metabolic alkalosis
it is high in the urine
135
what does the horseshose kidney get stuck on
IMA
136
unilateral renal agenesis can cause what
hypertrophy of one kidney and it creates increased CKD as they get older
137
what happens with bilateral renal agenesis
oligohydramnios- lund hypoplasai, flat face, low set ears, developmental defects of extremities and compatible with life
138
dysplastic kidney unilateral
most commone
139
what does the histology of the dysplastic kidney look like
noninhertied cysts in kidney like cartilage
140
what is bilateral dysplastic
can present like PKD but has not of the other associated problems and is non-inherited
141
ARPKD
infants, HTN, renal failure, Potter sequence.
142
what is associated with ARPKD
hepatic cysts and fibrosis- baby with portal HTN
143
ADPKD
young adults with HTN, and hematuria and renal failure with increased renin
144
what is associated with ADPKD
berry anyreusm, hepatic cysts, mitral valve prolapse
145
medullary cystic kidney disease
in medullary colleting ducts, small kineys and worsening renal failure
146
Acute renal failure- first symptoms
azotemia, oliguria,are hallmark signs.
147
Prerenal acute renal failure- lab values
decreased BF to the kidney, and BUN:cr>15, BUN can resorb but Cr cannot. BUN is resorbed to blood more when aldosterone is present. FENa<1 and osmolarity is >500 because to tubes are still working.
148
postrenal acute renal failures- lab values
decreased GFR from back pressure. Force more BUN back into the blood so >15 in ratio. The FENa and ism are normal.
149
what changes are in the lab values with post-renal acute renal failure
long standing leads to tubular damage, so ratio<15 and FEN>2%
150
acute tubular necrosis uses
injury and necorsis, and necrotic cell plus the tubes and blocks the GFR from back pressure
151
what is seen in the urine for ATN
brown granular casts are seen with cells that lose nuclei and detach from the basement membrane
152
what are the lab values for ATN
B:cr ratio<15 and FEN>2 and osm<500
153
what are the ischemic causes of ATN and where do they hit first
tend to affect the PCT and TAL first and are preceded by prerenal syndrome
154
what are the nephrotoxic causes of ATN
aminoglycosides, Pb, myoglobin, ethelyne glycol, radio contrast, rate from tumor lysis syndrome, hydrate and use allopurinol
155
what lab values do you see with nephrotoxic ATN
oliguira, brown granular casts, increased BUN, increased Cr, increased K, metabolic acid
156
how long does the oliguria last with ATN
it lasts for 2-3 weeks because the Pct are stable cells that can regenerate, but it takes a minute for them to get going
157
acute interstitial nephritits- causes, symptoms and histology
drug induced HS< oliguria, fever, rash a few weeks after starting the drug, and it is eosinphils in the urine and can progress to renal papillary necrosis
158
renal papillary necrosis and what are the associated conditions
necrosis of renal papilla and gross hematuria, flank pain-ASA, DM, sickle cell, pyelonephritis
159
what is the hallmark of nephrotic syndrome and lab values
proteinuria>3.5, hypoalbumina, hypogammaglobulinemia, hypercoagulable (lose ATIII), and hyperlipidemia, and increased cholesterol
160
why are nephrotic syndrome patients hypercoaglable
this is from the loss of ATIII
161
minimal change disease- what are the symptoms, pictures, and what can be associated with it
hodgekins disease from increased cytokine production, and lose foot processes from these cytokine production, and normal on everything but EM. No immune complexes so IF is relate- only lose albumin, and responds to steroids.
162
what causes the damage in minimal change disease
it is from damage from T cells release of cytokines
163
what is black, hispanic, HIV, heroin, sickle cell association
FSGS
164
FSGS- what are the histological findings, and see it on images and what is the progression
dense collagen in the glomerulus, and no immune complexes, only some segments are affected it can go to CKD
165
Caucasian, hepatitis B and C, solid tumor, SLE, NSAIDs, penicillamines what is the association
membranous nephrotic syndrome
166
membranous- what are the histological findings, and see it on images and what is the progression
thick glomerular BM due to immune complex deposition, spike and dome appearance, granular IF from immune complexes from immune complexes deposition in the sub epithelial.
167
where are the spike and domes
underneath podocyte and lay down new membrane dome is on top of the deposits and the spike is in between
168
membranoproliferative- what are the histological findings, and see it on images and what is the progression
thick capsular membrane- mesangial cell proliferation-tram track appearance from excess tacked up membrane. Granular IF.
169
what is type 1 membranoproliferative glomerulonephritis associated with and histology
hepatitis B and C and tram track appearance
170
what is type 2 membranoproliferative glomerulonephritis associated with and histology
complex deposits in the basement membrane and antibody C3 nephritic factor over activation of complement so C3 converts is not destroyed and this decreases the amount of C3 in the serum. Nephritic and nephrotic
171
where are the deposits in MPGN 1
sub endothelial
172
where are the deposits in MPGN 2
BM
173
where are the deposits in membranous
sub epithelial
174
diabetic nephropathy is from waht
high glucose leads to non-enzymatic glycosilation to hyaline aterioloscleorsis, and thick wall so decrease lumen. Preferential to efferent arterial. Hyper filtration firs is albumin.
175
what slows down the progression of diabetic nephropathy
ACE slows down this profession because it slows to clamp of efferent arteriole goes to nephrotic
176
what is the classic histology of diabetic nephropathy
kimmelsteil wilson nodules
177
systemic amyloid on the kidney- where does amyloid deposit, and what is the histology
amyloid is in the mesangium and apple green biofringence
178
classic symptoms of nephritic syndrome
glomerular inflammation, bleeding, oliguria, azotemia, salt retention, periorbital edema, RBC casts, and hypocellular inflamed glomerulus and C5a mediated damage
179
post strep glomerulonephritis- what is it from and what else is there and what causes it
it is M protein from strep impetigo and strep pyogenes, and it is 2-3 weeks after post infection. Cola colored urine, and granular IF, and sub epithelial humps and pile up dissipates later. adults>risk of RPGN
180
what is the crescent of RPGn full of
fibrin and macropahges
181
if the IF is linear on the RPGN then what is it from
linera is an antibody against BM so goodpasures sundrome- hematuira, hemoptysis and no sinus issues
182
if the iF is granular, on the RPGN then what is it from
post strep glomerulonephritis- adult or diffuse proliferative in lupus.
183
if the IF is negative, on the RPGN then what is it from
it is paucimmune and if its
- cANCA then it is Weighers and it has nasopharynx lesions, hemoptysis, hematuria, sinusitis
- panca- Churg straus- granuloma, eosinophils,asthma
184
IgA neprhotpathy
mesagnial deposits, RBC casets following an mucosal infection
185
what is seen on the IF of IgA nephropathy
grnaular mesangial deposits
186
what is seen on Alport syndrome
thinning and split BM from issues with Collagen IV, and hematuria only sensory hearing loss, ocular disturbances
187
what are the symptoms of cystitis
dysuria, suprapubic pain, no systemic symptoms and frequency
188
what are the labs for cystitis
>WBC, leukocyte esterase, nitrites, culture>100000
189
what are the common causes of cystitis
ecoli, staph sapro, proteus which causes alkalization of urine
190
what is sterile pyuria and whats it from
negative culture, suggests urethrititis from chlamaydia or gonorrhea
191
pyelonephritits symptoms and causes
fever, flank pain, WBC casts, leukocytosis and ecoli, kleb, and enterococcus
192
what are some of the increased risk of pyelonephritis
vesicoureteral reflux where theureters reach the bladder
193
chronic pylonephritits obsturction- histology and gross moprhology
cortical scarring at upper and lower poles and blunted calyxes and thyroidization of the kidney- tubules look huge and filled with colloid
194
calcium oxalate and calclium phosphate stoens- what do you look for and what are the associateions
it is increased Ca in the urine, need to check for increased Ca in the blood, and Crohns increase oxylate absorption which increases risk of stone
195
treatment of calcium oxylate stones
HCTZ
196
ammonium magnesum phosphate stoens
infection of urease positive oganisms that cause staghorm calculi and alkaline urine
197
uric acid stone
radiolucent and cannot be seen on XR, and acid eliminate, and decreased urine, acidic ph, gout, hyperuricimia, and so rate with hydration and alkalinize the urine with bicarb
198
staghorm calculi in children
cysteine stones from weird absorption difficulties
199
uremia as a side effect of CKD
increased nitrogenous weight, nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy, and asterisks, deposition of urea crystals in skin. Salt and H20 retention leading to HTN , metabolic acidosis, increased K, and Anemia
200
EPO where is it produced
renal peritubular intersitial cells
201
why is there decreased vitamin D in CKD
decreased Ca from decreased 1 alpha hydroxylate and can't excrete phosphate so decreased free Ca
202
renal osteodystrophy related symptoms
- osteitis fibrosis cystica- resorb bone- fibrosis and cyst formation
- osteomalacia- can't mineralize from bad D function
- osteoporosis- metabolic acidosis is trying to buffer acid against the bone
203
what do kidneys look like if they have been on dialysis
cysts and shrunken kidneys
204
what is there an increased risk of with CKD
renal cell carcinoma
205
aniogmyolipoma
tumor of the BV, with smooth muscle, dispose and associated with TS
206
RCC symptoms
hematuria, flank pain, fever, weight loss
207
what are the paraneoplastic syndromes associated with RCC
EPO, renin, PThrP, and aCTH
208
what can RCC cause if it hits the renal vein
left sided hematuria
209
what does RCC look like grossly and histollogically
it looks like clear cytoplasm and large yellow tumor
210
where does sporadic RCC occur
it is single in the upper pole associated with smokers
211
what are the mutations for RCC
it is VHL, which increases the IGF, and HIF, and increased VEGF, and increased PDEF
212
where is the genetic RCC
younger patient bilaterally, and mutliple- it is VHL
213
what is associated with VHL
RCC, hemanigoblastoma of the cerebellum
214
Wilms tumor is derived from what
blastema from glomeruli and storma
215
what is seen for Wilms tumor
lunger central flank mass, and HTN from increased renin
216
WAGR
wilms tumor, aniridia, genetial abnormalities, and retardation
217
Beckwith wideman syndrome
wilms tumor, hypoglycemia (neonatal), muscular hemihypertrophy, and organomegaly especially the tongue
218
Urothelial canrinoma
from transitional epithelium of lower track
219
what are the increased risk factors for urothelial carcinoma
polycyclic hydrocardbon, naptholene, azo dyes, cyclophosphamise, pehnactin
220
what is the papillary Urothelial canrinoma like and progression
papillary growth with blood vessel and it goes from low, high, to invasive
221
what is the flat urothelilal carcinoma like and progression
high grade then invades high risk of P53 mutation first
222
SCC carcinoma of the bladder risk factors
chronic cystitis, schistosoma hematobeium, long standing nephrolithiais
223
adenocarcinoma of the bladder
urachal remnant, cystitis glandularis, and extrophy from failure of anterior folds
224
where is adenocarcinoma of the bladder
it is on the dome of the bladder.
225
distal renal tubular acidosis
urine ph>5.5 defect in ability of alpha intercalated cells to decorate H and no new HCO3 is generated to metabolic acidosis and hypokalemia and increased risk of calcium phosphate kidney stones due to increased urine ph and increase bone turnover
226
what are the causes of distal renal tubular acidosis
amphoterecin B toxicity, analgesic neprhopathy, congential anomalies like the obstruction of the urinary tract
227
proximal renal tubular acidosis
urine ph<5.5 and defect in PCT HCO3 reabsorption and increased excretion of HCO2 in urine and subsequent metabolic acidosis. urine is acidified by alpha intercalated cells in CT. associated with K and increased risk of hypophosphatemia rickets.
228
what are the causes of proximal renal tubular acidosis
fanconi and carbonic anhydrase inhibitors
229
hyperkalemia renal tubular acidosis
urinary ph<5.5 hypoaldosteronis and so hyperkalemia, and decreased NH3 synthesis in PCT and decreased NH4 excretion
230
hyperkalemia renal tubular acidosis causes
ecreasd aldosterone proteictio nfro diabetic hyporeninsim, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency, ro aldosterone resistance. K sparing siruretics neurpopathy from obstruction or TMP/SMX
231
RBC casts
glomerulonephritis and malignant HTN
232
WBC casts
tubulointerstitial nflammation, acute pyelonephritis, transplant rejection
233
Fatty casts
nephrotic syndrome associated with maltese crosses
234
granular muddy brown casts
acute tubular necorsis
235
waxy casts
end-stage renal disease with CKD
236
hyaline casts
normla finding from concentrated urine samples
237
what are the depositions made from in the goodpasture syndrome
IgG and C3
238
what is the deposition in the IgA nephtopathy and where do they deoposit
IgA and C3. They deposit in the vascular system like mesangium, palpable purport, dermis, GI tract. Gross heamturia
239
what is GBM splitting seen in
Type I MPGN
240
what can the loss of ATIII do in nephrotic syndrome cause
it can be from renal vein thrombosi
241
what are the spike and domes from in membranous nephrotipathy
IGG and C3
242
what are the serum antibodies against in membranous neprhtopathy
it is antibodies against phospholipase A2 receptor
243
what can kidney stone present with
unilateral flank pain, abdominal pain, and vomiting
244
what are the urease positive organisms
Klebsiella, proteus, and staph saprophyticus
245
which kidney stones are radiolucent
uric acid, and cysteine stones
246
what is the genetic cause of cysteine stones and what is the other things that get stuck1
there is hereditary cysteine reabsorbing PCT transport which also leads to poor ornithine, lysine, arguing and cystine but the cystine forms the stoens
247
what test is positive in cystene stones
sodium cyanide
248
what are the kidney stones that are hexagonal
cysteine
249
what stones are coffin shaped
amonium magneiusm phosphate stoen
250
enveloped or prism shaped stone
calcium oxalate and calcium phsophate
251
what stones are rhomboid shaped
uric acid stoens
252
when does the creatinine increase with hdyronephrosis
if it is obstructed bilaterally or it happens when patient only has one kidney
253
why are the cells of RCC clear
from increased glycogen and lupids
254
where does RCC usually met to
lung and bone
255
where does the RCC originate
PCT cells
256
renal oncocytoma
benign epithelial cels tumor from the collecting ducts.Large eosinophilic cells with abundant mitochornida withough perinuclear clearing and presents with painless hematuria, flank pain and abdominal mass resected to exclude malignancy
257
what is RCC also called
renal cell adenocarcinoma
258
stress incontinence
outlet incompetence from urethral hepermobility due to weak elevator Dani muscle and leask within creased itnrabdominal pressure and increased with risk of obesity, vaginal silvery, prostate surgey. Pelvic floor muscle strengthening
259
urgency incontinence
overactive bladder from detrusor instability and lead wit huge to void immediately and treatment is training and this can be from MS from loss of higher center myelin can lead to voerfrlo
260
mixed incontience
both urgency and stress
261
overflow infontience
incomplete emptying detrusor underactivity or outlet obstruction, and lead with overfilling and increased post void residual and urianry retention on catheter or ultradoun. Relieve obstruction with alpha blockers and BPPH
262
xanthogramulomatous pyelonephritis
widespread kidney damage due to granulomaous tissue containing foamy macrophages
263
diffuse coritcal necorsis
acute generalized infarction of both kidneys due to combination of vasospasm and DIC. associated with obstetric catastrophes and septic shock
264
what form of vitamin D is decreased in renal osteodystrophy
25- hydroxycalciferol
265
what are the consequences of renal failrure
metabolic acidosis, dyslipidemia, hyperkalemia, ureamia, increased BUN, nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction, Na/H2o retiention leadign to hF and pumonary edema and hypertension. growth retardation, and developmental delay, and epo failure causing anemia, and renal osteodystrophy
266
what are the major drugs causing acute interstitial nephritis
diuretics, NSAIDs, penicillins, cephalosporins, PPIs, rifampin
267
what are the signs of renal papillary necorsis
bloody urine, colickly flank pain from urethral obstruction, hematuria, proteinuria
268
simple kidney cysts
filled wit hultrafiltrate and very common for majority of renal masses
269
complex cysts of the kidney
septates, enhances and or have solid components on imaging need to be removed for risk of RCC
270
sonic hedgehog gene- what does it do and what is a defect from it
it is patterning along the anterior posterior axis and CNS development- Holoprosencephaly is the defect
271
Wnt-7- what does it do and what is a defect from it
it produces the apical ectodermal ridge necessary for dorsal ventrla so nose and toes directions.
272
FGF- what does it do and what is a defect from it
lengthening the limbs. Achondroplasia is FGF3
273
Hox gnees
segmental organization in craniocaudal direction. It can put the limbs in weird spots- mutation can lead to hand foot genital where urogenital strucutres are malformed and the limbs are messed up
274
when does HCG become detectable
around day 6-8 when the blastocyst implants
275
when is the bilaminar disc created
2 weeks
276
when does gastrulation occur
3 weeks
277
when does the notochord start
18 days
278
when does the neural tube close
4 weeks
279
when is the fetus most susceptible to teratogens
3-8 weeks
280
what happens at week
4 LIMBS AND 4 chambered heart
281
what happens at week 8
movement
282
what happens at week ten
genitalia
283
what glands does the ectoderm form
parotid, mammary, and sweat glands
284
what does the craniopharyngeoma arise from
surface ectoderm
285
what does the nueroectoderm create
the CNS and retina, and spinal cored
286
what does the paraxial mesoderm form
it forms the cartilage, tendon, skeletal muscle, endothelium, and dermis
287
what does the mesoderm form
spleen, cardio, lymphatics blood, upper bag wall of ut tube, and ovaries, tests, adrenal cortex, dermis
288
what does the notochord become in the adult
nucellous pulposis
289
what is the mesodermal defects
vertebral defeects, anal atresia, cardiac defects, TE, renal defects, limb defects
290
what is the intermediate mesoderm
GU
291
endoderm what does it form
guy tube epithelium above the pectinated like, liver, lungs, gall bladder, pancreases, eustachian tube, thymus, parathyroid, thyroid follicles
292
teratogen: ACE
renal failure and oligohydramnios
293
teratogen: alkylating agents- cyclophosphamide, methotrexate
absence of digits, multiple anomalies
294
teratogen: aminoglycosides
ototoxicity
295
teratogen: antiepiletpitcs
NT defects
296
teratogen: DES like diethylstibesterol
vaginal clear cell adenocarcinoma or congenital mullein anomalies
297
teratogen: trimethropin, methotrexate
NT defects
298
teratogen: isoretinoin
multiple severe birth defects
299
teratogen: lithium
ebstein anomaly
300
teratogen: tetracyclines
discolored teeth and inhibited bone growth
301
teratogen: thalidomide
limb defects like phocomelia
302
teratogen: wafarin
bone deformities, nasal hypoplasia, fetal hemorrhage, abortion
303
what do you use for anticoagulation during pregnancy and why
heparin because its large and polar
304
what does the typical FAS baby look like
smooth filtrum, wide narrow eyes, and epicenthal folds
305
teratogen: cocaine
vasoconstrictioon IUGR, low birth weight, preemie
306
teratogen: smoking
low birth weight, preteen labor, placental problem, SIDS, IUGR
307
teratogen: iodine
congenital goiteror hypothyridism
308
teratogen: maternal diabetes
caudal regression syndrome with flaccid paralysis of the legs and dorsiflexion oft feet with urinary incontinence. congenital heart defects neural tube defects. Big baby
309
teratogen: methymercury
fish and it is neurotoxic
310
teratogen: vitamin A excess
spontaneous abortions and birth defects
311
teratogen: XR
microcephaly and intellectual disability
312
what is the worst end of FAS
holoprocencephaly
313
when do dichroinoic diamnionic twins split
0-4 says and this is at he 2 cell stage
314
when do monochroiconic and diamnioic twins split
one placenta two sacs-4-8 days
315
when do mono mono twins split
8-12 days
316
when do conjoined twins split
greater than 13 days
317
what is the most common type of twins
monochorionic twins and diamniotic
318
whate does the cytotrophoblasts do
it is the inner layer and it makes cells
319
what does the syncitiotrophoblast do
it is the outer layer that secretes hCG and stimulates the corpus leutum to secrete progesterone during the first trimester and it does not have mHCI
320
what is the decidua balalis
it is the maternal component where the maternal blood goes into lacunas
321
umbilical arteries do what
they return deoxygenated blood from the fetal internal iliac arteries to the placenta.
322
what is the deal if there is only one umbilical artery
congenital and chromosomal abnormalties
323
what does the umbilical vein doing
it supplies oxygenated blood from the placenta to fetus and drains into the IVC via liver or ductus venossuus
324
what is the urachus
it was a duct between the umbilicus and fetal bladder
325
what is a patent urachus
total failure of arches to obliterate so there is urine around umbilicus
326
what is a urachal cyst
partial failrue or urachus to obliterate and fluid filled cavity lined with uroepithelium between umbilicus and bladder. can lead to adenocarcinoma on dome of the bladder
327
what type of cancer is associated with a urachal cyst and where is it located
it is a adenocarcinoma on the done of the bladder
328
what is a vesicuurachal diverticulum
it is a slight failure to obliterate which leads to an outputting of the ebaldder
329
what is the vitelline duct
it connects the yolk sac to the midgut lumen
330
what is a vitelline fistula
vitelline duct fails to close so there is meconium discharge from the umbilicus
331
what is a meckell diverticulum from
parial closure of the vitalize duct with patent portion attached to the ileum and it can have gastric or pancreatic tissue hetertopically
332
what are the derivatives of the 1 and 2 arctic arches
maxillary aretery and stapedial artery
333
what are the derivatives of the 3 and 4 arctic arches
3- common carotid and internal carotid artery
| 4- aortic arch and right subclavian
334
what are the derivatives of the 6th aortic arch
PDA
335
what are the branchia clefts from
ectoderm
336
what are the branchial arches from
mesoderm and neural crest
337
what are the branchial pouches from
endoderm
338
what is the derivateve of the first cleft
external auditory meatus
339
what is the branchial cleft derivative of 2-4
cervical sinues and these are temporaty
340
what is a persistent cervical sinus present as
branchial cleft cyst which is a lateral mass that does not move with swallow
341
what are the derivates of the first branchial arch
maxiallya, mandible, and mastication muscles and associated nerves
342
what are the disorders of the first branchial arch
Chew- Pierre Robin sequence- micrognathia, glossoptosis, cleft palate, and airway obstruction.
Treacher Collons- neural crest dysfunction- mandibular hypoplasia, facial abnormalities
343
what are the derivates of the second branchial arch
Smile- CN VII- stapes styloid, stylohoid- and stapedius and posterior belly of the digastric
344
what are the derivates of the third branchial arch
Swallow- grater horn of the hyoid and the stylopharngeus. CN IX
345
what are the derivates of the fourth-sixth branchial arch
Simply swallow and Speak- intrinsic laryngeal muscles, and pharyngeal constrictors- 4th is superior laryngeal vagus and the sixth is the laryngeal X. also forms the poster o the otunge
346
what is the mmnurmonic for the arches
chew, smile, swallow stylishly, simply swallow, and speak
347
what do you cut through for a cricothyrotomy
places between the cricoid and thyroid cartilage. Incise through skin, superficial cervical fascia, investing pretrachial, deep fascia, and cricothyroid membrane
348
what does the first pouch develop into
ear
349
what does the second pouch develop into
palantine tonsil
350
what does the third pouch develop into
inferior is the parathyroid and the thymus
351
what does the fourth pouch develop into
superior parathyroids and parafollicular cells of the thyroid
352
DiGeorge is an aberrant development of which pouches
3 and 4 so thymic aplasia and failure of parathyroids leading to hypocalcemia
353
cleft lip is from what
failure of fusion of maxillary and medial nasal processes
354
what is cleft palate from
failure of fusion of the two lateral palatine shelves or failure of fusion of lateral palatine shelves with the nasal septum or the median palantine shelf
355
what is the default embryologic GU development
female mesonephric degenerates and paramesoneprhic develops
356
what is the male formation like from the internal and external path
SRY end turns on testis determining factor and it hits the testes and increases the serotli cells
- internal - settle cells secrete mullein inhibitory factor and this degenerates the paramesonephric ducts
- external- the leydig cells are stimulates to secrete testosterone and this cause the wolfing duct to develop which is the internal structures like the everything but the prostate. It then converts to DHT and this is what starts the male external genitalkia
357
what happens if there are no sertoli cells or they lack MIF
develop male and female internal genitalia and male external genitalia
358
what happens if 5 alpha reductase is deficitnet
inability to convert t to DHT causes male internal genitalia nbut ambigious on the outside- Dominican children that sprout penises at puberty.
359
Paramesoneprhic development
no SRY gene, so it develops into female internal structures, fallopian tubes, uterus, upper portion of the vagina
360
what happens for mullein agensis
may present as primary amenorrhea due to lack of uterus with females with full functional ovaries and secondary sexual characteristics
361
septate uterus
incomplete reposition of the septum
362
bicronate uterus
incomplete fusion of the mullein ducts
363
uterus didelphys
complete failure of fusion, so double uterues, vagina, and cervis
364
gubernaculum
anchors the testis in the scrotum and it is the ovarian ligament and round ligament of the uterus
365
processus vaginalis
former the tunica vaginalis in the male and nothing in the female
366
what is different about the venous drainage on the right and left
the left drains to the renal vein before the IVC, which means it is the side with increased pressure varicoceles happen on this side preferentially
367
what is the LN drainage of the ovary/testes
para-aortic
368
what is the LN drainage of the body of uterus, cervis, superior bladder
external iliac
369
what is the LN drainage of the prostate, cervis, corpus cavernous/proximal vagina
internal iliac nodes
370
what is the LN drainage of the distal vagina, vulva, scrotum, distal anus
superficial inguinal LN
371
what is the LN drainage of the glans penis
deep inguinal LN
372
what is the ligament that gets ligated for oophorectomy and ovarian torsion
it is the infundibulopelvic or the suspensory ligament of the ovary
373
what ligament connects the vervix to the side wall of the pelvis
cardinal ligament
374
what ligament is the derivative of the gubernaculum and travels through the inguinal canal
round ligament
375
what is the artery of samson
it is the anastomosis of the ovarian and uterine vessels
376
what ligament attaches the uterus , fallopian tubes and ovaries to the pelvic side wall
broad ligament
377
what ligament attacks the ovary to the lateral uterus
ovarian ligament
378
what is the epithelium of the ectocervix
strat squamous
379
what is the epithelium of the endocervix
it is simple collumnar
380
what is the epithelium of the uterus during the proliferative phase
it is long tubular glands
381
what is the epithelium of the uterus during secretory phase
coiled glands
382
where does a vasectomy cut and how long do you have to wait
it cuts the vas deferent but need to wait for 3 months
383
what is the path of sperm during ejaculation
seminiferous tubules, epidydimus, vas deferens, ejaculatory duct, urethra, penis
384
where is the urethra injured from a car accidnet
it is injured at the membranous urethra
385
where is the straddle injury of the urethra
it is in the bulbar and penile urethra. Urine can get into Bucks fascia
386
innervation of an erection
PNS increased NO and increased cGMP, and vasodilation- projectile
387
what takes away an erection
it is NE and increased Ca cause smooth muscle contraction leading to vasoconstriction and the penis becomes soft
388
emission innervtion
SNS and it is from the hypogastric nerve
389
ejaculation innervation
visceral and somatic nerves like the pudendal nerve
390
spermatogonia
maintain germ pool and produce primary spermatocytes
391
serotili cells
secrete inhibit B to inhiit FSh and secrete androgen binding protein to trap T and then it also produces MIF and it forms the tight junctions of the blood testis barrier. Support and develop sperm. decreased sperm production and decreased inhibit B with increased termpeature
392
Leydig cells
secrete testosterone in the presence of LH and is unaffected by temperature
393
estrogen source
ovary, placenta, adipose tissue
394
what is the order of the estrogens in relation to potency
estradiol>estrone>estriol
395
wahat is the function of estrogen
development of genitalia and breast, female fate distraction. it encourages growth of the follicles, endometrial proliferation, and increased myometrial excitability. upregualton of estrogen, LH and progesterone receptors and feedback inhibition of FSh and stimulation of the LH urger. Increased transport proteins, and increased HDL and decreased LDl
396
what estrogens increase and by how much during pregnancy
50x increased in estradiol and estrone. and 1000 increase in estriol which indicates fetal well-being
397
where are estrogen receptors
they are in the cytoplasm and translocate to the nucleus when bound by estrogen
398
what is the pathway of estrogen production in the ovary
GnRH stimulates the release of LH which acts on the tech cells and it converts cholesterol to androgens by descales. and the androgens go to the granulosa cells which are stimulated by FSh to tuns the androgen to estrogen via aromatase
399
progesterone sources
Corpus lueteum, palcenta, adreanal cortex, and testes
400
what is the function of progesteron
stimulation of endometrial glandular secretions and spiral artery development. Maintains the pregnancy and it decreases the myometrial excitability, produces thick mucus to prevent seem entery, increased body temp and decreased LH and FSH release. it prevents conditions and prevent endometrial hyperplasia
401
decreases progesterone increases what
it increases prolactin
402
what stage of meiosis is completed just prior to ovulation
meisosis I
403
what stage is the ice in until ovulation
prophase I
404
what stage is the oocyte arrested in until fertilization
metaphase II
405
what hormones do what for ovulation
increased estrogen, increased GNRH receptors on anterior put. Estrogen surge stimulates LH release and and ovulation and rrupture of follicle and progesteron induces an increase in body temeprature
406
mid cycle pain with peritoneal irritation
Mittelzchmerz
407
imperforarte hymen
primary ammenorhea from incomplete degeneration of the fibrous posdrople of the vagnina. Can have bulging introits at birth which regresses then during periods it is symptomatic because there is abdomnial pain and pelvic pain with the accumulation of blood in the vagina and mass is palpable in rectum
408
how long is the luteal phase
14 days
409
what is ovulation plus 14
period
410
when is the follicular phase of growth the fastest
2nd week of follicular phase
411
what stimulates the endometrial proliferation
estrogen
412
what maintains the endometrium to support implantation
progesterone
413
where does fertilization usually occur
in the ampulla of the fallopian tube within one day of ovulation
414
when does the implantation occu
6 days after fertilization
415
what secretes hug and when is it detectable in blood and urien
syncitiotrophoblasts and 1 week for blood and 2 for urine
416
what is gestatational age
it is calculated from date of last menstrual period
417
what is embryonic age
calculated from date of concentption
418
what happens to CO in preganancy
increased preload decreased after load and increased CO
419
what happens to Hr in preganancy
increased for increased perfusion
420
what happens to blood cells in preganancy
anemia from increased plasma and increased RBC and decreased viscosity
421
what happens to coagulation in preganancy
it is increased to decrease blood loss during delivery
422
what happens to breathing during pregnancy
hyperventialtion because of the increased CO2 output
423
what does lactogen do during pregnancy
it is secreted and causes insulin resistance which leads to increased blood glucose levels. It does this by stimulating beta cells to decreased more insulin and this is because there are greater energy requirements during pregnancy
424
what is supin hyertension syndrome of pregnancy
compression of the IVC means there is decreased VR which decreases the preload and CO and so hypotension. This shows up as pallor, hypotension, sweating, nausea, and dizziness
425
what does the HCG do and when does it peak
it peaks in the first 8-10 weeks to act as LH and then the placenta creates its own estriol and progesterone so the corpus lute degenerations. HCG maintains the corpus lute so it maintains the source of progresterone
426
what is the deal with the alpha subunit of HCG
it is the same as LH, FSH, and TSH and so if there is increased HCG then it can cause hyperthyroidism
427
what are the causes of increased HCG
multiple gestations, molar pregnancy, choriocarcinomas, down syndrome
428
what are the causes of decreased HCG
ectopic pregnanc, tri 13 and 18
429
low brith weight is defined as what and what are the complicatiosn
increased risk of SIDS, and increased motility have more infection, RDS, necrotizing entercolotits, intraventricular hemorrhage, and persistent fetal circulation like PDA
430
what increases the risk of SIDS
secondhand smoke, sleeping with the baby, asthma, otitis media, and pneumonia
431
what are the causes of intraventricular hemorrhage in the child and what are the symptoms
developmental impairment, hypotonia, decreased movement, bulging fontanelles, hypotension, seizure, coma, Bleed is from the germinal matrix which has immature blood vessel and these lack glia
432
lactation what does prolactin do and what does oxytocin do
prolactin- induce and maintain lactation and decrese fertility. Oxytocin assits in milk let down and promotes uterine contraction
433
what does breast milk contain- immune cell wise
IgA, macrophages, and lymphocytes. it can decrease risk of infection, asthma, allergies, diabetes, and obsestiy
434
what supplementation is required with breast milk
D and K
435
what risks are lowered maternally if they breast feed
decreased risk of ovarian and breast cancer
436
what is the criteria and symptoms and hormone levels for menopausr
it is ammenorhea for 12 months with decreased estrogen from decreased follicles. it is usually 51 and 4-5 years of abnormal menstruation. Some of the estrogen is peripherally converted to androgens which cause hirsutism There is increased FSH and LH and decreased estrogen. Hot flash, atrophy of vagina, osteoporosis, and CAD, and sleep issues
437
menopause before 40 signals what
premature ovarian failure
438
what does T do
differntiation of the epidydimus, vas deferens, seminal vesicles, penis , seminal vesicles, and sperm and muscles and deep voice and close epiphyseal plates, libido
439
DHT function
differentiation of penis, scrotum, prostate, balding large prostate and sebaceous gland
440
what converts T to DHT and what is it inhibited by
5alpha reductase and it is inhibited by finasteride.
441
what does exogenous T do to the normal hormone functioning
it inhibits the hypothalamic axis, and the pit gonad recreation so decreased intratesticualr testosterone and decreased testosertone size and azospermia
442
when does spermatogenesis begin
puberty
443
how long does full sperm development take
2 months
444
Tanner stage 1
no sexual hair, flat chest wit raised nipple
445
Tanner stage 2
pubic hair appears-pubarche
testicualr enlargement
breast bud forms-thelarche
446
Tanner stage 3
coarsening of pubic hair
penis lengeth increases
breast mounds form
447
Tanner stage 4
coarse hair across pubis, penid gets bigger, breast gets bigger and aerola gets bigeer
448
Tanner stage 5
coarse hair across the pubis and middle thigh penis and testis unloader. adult breast contours and aerola gets less fluffy
449
testicular atrophy, long extremities, gynecomastia, female hair distribution, and intellectual disabiltiy- what in the condition and what are the hormonal level with it
Klinefelter 47 XXY, it is increased LH and Increased FSH and decreased T and since there is dysgenesis of the seminiferous tubules that is why the FSH is high and the bas normal leydig cells decrease the T and increase the LH and estrogen from the extra androgens hanging around
450
what if the testosterone is high and the LH is high
defective androgen receptor
451
what if the T is high and the LH low
testosterone secreting tumor or exogenous steroids
452
what is the T is low and the LH is high
primary hypogonadism
453
what if the T and the LH are low
hypogonadotropic hypogonadism
454
what is a 46 XX DSD present as
ovaries are present, but external genitalia are virilized or ambiguous. Due to excessive and inappropriate exposure to androgenic steroids during early gestation like CAH, exogenous administration of androgens during pregancny
455
what does a 46 XY DSD present as
testes are present but external lgenitalia are female or ambiguous. Most common is androgen insensitivity syndrome or testicular feminization
456
what is placental aromatase deficiecny
it is the inability to synthesize estrogens from andrgens so masculization of female XX infants with ambiguous gentialia. Increased serum testosterone and androsteindiuone. Can present with maternal virisliazation.
457
what is androgen insensitivity syndrome 46 XY
defect in androgen receptor resulting in nroaml appearing female. wit female external gentialia, scant sexual hair, rudimentary vagina, fallopian tubes absent. Patients develop normal functioning testes found in the labia major and surgically removed. INCreased T and estrogen and Lh
458
5 alpha reductase deficiency
D- likmited to males unable to convert T to DHT and ambigous gentialia until puberty when increase T causes masculinization and growth of external genitalia. and the LH is normal to Increase and the external genitalia are normal
459
Kallman syndrome
failure to complete puberty its a form of hypogonadotropic hypogonadism defective gradation of GNRH cells and formation of olfactory bulb so decreased GNRH from hypothalamus and anosmia so leads to DNRH FSH and LH and T are all decreased because of the lack of hypothalamic This is a central form of hypogonadism
460
what is the mutation in Kallman syndrome
KAL1 gene and FGF 1 receptor
461
hydatidifrom mole (complete)
46 XX or sometims Xy and it is encuclearted egg plus single per which duplicates its DNA. There are no fetal parts highly increased HCG. snow storm grape uterus on ultrasound. Higher risk of tropholastic neoplasia or chroicarcinoma
462
what are the general symptoms of a molar pregnancy and what casuses this
pelvic pain, vaginal beleeding, early preeclampsia, theca leutial cysts, hyperemesis, hyperthyroid
463
Partial Mole
69 XXX, XXY and these are two sperm and 1 egg. here are some fetal parts and increased HCG, but the risk of malignancy is rare
464
choriocarcinoma
can develop during or shortly after pregnancy in the mother or baby. Malignancy of trophoblasticstissue with no chorionic villi present it is often bilateral multiple theca literal cuts increased BHCG and shortness of breath and hemoptysis from the spread to the luugns
465
what kind of discharge might you see from choriocarcinoma
muddy brown discharge
466
placental aburption
premature sepearation of the placenta from the uterine wall before delivery
467
what are the risk factors for placental aburption
trauma like MVA, cocaine, HTN smoking preeclampsia
468
what is the presentation of placental aburption
abrupt painful bleeding in third trimester wit hDIC, maternal shock, fetal distress
469
what does DIC happen with placental abruption
DIC is kicked off by the placental injury because there are lots of tissue factors in the trophoblasts which hare released from the placental injury kicking off the clotting cascade in mom
470
what are the risk factors for placenta acreta
prior C section, infalmmation, placenta previa
471
placenta accreta
placenta attaches to the myometrium without penetrating it
472
placenta increta
placenta goes into the myometrium
473
placenta percreta
placenta perforrates into the uterien sourer or rectum or bladder
474
what is the presentation of placenta accreta and what does it cause as complications
often detected on ultrasound and no separation of placenta after delivery leading to postpartum hemorrhagee and Sheehan syndrome
475
placenta previa risk factors
multiparity prior c section
476
placenta previa presentation
painless third trimester bleeding
477
placenta previa what is it
placenta to lower uterine semgent over or next to the cervical os
478
vasa previa presentaion
triad of membrane rupture, painless vaginal bleedign and fetal bradycardia
479
what is vasa previa
it is where the fetal vessels run over or in close proximity to the cervical os leading to vessel rupture, exsanguinatio and death.
480
what should be done about vasa previa
it is an emergency C section
481
what is associated with vasa previa
velamentous cord that where the cord inserts into the chroioamniotic membrane rather than placenta so the fetal vessels travel to the placenta unprotected by Wharton Jelly
482
Postpartum hemorrhage what is it from
uterine atony, trauma, thrombin and tissue like retained products of conception
483
if the uterus is large and boggy from the myometrium not clamping down, what can be ligated to stop a life threatening hemorrhage
internal iliac artery ligation
484
ectopic pregnancy occurs where
ampulla of the fallopian tube
485
what is the history normal for ectopic prengnacy
lower than expected HCG, appendicitis, amenorrhea, and sudden low abdominal pain
486
what are the risk factors for ectopic pregnancy
prior ectopic, history of infertility, salpingitis from PID, ruptured appendix, prior tubal surgery
487
polyhydramnios
oto much amniotic fluid associated with esophageal duodenal atresia, anencephaly and inability to swallow fluid maternal diabetes, fetal anemia , multiple gestations
488
oligohydramnios
too little amniotic fluid associated wit placenta insufficieny, bilateral renal agencies posterior urethral vales and resultant inability to extreme urine. can cause potter sequence and lung hypoplasia
489
gestational hypertension
BP>140/90 after the 20th week of gestation. No preexisting HTN
490
treatment for gestation HTn
hydralazine, alpha methyldopa, labetalol, nifedipine try to deliver 37-39 weeks
491
preeclampsia
new onset HTN with either proteinuria or end organ dysfunction after 20 weeks. May proceed to exlampsia or sieures
492
what is the cause of preeclampsia
abnormla palcenal spiral arteris leding to hypoxia nd ischemia of the placenta and release cytokines that damage the amturnal endothelium leading to proteuinuia HTN and end organ damage
493
what are the complications of preeclampsia
placental abruption, coagulopathy, renal failure ueroplacental insufficienct, eclampsia
494
what increases the incidence of preeclampsia
pre-existing HTN, DM, CKD, autoimmune disorders
495
treatment of preeclampsia
antihypertensives, IV mg sulfate, definitive is delivery
496
eclampsia
preeclampsia and maternal seizures
497
what is maternal death from in eclampsia
ARDS, sroke, intracranial hemorrhage
498
treatment of eclampsia
IV MG sulfate, antihypertensives, immediate delivery
499
HELLP
hemolysis, elevated LFTs, low platelets. manifestation of severe preeclampsia
500
presentation of HELP
pre with nausea vomitting, absornmianl pain for 12 hours and high BP and RUQ
501
what is seen on histology of HELLp
schostocytes
502
what can the HELLLP lead to
hepatic subcapsular heamotmas leading to rupture and severe hypotension
503
for gynecologic tumors what is the incidence by type
endometrial>ovarian>cervical
504
what is the most common gynecologic tumors worldwide
cervical from lack of screening
505
what is the worst for prognosis in gynecologic tumors
ovarian>endometrial cervical
506
gestation diabetes
big headed big babdy from decreased insulin sensitivity. use diet and insulin. Baby can have beta cell hyperplasia leading to hypoglycemia neonatallay
507
pre-gestation diabetes
DM prior to pre need to manage wit insulin and big baby with cardiac defects and sacral agenesis
508
what is a high grade CIn
atypical cells are by on the lower 1.3 of the cervia lepthelum and to the epithelial surface and go to invasive
509
what is low grade CIN
cells are not in the lower 1/3 of the vagina
510
what is it called if the CIN invades the BM
it is invasive
511
what is micro invasive CIN
it goes into the BM
512
septic abortion
it is retained products of concept, fever, abdominal paine, uterine tnederness, and foul discharges. Usually staph a, step B, icily. can become septic if it goes into the intervillous space of the blood stream. Treat wit broad antibiotics and evacuation.
513
what are the long term complications of septic abortion
it is adhesions secondary ammenorhea and infertility
514
sqamous cell caricnoma
it is in the vagina and is rarely primary
515
what is clear cell adenocarcinoma associated with and where is it
vagina and from DES exposure
516
Sarcoma botryoides- embroyngal rhabdomyosarcoma
affects girls<4 years old- spindle shaped cells and design positive grape mass from the vagina
517
dysplasia and carcinoma in situ for cervical cancer
disordered epithelial growth begins at the basal layer of squamocolumnar junction in the transformation zone and extends out It is glassitied as 1-3
518
dysplasia and carcinoma in situ for cervical cancer- what causes it
HPV 16 and 18 which produce E6 gene a which is p53 inhibitor and E7 which is gene product that suppresses Rb. May perigees to invasive if untreated. Presents as postcoital bleeding
519
invasive cervical carcinoma
scc and pap smear of cervial dupsplasia lateral invasion can block the ureters and cause renal failure
520
premature ovarian failure
premature atresia of the ovarina follicles in some of reproductive age and signs of puberty before 40
521
causes of anovulation
eprgancny, PCOS, obestivy, HPO axis issues, premature ovarian failure, increased prolactin, thyroid issues, eating disorder, athletes, cushign, adrenal insufficiency
522
follicular cyst
distention of enraptured gradian follicle asoscited wit hhyperesterogeism and endometrial hyperplasia most common in young women ncan lead to torsio
523
theca-leutin cysts
often bilateral, multiple and due to gonadotropin stimulation associated with choriocarcinoma and hyatidiform moles- from increased HCG
524
serous cystadenoam
ovarian neoplasm which his the most common- lined with fallopian tube like epithelium and often bilateral
525
what is the most common person and presentation for ovarian neplsma
women>55 adnexal mass
526
what increases the chance of malignancy in ovarian masses
advanced age, infertility, endometriosis, PCOS, genetic predispsotion like BRCA1 and 2, Lynch syndrome and strong family history
527
what decreases the chance of malignancy in ovarian masses
previous pregnancy, history of breast feeding, OCPs, tubal ligation
528
what do you measure for recurrence of ovarian mass
CA125
529
mucinos cystadenoam
multiloculated large cells that have mucus secreting epithelim
530
endometrioma
endometriosis with ovary cyst formation mass presents wit pelvic pain dysmenorrhea, dyspareniuna and chocolate cysts
531
mature cystic teratoma
germ cell tumor, most common in 10-30 year olds cystic mass with all three germ layers. can be secondary to ovarian torsion from the large side
532
what ovarian tumor can present with hyperthyroidism and why
mature cystic teratoma can present with ectopic thyroid tissue
533
Brenner tumor
loos like the bladder solid tumor that is pale yellow tan and encapsulated and coffee bean nuclei
534
fibrosmas
bundles of single shaped fibrolasts with Meigs syndrome of ovarian fibroma, acites, hydrothorax and pulling in the groin
535
what is Meigs syndrome and what is it associated with
ovarian fibroma, ascites, hydrothorax and pulling sensation in the groin
536
thecoma
like granolas cell tumors may produce estrogen presents with abnormal uterine bleeding in postmenopausal woman
537
granulosa cell tumor
malignant stromal tumor of women in their 50s often produces estrogen and or progesterone and presents with postmenopausal bleeding, sexual precocity in pre-adolescents, breast tenderness. Call exner bodies with esoniphilic fluid looking like primordial follicles. it produces E and it is a yellow mass
538
serous cystadenoma
malignant ovarina neoplasm bilateral with psammoma bodies
539
mucinous cystadenocarcinom
psydomyxoma periotinei intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor
540
immature teratoma
aggerssive contains getal tissue neuroectodem and it is before 20 years old and represented by immature/embyonic like neural tissue
541
dysgerminoma- W
adolescents wit hquiaalent to seminoma- it is increased HCG and LDH asa tumor markers wit fired egg cells
542
yolk sac tumor or woman
aggressive tumro in the sacrococcygela area in young children wit heels friable hemorrhage solid mass wit scholar duvall bodies representing glomeruli. AFP is the tumor marker
543
Krukenberg tumor
Gi malignancy that mets to the ovaries and mucin secreting signet ring celsl
544
endometrial poly
endometrial tissue within the uterine wall may contain smooth muscle cells and can extend into the endometrial cavity in the form of a poly- painless abnormal bleeding
545
adenomyosis
extension of endometrial tissue into the myometrium so glands into the myometrium. caused by hyperplasia of the basal layer of endometrium and present with dysmenorrha, menorrhagia, uniformly enlarged soft gobular uterus- heavy bleeding and dysmenorrha- treat with GNRH agonists or hysterectomy
546
Leiomyoma
most common tumor in females. multiple discrete tumors with increase in black people. Benign smooth muscle tumor, malignant transformation to leiomyocarcomes si rate. Estrogen sensitive to increase size with pregnancy and menopause decreases it . It can cause abnormal bleeding or iron def. Whorled pattern of smooth muscle bundles with well-demarcated borders
547
endometrial hyperplasia
abnormal endometrial gland proliferation leading to express estrogen stimulation so increased risk of endometrial carcinoma. nuclei atypia increases the risk of carcinoma. Postemenpausal vaginal bleeding.
548
risk factors for endometrial hyperplasia
anovualtroy cycles, HRT, pcos, and granulosa cell tumor
549
endometritis
inflammation of the endometrium associated with retained products of concetption, delivery, miscarriage, abortion or with foreign body. retained material in the uterus promotes intfectio by bacterial flora from vagin or intestinal tract- treat with genta, cloned nada amp
550
endometriosis
nonneoplastic endometrial glands and storm outside the endometrium. ovary, pelvis, peritoneum and is due to retrograde flow metaplastic transomfation of mutlipotent cells, leads to cyclic pelvic pain, bleeding, dysmenorrhea, dyspareunia, dyscheezia, inferititly, normal size uterust
551
treatmetn for endometriosis
NSAIDs OCP, progestin GNRH, danazol, laproscoptic removal
552
leiomyosarcoma
malignant from myometrium which is denovo not from leioma and it is a rapidly enlarging uterus
553
fibroadenoma of the breast- typical patient
women under 35
554
what is the typical presentation of fibroadenoma of the breast
increased size and tenderness with the estrogen and small well defined mobile pass
555
what is the histology of the fibroadenoma
glands and cystic spaces with epitheliumn that atrophies and the storm is hyalinzied and benign myxoid stroma
556
fibrocystic breast changes
premenopausal women over 35 and prenmetstal breaks pain and lumps that are bilareral and multifocal. simple blue done cuts with papillary apocrine change and metaplasia
557
aclerosis adenossi
increased acini and stomal fibrosis associated wit calcifications and slight increased risk of cancer
558
intraducatal pailloma
small papillary tumor within lactiferous ducts typically beneath areola most common cause of bloody discharge. papilalry cells with fibrovascualr core
559
epithelial hyperplasia
increased cells in the terminal ductal or lobular epithelium and increased risk of carcinoma with atpyical cells
560
phyllodes tumor
large mass of connective tissue wit cyst s that are lead like most common in 5th decade of life and can befcome malignan
561
fat necrosis of the breast
benign painless lump due to breast injust calcified oil cyst with necrosis fat and giant cells on bipsy- may not realize there has been trauma
562
lactational mastitis
breastfeeding increased risk of staph aureus from cracks n the nipple. treat with antibiotics and keep breast feeding
563
gynecomastia
breast enlargemetn in men due to increased estrogen compared to androgen- cirrhosis, hypogonadisn, testicualr tumors, spirlactone, cimetidine, ketoconazole
564
after amstectomy with eaxillary LN dissection can cause what
chroninc lymphaenam and angiosarcoma with shot slit infiltration with abnormal vascular spaces
565
what receptors have worse prognosis for breast cancer
triple negative
566
what is the most important prognostic factor for early state disease
axillary LN involement
567
what is the most often axillary LN involved
upper-outer quadrant of the breast
568
what increases your risk for malignancy of the breast
increases estrogen, increased menstrual cycles, older age at first live brith, ocestiy, BRCA1, and BRCA2, and AA ethnicity for triple negative
569
DCIS
fill ductal lyme and arises from ductal atypia
570
what is seen on mammography of DCIS
microcalcifications
571
what is seen on histology of DCIS
pleomorphic cells with central necrosis does not pass basement membrane and can lead to Pagget
572
comedocarcinoma
ductal with central necrosis subtype of DCIS
573
Paget disease
underlyins DCIS or underlying invasive breast cancer. edematous nipple patches
574
invasive ductal carcinoma
firm fibrous rock hard mass with sharp margins and small glandular duct cells with stellate infiltration- most of the breast cancer
575
invasive lobular carcinoma
orderly row of cells due to decrease e cad herein expression- bilateral with multiple lesions in the same locatio
576
nmedulalry carcinoma
fleshy, cellualr ,lymphocytic infiltrate
577
inflammatory breast cancer
dermal lymphatic invasion by breast carcinoma Peau d organdy neoclassic lymphatic drainage- itchy rash and obstruction of lymph drainage
578
dimpling
signs of invoelment of suspensory ligaments leading to traction dab breast dimple
579
peyronie diease
abnroaml curvature of the penis due to fibrous plaque within the tunica albuginea associated wit erectile dysfunction, can cause pain and anxiety, consider surgical repain
580
ischemic priapism
painful sustained erection lasting more than 4 horus. sickle cells, dildenafil and trazadone, teat wit corporal aspiration, intravarenosal phenylephrine or surgical decompresion
581
SCC of the dick
more common in Asia, africa, south America the precursor lesions are below can be from HPV
582
bowen disease
penile shaft lesion with leukoplaskia
583
erythropalsia of Queryrat
cancer of the glans that presents are erythroplakia
584
Bowenoid papulosis
carcinoma incite of unclear malignant potential in young person as reddish papules
585
cryptorchismim
mipaired spermatogenesis can have normal T levels increased risk of gems cells tumors permuting, decreased nhibin B increased FSH and LH and decreased T in bilateral cases
586
varicocelel
dilated veins in the pampiniform plexus from increased venous pressure because of the resistance of flow from the left gonadal vein drainage into the left renal vain can cause infertility because of increased temperature. does not ranslumnate
587
what can compress the left renal vein
aorta and SMA
588
congenital hydrocele
scotal swelling in infants due to incompelte obliteration fo processus vaginalis
589
acquired hydrocele
scotal fluid collection from infection, trauma or tumor
590
spermatocele
csyt due to dilated epidydimal duct or rete testes- paratesticualr fluculant nodule
591
what are the risk factors for testicular germ cells tumors
cryptorchisdism, klineferlts, most are mixed germ cell tumros
592
seminoma
malignant painless, homogenous testicualr enlargemetn does not occur in infancy. large cells in lobules with watery cytoplasm and fried egg appearance. increased placental ALP. radiosensitive
593
yolk sac tumors
yello muconous and aggerssive malignancy of the testes analogous to ovarian yolk sac tumor. Schiller duval bodies that look like primitive glomeruli. increased AFP under 3 ears old
594
choriocarcinoma
malignant increased in HCG from disorder syncitiotrophoblastic and cytoptphiblastic tissue mets to the lungs and brain. gynecomastia ad hyperthryoid
595
what does choriocaricnoma cause hyperthyroid
increased BHCg which has the same alpha unit at TSH
596
teratoma
males may be malignant the later they are caught
597
embroynal carcinoma
malignant hemorrhagic mass with necrosis and painful worse prognosis than semifinal glandular and papillary morphology.y pure embryonal is create often mixed wit other tumors. increased HCG and normal AFP
598
Lydia cell tumors
golden brown color containing REinke crystals and eosinihilic cytoplasmic inclusions produce androgens or estrogens- gynecomastia, and prcosuous pebbly in boys
599
Stroll cell tumors
androblastoma from sex cord stroma
600
testicualr lymphoma
most common testicular cancer in older men- not a primary center arises from matastatic lymphoma to the testes and is aggressive
601
BPH
smooth elastic firm nrhular enlargement and hyperplasia but not hypertrophy or periuretrhal lateral and middle lobes which compares the ueretha into a vertical slit. Increased frequency of urination and nocturne, difficulty stating and stopping urine storem ,dysuria, and may lead to situation and hypertrophy of the bald, hydropnephrosis, UTI and increased PSA
602
what is the treatment for BPH
alpha 1 antagonists lieke terazosin and tasulosin which hcuase realization of the smooth muscle. five alpha reductase inhibitors like finasteride, and tadalafil
603
prostatitis
dysturia frquency regency low back pain, warm tender enalrged prostate
604
what is the cause of acute protatitis
it is ecoli in older people and neisseria or clap in younger people
605
what is the cause of conic prostatitis
tends to be a bacterial
606
prostatic adenocarcinoam
common in mend over 5 0and arises in the posterior peripheral zone of the prostate and is diagnosed by increased PSA and subsequent needle core biopsies with increased PAP and PSA.
607
what type of bone mets does prostate cancer have
blastic lesions that are indicated by low back pain and increased ALP and PSA. there are from the vertebral venous plexus and the posterity venous plexus
