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Step1 > Renal and Repro-Final things I should know > Flashcards

Renal and Repro-Final things I should know Flashcards

1
Q

mesonephros

A

function as interim kidney for first trimester, later contributes to male genital system.

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2
Q

metanephros

A

permanent, first appears in fifth week of gestation, nephrogenetisis continues through 32-36 weeks

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3
Q

what is the uteric bud derived from

A

the caudal end to the mesonephric duct

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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.

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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.

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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

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7
Q

vesicoureteral reflux

A

incomplete closure lead to dilation and chronic non-obstructive hydronehrosis and increased risk of infection

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8
Q

what poles of the kidneys fuse on horseshoe kidney

A

it is inferior poles that are fused.

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9
Q

what does the horseshoe kidney get stuck on

A

IMA

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10
Q

what are horseshoe kidneys associated with

A

hydronephrosis, renal stones, infection, chromosomal aneuploidy and sometimes cancer

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11
Q

unilateral renal agenesis

A

uteric bud fails to develp and induce differentiation of metanephrtic mesenchyme so complete absence of kidney and ureter

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12
Q

multicystic dysplasic kidney

A

uretic bud fails to induce differentiation of metanephric mesenchyme so nonfunctional kidney consisting of cysts and connective tissue.

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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

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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

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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

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16
Q

which kidney is taken for transplant and why

A

the left is taken because of the longer renal vein

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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

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18
Q

what is the arriving after to the glomerulus and which is the one leaving

A

it is afferent and efferent

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19
Q

what does the ureter pass under

A

the uterine artery or under the vas deferens

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20
Q

what can damage the ureters

A

ligation of uterine or ovarian vessels can damage it causes obstruction or leak

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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

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22
Q

what can plasma volume be measured by

A

it can be measured by radiolabelled albumin

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23
Q

extracellular volume can be measured by what

A

mannitol and inulin

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24
Q

what is the percent water per body weight

A
  • 60% of total body water
  • 40% is the ICF
  • 20% is the ECF
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25
Q

what is the normal body mass

A

70Kg

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26
Q

what is the glomerular filtration barrier composed of

A

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

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27
Q

when the charge barrier lost and what happens if it is lost

A

it is lost in nephrotic syndrome and it causes albuminuria, hyporpoteinemia, generalized edema, and hyperlipidemia

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28
Q

what is the formula for renal clearance

A

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

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29
Q

what can be used to calculate clearance

A

inulin because its filtered and not reabsorbed or secreted

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30
Q

what is the GFR formula

A

UV/P

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31
Q

what is normal GFR

A

100

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32
Q

what is the substance used for estimating GFR

A

it is creatinine clearance is an approximate measure of GFR and it slightly overestimates GFR because creatinine is moderately secreted at the tubules

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33
Q

what does incremental reductions in GFR define

A

chronic kidney disease

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34
Q

what estimates RPF

A

PAH clearance is used because between filtration and secretion there is 100% excretion of all PAH that enters the kidneys

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35
Q

what is the formula for RPF

A

UV/P

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36
Q

what is the formula of RBF

A

RPF/(1-hct)

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37
Q

Cx

A

net tubular reabsroption

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38
Q

Cx>GFR

A

net tubular secretion

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39
Q

Cx=GFR

A

no net secretion or reabsorption

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40
Q

what is normal FF

A

20%

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41
Q

what is the formal of FF

A

GFR/RPF

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42
Q

what represents the P part of the net filtration pressure

A

hydrostatic and glomerular

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43
Q

what is the pi part of the net filtration pressure

A

oncotic pressure and bowman space

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44
Q

what happens to GFR, RPF, and FF with afferent arteriole constriction- also what drug causes this

A

decreased GFR, decreased RPF, and no change in FF- NSAIDs

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45
Q

what happens to GFR, RPF, and FF with efferent arteriole constriction- what can cause this

A

Increased GFR, decreased RPF, increased FF- and this is from ATII

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46
Q

what happens to GFR, RPF, and FF with increased plasma protein concentration

A

decreased GFR, no change in RPF and decreased FF

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47
Q

what happens to GFR, RPF, and FF with decreased plasma protein concentration

A

increased GFR, no change to RPF, and increased FF

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48
Q

what happens to GFR, RPF, and FF with constriction of the ureter

A

decreased GFR and decreased FF

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49
Q

what happens to GFR, RPF, and FF with dehydration

A

decreased GFR, decreased RPF, and increased FF

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50
Q

what happens to GFR, RPF, and FF with dilation of the efferent arteriole and what causes this

A

decreased GFR, increased RPF, decreased FF this is from ace inhibitors

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51
Q

how do you calculate the reabsortion

A

filtered-excreted

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52
Q

how do you calculate secretion

A

excreted-filtered

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53
Q

what is the FENa formula

A

Na excreted/Na filtered

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54
Q

where is glucose usually reabsorbed and by what receptor

A

it is usually from the PCT by the Na/hlucose cotransporter

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55
Q

where does glucosuria begin and when is it saturated

A

it starts at 200 and 375 is saturated

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56
Q

normal pregnancy does what to glucose clearance

A

it decreases the ability of the PCT to reabsorb glucose and amino acids- glycosuria and aminoaciduria

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57
Q

what is the splay region of glucose clearance from

A

its the region of substance clearance between threshold and Tm due to heterogeneity of the nephrons

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58
Q

what does the PCT reabsorb

A

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

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59
Q

where does PTH work in the kidney and what does it do

A

it works on the PCT and it inhibits the Na/Po4 cotranport so that Po4 is exctered

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60
Q

what does ATII do at the PCT

A

it increased Na and H2O and Hcro reabsorption leading to contraction alkalosis

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61
Q

what does the thin descending loop of here do

A

passively reabsobs H20 via medullary hypertonicity and its impermeable to Na making this the concentrating segment

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62
Q

what does the TAL do

A

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

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63
Q

Early DCT function

A

reabsorbed the Na and Cl and it makes urine fully dilute.

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64
Q

what does PTH do at the DCT

A

it increases the Ca/Na exchanges to increase Ca reabsorption

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65
Q

Collectung tubule function

A

it reabsorbed Na in exchange for K and H

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66
Q

what does aldosterone do at the CT

A

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

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67
Q

what does ADH do at the CT

A

it acts at the V2 receptor and inserts aquaporins into the apical side

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68
Q

what blocks the V2 receptors

A

Lithium

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69
Q

Fanconi syndrome- what is it doing

A

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

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70
Q

what are the causes of Fanconi

A

Wilson, tyrosinemia, glycogen storage disorder, ischemia, multiple myeloma, nephrotoxns

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71
Q

what drugs can cause FAnconi

A

ifosfamide, cisplatin, tenofovir, expried tetrcytlines, lead poisoning

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72
Q

Bartter syndrome

A

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

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73
Q

Gitleman

A

defect of NAcli in the DCT like thiazide diuretics use. AR. it is low K and low Mg, and metabolic alkalosis, and hypocalciuria

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74
Q

Liddle Syndrome

A

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

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75
Q

syndrome of apparent mineralocorticoid excess (SAME)

A

deficiency of 11ba hydroxysteroid dehydrogenase- so increased mineralocorticoids. increased minrealocoticoid receptor acitvity- HTN, decreased K, metabolic alkalosis, low serum aldosteron

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76
Q

what can you get acquired SAME from

A

glycyrrhetinic acid which is present in licorice

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77
Q

what is the order of the solute secreted and reabsorbed lines on the graph

A

from secreted to reabsorbed: PAH, creating, inulin, urea, Cl, K, Na, osmolarity, HCO3, Amino acids, glucose

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78
Q

what activates the RAAS

A

decreased BP, decreased NA, increased sympathetic tone

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79
Q

what blocks renin release

A

beta cell blocker

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80
Q

what blocks renin binding

A

aliskrenin

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81
Q

what blocks ACE

A

prils- increased bradykinin by blocking ACE

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82
Q

what blocks angiotensin II binding

A

arbs and these end in artans

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83
Q

what does angiotensin II do to vascular smooth muscle

A

it causes vasoconstriction and increased BP

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84
Q

what does angiotensin II do to glomerulus

A

it is constricts efferent arteriole to increase FF to preserve renal function in low-volume states

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85
Q

what does angiotensin II do to adrenal gland

A

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

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86
Q

what does angiotensin II do to the posterior pituitary

A

it increases aquaporin insertion into the CT in the principal cells. Increased H2O reabsorption

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87
Q

what does angiotensin II do to PCT

A

it increases the NA/H activity which increases Na, HCO3 reabsorption, and contraction alkalosis

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88
Q

what does angiotensin II do to hypothalamus

A

stimulates thirst

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89
Q

where does renin come from and what does it do

A

it is secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic deischarge- beta effect

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90
Q

where does ATII work and what does it affect

A

affects baroreceptors function and limit reflex bradycardia which would normally accompany its present effects, helps maintain blood volume and blood pressure

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91
Q

where does ANP and BNP work and what does it affect

A

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

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92
Q

where does ADH work and what does it affect

A

it regulates osmolarity and responsible for low volume states

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93
Q

where does aldosterone work and what does it affect

A

aldosteone regulates the ECF and NA content and responds to low blood volume states

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94
Q

where are the JG cells and what does it sense

A

they are on the afferent arteriole. It senses changes in decreased BP and increased sympathetic tone

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95
Q

where is the macula dense and what does it sense

A

it is in the DCT and it is from decreased NaCl delivery and increased renin release and efferent arteriole constricts and increased GFR

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96
Q

what happens with beta blockers

A

it is decrease in BP from inhibition of B1 receptors in the JGA cells by decreasing renin release

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97
Q

erythropoein

A

released by interstitial cells in the peritubular capillary bed to hypoxia. stimulates RBC proliferation in bone marrow. Erythropetin often supplement in chronic kidney disease

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98
Q

caciferol

A

PCT cells convert 25-OH to 1,25 ocnverserion by 1-alpha-hydroxylase

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99
Q

prostaglandins

A

paracine secretion vasodilates the afferent arterioles to increase RBF

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100
Q

what do NSAIDs do

A

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

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101
Q

low dopamine

A

dilates interlobular arteries, afferent arterioles, efferent arterioles to increase RBF little or no change in GFR

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102
Q

high dopamine

A

acts as a vasoconstrictor

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103
Q

where is dopamine secreted in the kidney

A

it is secreted from the PCT cells to increase naturesis

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104
Q

where does ANP work

A

on the afferent arteriole

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105
Q

where does PTH work in the serum

A

causes Ca reabsorption from DCT, and decreased PO4 from the PCT, and 1,25 Oh production is increased

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106
Q

what causes shift of K out of the cell

A

digitalis, hyperosmolarity, lysis of cells, acidosis, beta blockers, high blood sugar like DKA (need to be careful with correction of DKA from creating kalemia)

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107
Q

what shifts K into the cell

A

hypo-osmolarity, alkalossi, beta adrenergic agonist, insulin

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108
Q

low sodium concentration symptoms

A

nausea, maliase, stupor, coma, seizures

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109
Q

high sodium concentration symptoms

A

irritability, stupor, coma

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110
Q

low potassium concentration symptoms

A

u waves, flat T waves, arrhythmias, muscle cramps, spasm, weakness

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111
Q

high potassium concentration symptoms

A

wide QRS, peaked T waves, arrhythmia, muscle weakness

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112
Q

low Ca concentration symptoms

A

tetany, seizures, QT prolongation, twitching, and spasm

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113
Q

high Ca concentration symptoms

A

stones, bones, groans, increased urinary frequency, psychiatric overtones, anxiety, altered mental status

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114
Q

low Mg concentration symptoms

A

tetany, torsades de pointes, hypokalemia

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115
Q

high Mg concentration symptoms

A

decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

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116
Q

low phosphate concentration symptoms

A

bone loss, osteomalacia, rickets in kids

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117
Q

high phosphate concentration symptoms

A

renal stones, metastatic calcifications, hypocalcemia

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118
Q

what happens to the renin, aldoterone and urinary ca levels in Bartters syndrom

A

increased renin, aldosterone and urinary Ca

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119
Q

what happens to renin, aldosterone, Mg, and urinary Ca in Gitelman syndrome

A

increased renin, increased aldosterone, decreased Mg, and decreased urinary Ca

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120
Q

what happens to BP, renin, aldosterone in Liddle syndrome

A

increased BP, decreased renin, and decreased aldosterone

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121
Q

what happens to BP, renin, aldosterone in SIADH

A

increased BP, decreased renin, decreased aldosterone

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122
Q

what happens to BP, renin, and aldosterone during primary hyperaldosterone

A

BP is increased, renin is decreased, aldosterone increased

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123
Q

what happens to Bp, renin, aldosterone in a renin secreting tumor

A

Bp increased, renin increased and aldosterone increased

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124
Q

what are the pH, Pco2, and HCO3 levels in metabolic acidosis

A

decreased pH, decreased Pco2, decreased Hco3

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125
Q

what are the pH, Pco2, and HCO3 levels in metabolic alkalosis

A

increased pH, increased PCo2, increased HCO3

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126
Q

what are the pH, Pco2, and HCO3 levels in respiratory acidosis

A

decreased pH, increased PCO2, and increased HCO3

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127
Q

what are the pH, Pco2, and HCO3 levels in respiratory alkalosis

A

increased pH, decreased PCo2, and decreased HCo3

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128
Q

what is the henderson hassebech used for acid-base physiolgoy

A

Ph=hCO3/PaCO2

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129
Q

what causes respiratory accesses and how they breath

A

hypoventilation- airway obstruction, acute lung disease, chronic lung disease like COPD, opioids, sedatives, weak respiratory muscles

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130
Q

what are the causes of AGMA

A

methanol, uremia, DKA, propylene glycol, iron tablets, isoniazid, lactic acidosis, ethylene glycol, late salycilic acid

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131
Q

what are the causes of normal anion gap metabolic acidosis

A

hyperalimentation, addison disease, rental tubular acidosis, diarrhea, acetazolamide, spirolactone, saline infusion

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132
Q

what causes respiratory alkalosis and what is the breathing pattern

A

hyperventialtion- hysteria, hypoxemia and high altitude, early salicylate, tumor, pulmonary embolism

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133
Q

what causes metabolic alkalosis

A

loop diuretics, committing, antacids, hyperaldosteronism

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134
Q

what is the Cl level in the urine for metabolic alkalosis

A

it is high in the urine

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135
Q

what does the horseshose kidney get stuck on

A

IMA

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136
Q

unilateral renal agenesis can cause what

A

hypertrophy of one kidney and it creates increased CKD as they get older

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137
Q

what happens with bilateral renal agenesis

A

oligohydramnios- lund hypoplasai, flat face, low set ears, developmental defects of extremities and compatible with life

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138
Q

dysplastic kidney unilateral

A

most commone

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139
Q

what does the histology of the dysplastic kidney look like

A

noninhertied cysts in kidney like cartilage

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140
Q

what is bilateral dysplastic

A

can present like PKD but has not of the other associated problems and is non-inherited

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141
Q

ARPKD

A

infants, HTN, renal failure, Potter sequence.

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142
Q

what is associated with ARPKD

A

hepatic cysts and fibrosis- baby with portal HTN

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143
Q

ADPKD

A

young adults with HTN, and hematuria and renal failure with increased renin

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144
Q

what is associated with ADPKD

A

berry anyreusm, hepatic cysts, mitral valve prolapse

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145
Q

medullary cystic kidney disease

A

in medullary colleting ducts, small kineys and worsening renal failure

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146
Q

Acute renal failure- first symptoms

A

azotemia, oliguria,are hallmark signs.

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147
Q

Prerenal acute renal failure- lab values

A

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.

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148
Q

postrenal acute renal failures- lab values

A

decreased GFR from back pressure. Force more BUN back into the blood so >15 in ratio. The FENa and ism are normal.

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149
Q

what changes are in the lab values with post-renal acute renal failure

A

long standing leads to tubular damage, so ratio<15 and FEN>2%

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150
Q

acute tubular necrosis uses

A

injury and necorsis, and necrotic cell plus the tubes and blocks the GFR from back pressure

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151
Q

what is seen in the urine for ATN

A

brown granular casts are seen with cells that lose nuclei and detach from the basement membrane

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152
Q

what are the lab values for ATN

A

B:cr ratio<15 and FEN>2 and osm<500

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153
Q

what are the ischemic causes of ATN and where do they hit first

A

tend to affect the PCT and TAL first and are preceded by prerenal syndrome

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154
Q

what are the nephrotoxic causes of ATN

A

aminoglycosides, Pb, myoglobin, ethelyne glycol, radio contrast, rate from tumor lysis syndrome, hydrate and use allopurinol

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155
Q

what lab values do you see with nephrotoxic ATN

A

oliguira, brown granular casts, increased BUN, increased Cr, increased K, metabolic acid

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156
Q

how long does the oliguria last with ATN

A

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

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157
Q

acute interstitial nephritits- causes, symptoms and histology

A

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

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158
Q

renal papillary necrosis and what are the associated conditions

A

necrosis of renal papilla and gross hematuria, flank pain-ASA, DM, sickle cell, pyelonephritis

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159
Q

what is the hallmark of nephrotic syndrome and lab values

A

proteinuria>3.5, hypoalbumina, hypogammaglobulinemia, hypercoagulable (lose ATIII), and hyperlipidemia, and increased cholesterol

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160
Q

why are nephrotic syndrome patients hypercoaglable

A

this is from the loss of ATIII

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161
Q

minimal change disease- what are the symptoms, pictures, and what can be associated with it

A

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.

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162
Q

what causes the damage in minimal change disease

A

it is from damage from T cells release of cytokines

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163
Q

what is black, hispanic, HIV, heroin, sickle cell association

A

FSGS

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164
Q

FSGS- what are the histological findings, and see it on images and what is the progression

A

dense collagen in the glomerulus, and no immune complexes, only some segments are affected it can go to CKD

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165
Q

Caucasian, hepatitis B and C, solid tumor, SLE, NSAIDs, penicillamines what is the association

A

membranous nephrotic syndrome

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166
Q

membranous- what are the histological findings, and see it on images and what is the progression

A

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.

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167
Q

where are the spike and domes

A

underneath podocyte and lay down new membrane dome is on top of the deposits and the spike is in between

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168
Q

membranoproliferative- what are the histological findings, and see it on images and what is the progression

A

thick capsular membrane- mesangial cell proliferation-tram track appearance from excess tacked up membrane. Granular IF.

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169
Q

what is type 1 membranoproliferative glomerulonephritis associated with and histology

A

hepatitis B and C and tram track appearance

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170
Q

what is type 2 membranoproliferative glomerulonephritis associated with and histology

A

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

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171
Q

where are the deposits in MPGN 1

A

sub endothelial

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172
Q

where are the deposits in MPGN 2

A

BM

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173
Q

where are the deposits in membranous

A

sub epithelial

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174
Q

diabetic nephropathy is from waht

A

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.

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175
Q

what slows down the progression of diabetic nephropathy

A

ACE slows down this profession because it slows to clamp of efferent arteriole goes to nephrotic

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176
Q

what is the classic histology of diabetic nephropathy

A

kimmelsteil wilson nodules

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177
Q

systemic amyloid on the kidney- where does amyloid deposit, and what is the histology

A

amyloid is in the mesangium and apple green biofringence

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178
Q

classic symptoms of nephritic syndrome

A

glomerular inflammation, bleeding, oliguria, azotemia, salt retention, periorbital edema, RBC casts, and hypocellular inflamed glomerulus and C5a mediated damage

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179
Q

post strep glomerulonephritis- what is it from and what else is there and what causes it

A

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

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180
Q

what is the crescent of RPGn full of

A

fibrin and macropahges

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181
Q

if the IF is linear on the RPGN then what is it from

A

linera is an antibody against BM so goodpasures sundrome- hematuira, hemoptysis and no sinus issues

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182
Q

if the iF is granular, on the RPGN then what is it from

A

post strep glomerulonephritis- adult or diffuse proliferative in lupus.

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183
Q

if the IF is negative, on the RPGN then what is it from

A

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
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184
Q

IgA neprhotpathy

A

mesagnial deposits, RBC casets following an mucosal infection

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185
Q

what is seen on the IF of IgA nephropathy

A

grnaular mesangial deposits

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186
Q

what is seen on Alport syndrome

A

thinning and split BM from issues with Collagen IV, and hematuria only sensory hearing loss, ocular disturbances

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187
Q

what are the symptoms of cystitis

A

dysuria, suprapubic pain, no systemic symptoms and frequency

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188
Q

what are the labs for cystitis

A

> WBC, leukocyte esterase, nitrites, culture>100000

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189
Q

what are the common causes of cystitis

A

ecoli, staph sapro, proteus which causes alkalization of urine

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190
Q

what is sterile pyuria and whats it from

A

negative culture, suggests urethrititis from chlamaydia or gonorrhea

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191
Q

pyelonephritits symptoms and causes

A

fever, flank pain, WBC casts, leukocytosis and ecoli, kleb, and enterococcus

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192
Q

what are some of the increased risk of pyelonephritis

A

vesicoureteral reflux where theureters reach the bladder

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193
Q

chronic pylonephritits obsturction- histology and gross moprhology

A

cortical scarring at upper and lower poles and blunted calyxes and thyroidization of the kidney- tubules look huge and filled with colloid

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194
Q

calcium oxalate and calclium phosphate stoens- what do you look for and what are the associateions

A

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

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195
Q

treatment of calcium oxylate stones

A

HCTZ

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196
Q

ammonium magnesum phosphate stoens

A

infection of urease positive oganisms that cause staghorm calculi and alkaline urine

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197
Q

uric acid stone

A

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

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198
Q

staghorm calculi in children

A

cysteine stones from weird absorption difficulties

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199
Q

uremia as a side effect of CKD

A

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

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200
Q

EPO where is it produced

A

renal peritubular intersitial cells

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201
Q

why is there decreased vitamin D in CKD

A

decreased Ca from decreased 1 alpha hydroxylate and can’t excrete phosphate so decreased free Ca

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202
Q

renal osteodystrophy related symptoms

A
  • 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
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203
Q

what do kidneys look like if they have been on dialysis

A

cysts and shrunken kidneys

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204
Q

what is there an increased risk of with CKD

A

renal cell carcinoma

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205
Q

aniogmyolipoma

A

tumor of the BV, with smooth muscle, dispose and associated with TS

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206
Q

RCC symptoms

A

hematuria, flank pain, fever, weight loss

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207
Q

what are the paraneoplastic syndromes associated with RCC

A

EPO, renin, PThrP, and aCTH

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208
Q

what can RCC cause if it hits the renal vein

A

left sided hematuria

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209
Q

what does RCC look like grossly and histollogically

A

it looks like clear cytoplasm and large yellow tumor

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210
Q

where does sporadic RCC occur

A

it is single in the upper pole associated with smokers

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211
Q

what are the mutations for RCC

A

it is VHL, which increases the IGF, and HIF, and increased VEGF, and increased PDEF

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212
Q

where is the genetic RCC

A

younger patient bilaterally, and mutliple- it is VHL

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213
Q

what is associated with VHL

A

RCC, hemanigoblastoma of the cerebellum

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214
Q

Wilms tumor is derived from what

A

blastema from glomeruli and storma

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215
Q

what is seen for Wilms tumor

A

lunger central flank mass, and HTN from increased renin

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216
Q

WAGR

A

wilms tumor, aniridia, genetial abnormalities, and retardation

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217
Q

Beckwith wideman syndrome

A

wilms tumor, hypoglycemia (neonatal), muscular hemihypertrophy, and organomegaly especially the tongue

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218
Q

Urothelial canrinoma

A

from transitional epithelium of lower track

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219
Q

what are the increased risk factors for urothelial carcinoma

A

polycyclic hydrocardbon, naptholene, azo dyes, cyclophosphamise, pehnactin

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220
Q

what is the papillary Urothelial canrinoma like and progression

A

papillary growth with blood vessel and it goes from low, high, to invasive

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221
Q

what is the flat urothelilal carcinoma like and progression

A

high grade then invades high risk of P53 mutation first

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222
Q

SCC carcinoma of the bladder risk factors

A

chronic cystitis, schistosoma hematobeium, long standing nephrolithiais

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223
Q

adenocarcinoma of the bladder

A

urachal remnant, cystitis glandularis, and extrophy from failure of anterior folds

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224
Q

where is adenocarcinoma of the bladder

A

it is on the dome of the bladder.

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225
Q

distal renal tubular acidosis

A

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

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226
Q

what are the causes of distal renal tubular acidosis

A

amphoterecin B toxicity, analgesic neprhopathy, congential anomalies like the obstruction of the urinary tract

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227
Q

proximal renal tubular acidosis

A

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.

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228
Q

what are the causes of proximal renal tubular acidosis

A

fanconi and carbonic anhydrase inhibitors

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229
Q

hyperkalemia renal tubular acidosis

A

urinary ph<5.5 hypoaldosteronis and so hyperkalemia, and decreased NH3 synthesis in PCT and decreased NH4 excretion

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230
Q

hyperkalemia renal tubular acidosis causes

A

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

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231
Q

RBC casts

A

glomerulonephritis and malignant HTN

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232
Q

WBC casts

A

tubulointerstitial nflammation, acute pyelonephritis, transplant rejection

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233
Q

Fatty casts

A

nephrotic syndrome associated with maltese crosses

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234
Q

granular muddy brown casts

A

acute tubular necorsis

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235
Q

waxy casts

A

end-stage renal disease with CKD

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236
Q

hyaline casts

A

normla finding from concentrated urine samples

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237
Q

what are the depositions made from in the goodpasture syndrome

A

IgG and C3

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238
Q

what is the deposition in the IgA nephtopathy and where do they deoposit

A

IgA and C3. They deposit in the vascular system like mesangium, palpable purport, dermis, GI tract. Gross heamturia

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239
Q

what is GBM splitting seen in

A

Type I MPGN

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240
Q

what can the loss of ATIII do in nephrotic syndrome cause

A

it can be from renal vein thrombosi

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241
Q

what are the spike and domes from in membranous nephrotipathy

A

IGG and C3

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242
Q

what are the serum antibodies against in membranous neprhtopathy

A

it is antibodies against phospholipase A2 receptor

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243
Q

what can kidney stone present with

A

unilateral flank pain, abdominal pain, and vomiting

244
Q

what are the urease positive organisms

A

Klebsiella, proteus, and staph saprophyticus

245
Q

which kidney stones are radiolucent

A

uric acid, and cysteine stones

246
Q

what is the genetic cause of cysteine stones and what is the other things that get stuck1

A

there is hereditary cysteine reabsorbing PCT transport which also leads to poor ornithine, lysine, arguing and cystine but the cystine forms the stoens

247
Q

what test is positive in cystene stones

A

sodium cyanide

248
Q

what are the kidney stones that are hexagonal

A

cysteine

249
Q

what stones are coffin shaped

A

amonium magneiusm phosphate stoen

250
Q

enveloped or prism shaped stone

A

calcium oxalate and calcium phsophate

251
Q

what stones are rhomboid shaped

A

uric acid stoens

252
Q

when does the creatinine increase with hdyronephrosis

A

if it is obstructed bilaterally or it happens when patient only has one kidney

253
Q

why are the cells of RCC clear

A

from increased glycogen and lupids

254
Q

where does RCC usually met to

A

lung and bone

255
Q

where does the RCC originate

A

PCT cells

256
Q

renal oncocytoma

A

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
Q

what is RCC also called

A

renal cell adenocarcinoma

258
Q

stress incontinence

A

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
Q

urgency incontinence

A

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
Q

mixed incontience

A

both urgency and stress

261
Q

overflow infontience

A

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
Q

xanthogramulomatous pyelonephritis

A

widespread kidney damage due to granulomaous tissue containing foamy macrophages

263
Q

diffuse coritcal necorsis

A

acute generalized infarction of both kidneys due to combination of vasospasm and DIC. associated with obstetric catastrophes and septic shock

264
Q

what form of vitamin D is decreased in renal osteodystrophy

A

25- hydroxycalciferol

265
Q

what are the consequences of renal failrure

A

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
Q

what are the major drugs causing acute interstitial nephritis

A

diuretics, NSAIDs, penicillins, cephalosporins, PPIs, rifampin

267
Q

what are the signs of renal papillary necorsis

A

bloody urine, colickly flank pain from urethral obstruction, hematuria, proteinuria

268
Q

simple kidney cysts

A

filled wit hultrafiltrate and very common for majority of renal masses

269
Q

complex cysts of the kidney

A

septates, enhances and or have solid components on imaging need to be removed for risk of RCC

270
Q

sonic hedgehog gene- what does it do and what is a defect from it

A

it is patterning along the anterior posterior axis and CNS development- Holoprosencephaly is the defect

271
Q

Wnt-7- what does it do and what is a defect from it

A

it produces the apical ectodermal ridge necessary for dorsal ventrla so nose and toes directions.

272
Q

FGF- what does it do and what is a defect from it

A

lengthening the limbs. Achondroplasia is FGF3

273
Q

Hox gnees

A

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
Q

when does HCG become detectable

A

around day 6-8 when the blastocyst implants

275
Q

when is the bilaminar disc created

A

2 weeks

276
Q

when does gastrulation occur

A

3 weeks

277
Q

when does the notochord start

A

18 days

278
Q

when does the neural tube close

A

4 weeks

279
Q

when is the fetus most susceptible to teratogens

A

3-8 weeks

280
Q

what happens at week

A

4 LIMBS AND 4 chambered heart

281
Q

what happens at week 8

A

movement

282
Q

what happens at week ten

A

genitalia

283
Q

what glands does the ectoderm form

A

parotid, mammary, and sweat glands

284
Q

what does the craniopharyngeoma arise from

A

surface ectoderm

285
Q

what does the nueroectoderm create

A

the CNS and retina, and spinal cored

286
Q

what does the paraxial mesoderm form

A

it forms the cartilage, tendon, skeletal muscle, endothelium, and dermis

287
Q

what does the mesoderm form

A

spleen, cardio, lymphatics blood, upper bag wall of ut tube, and ovaries, tests, adrenal cortex, dermis

288
Q

what does the notochord become in the adult

A

nucellous pulposis

289
Q

what is the mesodermal defects

A

vertebral defeects, anal atresia, cardiac defects, TE, renal defects, limb defects

290
Q

what is the intermediate mesoderm

A

GU

291
Q

endoderm what does it form

A

guy tube epithelium above the pectinated like, liver, lungs, gall bladder, pancreases, eustachian tube, thymus, parathyroid, thyroid follicles

292
Q

teratogen: ACE

A

renal failure and oligohydramnios

293
Q

teratogen: alkylating agents- cyclophosphamide, methotrexate

A

absence of digits, multiple anomalies

294
Q

teratogen: aminoglycosides

A

ototoxicity

295
Q

teratogen: antiepiletpitcs

A

NT defects

296
Q

teratogen: DES like diethylstibesterol

A

vaginal clear cell adenocarcinoma or congenital mullein anomalies

297
Q

teratogen: trimethropin, methotrexate

A

NT defects

298
Q

teratogen: isoretinoin

A

multiple severe birth defects

299
Q

teratogen: lithium

A

ebstein anomaly

300
Q

teratogen: tetracyclines

A

discolored teeth and inhibited bone growth

301
Q

teratogen: thalidomide

A

limb defects like phocomelia

302
Q

teratogen: wafarin

A

bone deformities, nasal hypoplasia, fetal hemorrhage, abortion

303
Q

what do you use for anticoagulation during pregnancy and why

A

heparin because its large and polar

304
Q

what does the typical FAS baby look like

A

smooth filtrum, wide narrow eyes, and epicenthal folds

305
Q

teratogen: cocaine

A

vasoconstrictioon IUGR, low birth weight, preemie

306
Q

teratogen: smoking

A

low birth weight, preteen labor, placental problem, SIDS, IUGR

307
Q

teratogen: iodine

A

congenital goiteror hypothyridism

308
Q

teratogen: maternal diabetes

A

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
Q

teratogen: methymercury

A

fish and it is neurotoxic

310
Q

teratogen: vitamin A excess

A

spontaneous abortions and birth defects

311
Q

teratogen: XR

A

microcephaly and intellectual disability

312
Q

what is the worst end of FAS

A

holoprocencephaly

313
Q

when do dichroinoic diamnionic twins split

A

0-4 says and this is at he 2 cell stage

314
Q

when do monochroiconic and diamnioic twins split

A

one placenta two sacs-4-8 days

315
Q

when do mono mono twins split

A

8-12 days

316
Q

when do conjoined twins split

A

greater than 13 days

317
Q

what is the most common type of twins

A

monochorionic twins and diamniotic

318
Q

whate does the cytotrophoblasts do

A

it is the inner layer and it makes cells

319
Q

what does the syncitiotrophoblast do

A

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
Q

what is the decidua balalis

A

it is the maternal component where the maternal blood goes into lacunas

321
Q

umbilical arteries do what

A

they return deoxygenated blood from the fetal internal iliac arteries to the placenta.

322
Q

what is the deal if there is only one umbilical artery

A

congenital and chromosomal abnormalties

323
Q

what does the umbilical vein doing

A

it supplies oxygenated blood from the placenta to fetus and drains into the IVC via liver or ductus venossuus

324
Q

what is the urachus

A

it was a duct between the umbilicus and fetal bladder

325
Q

what is a patent urachus

A

total failure of arches to obliterate so there is urine around umbilicus

326
Q

what is a urachal cyst

A

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
Q

what type of cancer is associated with a urachal cyst and where is it located

A

it is a adenocarcinoma on the done of the bladder

328
Q

what is a vesicuurachal diverticulum

A

it is a slight failure to obliterate which leads to an outputting of the ebaldder

329
Q

what is the vitelline duct

A

it connects the yolk sac to the midgut lumen

330
Q

what is a vitelline fistula

A

vitelline duct fails to close so there is meconium discharge from the umbilicus

331
Q

what is a meckell diverticulum from

A

parial closure of the vitalize duct with patent portion attached to the ileum and it can have gastric or pancreatic tissue hetertopically

332
Q

what are the derivatives of the 1 and 2 arctic arches

A

maxillary aretery and stapedial artery

333
Q

what are the derivatives of the 3 and 4 arctic arches

A

3- common carotid and internal carotid artery

4- aortic arch and right subclavian

334
Q

what are the derivatives of the 6th aortic arch

A

PDA

335
Q

what are the branchia clefts from

A

ectoderm

336
Q

what are the branchial arches from

A

mesoderm and neural crest

337
Q

what are the branchial pouches from

A

endoderm

338
Q

what is the derivateve of the first cleft

A

external auditory meatus

339
Q

what is the branchial cleft derivative of 2-4

A

cervical sinues and these are temporaty

340
Q

what is a persistent cervical sinus present as

A

branchial cleft cyst which is a lateral mass that does not move with swallow

341
Q

what are the derivates of the first branchial arch

A

maxiallya, mandible, and mastication muscles and associated nerves

342
Q

what are the disorders of the first branchial arch

A

Chew- Pierre Robin sequence- micrognathia, glossoptosis, cleft palate, and airway obstruction.
Treacher Collons- neural crest dysfunction- mandibular hypoplasia, facial abnormalities

343
Q

what are the derivates of the second branchial arch

A

Smile- CN VII- stapes styloid, stylohoid- and stapedius and posterior belly of the digastric

344
Q

what are the derivates of the third branchial arch

A

Swallow- grater horn of the hyoid and the stylopharngeus. CN IX

345
Q

what are the derivates of the fourth-sixth branchial arch

A

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
Q

what is the mmnurmonic for the arches

A

chew, smile, swallow stylishly, simply swallow, and speak

347
Q

what do you cut through for a cricothyrotomy

A

places between the cricoid and thyroid cartilage. Incise through skin, superficial cervical fascia, investing pretrachial, deep fascia, and cricothyroid membrane

348
Q

what does the first pouch develop into

A

ear

349
Q

what does the second pouch develop into

A

palantine tonsil

350
Q

what does the third pouch develop into

A

inferior is the parathyroid and the thymus

351
Q

what does the fourth pouch develop into

A

superior parathyroids and parafollicular cells of the thyroid

352
Q

DiGeorge is an aberrant development of which pouches

A

3 and 4 so thymic aplasia and failure of parathyroids leading to hypocalcemia

353
Q

cleft lip is from what

A

failure of fusion of maxillary and medial nasal processes

354
Q

what is cleft palate from

A

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
Q

what is the default embryologic GU development

A

female mesonephric degenerates and paramesoneprhic develops

356
Q

what is the male formation like from the internal and external path

A

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
Q

what happens if there are no sertoli cells or they lack MIF

A

develop male and female internal genitalia and male external genitalia

358
Q

what happens if 5 alpha reductase is deficitnet

A

inability to convert t to DHT causes male internal genitalia nbut ambigious on the outside- Dominican children that sprout penises at puberty.

359
Q

Paramesoneprhic development

A

no SRY gene, so it develops into female internal structures, fallopian tubes, uterus, upper portion of the vagina

360
Q

what happens for mullein agensis

A

may present as primary amenorrhea due to lack of uterus with females with full functional ovaries and secondary sexual characteristics

361
Q

septate uterus

A

incomplete reposition of the septum

362
Q

bicronate uterus

A

incomplete fusion of the mullein ducts

363
Q

uterus didelphys

A

complete failure of fusion, so double uterues, vagina, and cervis

364
Q

gubernaculum

A

anchors the testis in the scrotum and it is the ovarian ligament and round ligament of the uterus

365
Q

processus vaginalis

A

former the tunica vaginalis in the male and nothing in the female

366
Q

what is different about the venous drainage on the right and left

A

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
Q

what is the LN drainage of the ovary/testes

A

para-aortic

368
Q

what is the LN drainage of the body of uterus, cervis, superior bladder

A

external iliac

369
Q

what is the LN drainage of the prostate, cervis, corpus cavernous/proximal vagina

A

internal iliac nodes

370
Q

what is the LN drainage of the distal vagina, vulva, scrotum, distal anus

A

superficial inguinal LN

371
Q

what is the LN drainage of the glans penis

A

deep inguinal LN

372
Q

what is the ligament that gets ligated for oophorectomy and ovarian torsion

A

it is the infundibulopelvic or the suspensory ligament of the ovary

373
Q

what ligament connects the vervix to the side wall of the pelvis

A

cardinal ligament

374
Q

what ligament is the derivative of the gubernaculum and travels through the inguinal canal

A

round ligament

375
Q

what is the artery of samson

A

it is the anastomosis of the ovarian and uterine vessels

376
Q

what ligament attaches the uterus , fallopian tubes and ovaries to the pelvic side wall

A

broad ligament

377
Q

what ligament attacks the ovary to the lateral uterus

A

ovarian ligament

378
Q

what is the epithelium of the ectocervix

A

strat squamous

379
Q

what is the epithelium of the endocervix

A

it is simple collumnar

380
Q

what is the epithelium of the uterus during the proliferative phase

A

it is long tubular glands

381
Q

what is the epithelium of the uterus during secretory phase

A

coiled glands

382
Q

where does a vasectomy cut and how long do you have to wait

A

it cuts the vas deferent but need to wait for 3 months

383
Q

what is the path of sperm during ejaculation

A

seminiferous tubules, epidydimus, vas deferens, ejaculatory duct, urethra, penis

384
Q

where is the urethra injured from a car accidnet

A

it is injured at the membranous urethra

385
Q

where is the straddle injury of the urethra

A

it is in the bulbar and penile urethra. Urine can get into Bucks fascia

386
Q

innervation of an erection

A

PNS increased NO and increased cGMP, and vasodilation- projectile

387
Q

what takes away an erection

A

it is NE and increased Ca cause smooth muscle contraction leading to vasoconstriction and the penis becomes soft

388
Q

emission innervtion

A

SNS and it is from the hypogastric nerve

389
Q

ejaculation innervation

A

visceral and somatic nerves like the pudendal nerve

390
Q

spermatogonia

A

maintain germ pool and produce primary spermatocytes

391
Q

serotili cells

A

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
Q

Leydig cells

A

secrete testosterone in the presence of LH and is unaffected by temperature

393
Q

estrogen source

A

ovary, placenta, adipose tissue

394
Q

what is the order of the estrogens in relation to potency

A

estradiol>estrone>estriol

395
Q

wahat is the function of estrogen

A

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
Q

what estrogens increase and by how much during pregnancy

A

50x increased in estradiol and estrone. and 1000 increase in estriol which indicates fetal well-being

397
Q

where are estrogen receptors

A

they are in the cytoplasm and translocate to the nucleus when bound by estrogen

398
Q

what is the pathway of estrogen production in the ovary

A

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
Q

progesterone sources

A

Corpus lueteum, palcenta, adreanal cortex, and testes

400
Q

what is the function of progesteron

A

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
Q

decreases progesterone increases what

A

it increases prolactin

402
Q

what stage of meiosis is completed just prior to ovulation

A

meisosis I

403
Q

what stage is the ice in until ovulation

A

prophase I

404
Q

what stage is the oocyte arrested in until fertilization

A

metaphase II

405
Q

what hormones do what for ovulation

A

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
Q

mid cycle pain with peritoneal irritation

A

Mittelzchmerz

407
Q

imperforarte hymen

A

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
Q

how long is the luteal phase

A

14 days

409
Q

what is ovulation plus 14

A

period

410
Q

when is the follicular phase of growth the fastest

A

2nd week of follicular phase

411
Q

what stimulates the endometrial proliferation

A

estrogen

412
Q

what maintains the endometrium to support implantation

A

progesterone

413
Q

where does fertilization usually occur

A

in the ampulla of the fallopian tube within one day of ovulation

414
Q

when does the implantation occu

A

6 days after fertilization

415
Q

what secretes hug and when is it detectable in blood and urien

A

syncitiotrophoblasts and 1 week for blood and 2 for urine

416
Q

what is gestatational age

A

it is calculated from date of last menstrual period

417
Q

what is embryonic age

A

calculated from date of concentption

418
Q

what happens to CO in preganancy

A

increased preload decreased after load and increased CO

419
Q

what happens to Hr in preganancy

A

increased for increased perfusion

420
Q

what happens to blood cells in preganancy

A

anemia from increased plasma and increased RBC and decreased viscosity

421
Q

what happens to coagulation in preganancy

A

it is increased to decrease blood loss during delivery

422
Q

what happens to breathing during pregnancy

A

hyperventialtion because of the increased CO2 output

423
Q

what does lactogen do during pregnancy

A

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
Q

what is supin hyertension syndrome of pregnancy

A

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
Q

what does the HCG do and when does it peak

A

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
Q

what is the deal with the alpha subunit of HCG

A

it is the same as LH, FSH, and TSH and so if there is increased HCG then it can cause hyperthyroidism

427
Q

what are the causes of increased HCG

A

multiple gestations, molar pregnancy, choriocarcinomas, down syndrome

428
Q

what are the causes of decreased HCG

A

ectopic pregnanc, tri 13 and 18

429
Q

low brith weight is defined as what and what are the complicatiosn

A

increased risk of SIDS, and increased motility have more infection, RDS, necrotizing entercolotits, intraventricular hemorrhage, and persistent fetal circulation like PDA

430
Q

what increases the risk of SIDS

A

secondhand smoke, sleeping with the baby, asthma, otitis media, and pneumonia

431
Q

what are the causes of intraventricular hemorrhage in the child and what are the symptoms

A

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
Q

lactation what does prolactin do and what does oxytocin do

A

prolactin- induce and maintain lactation and decrese fertility. Oxytocin assits in milk let down and promotes uterine contraction

433
Q

what does breast milk contain- immune cell wise

A

IgA, macrophages, and lymphocytes. it can decrease risk of infection, asthma, allergies, diabetes, and obsestiy

434
Q

what supplementation is required with breast milk

A

D and K

435
Q

what risks are lowered maternally if they breast feed

A

decreased risk of ovarian and breast cancer

436
Q

what is the criteria and symptoms and hormone levels for menopausr

A

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
Q

menopause before 40 signals what

A

premature ovarian failure

438
Q

what does T do

A

differntiation of the epidydimus, vas deferens, seminal vesicles, penis , seminal vesicles, and sperm and muscles and deep voice and close epiphyseal plates, libido

439
Q

DHT function

A

differentiation of penis, scrotum, prostate, balding large prostate and sebaceous gland

440
Q

what converts T to DHT and what is it inhibited by

A

5alpha reductase and it is inhibited by finasteride.

441
Q

what does exogenous T do to the normal hormone functioning

A

it inhibits the hypothalamic axis, and the pit gonad recreation so decreased intratesticualr testosterone and decreased testosertone size and azospermia

442
Q

when does spermatogenesis begin

A

puberty

443
Q

how long does full sperm development take

A

2 months

444
Q

Tanner stage 1

A

no sexual hair, flat chest wit raised nipple

445
Q

Tanner stage 2

A

pubic hair appears-pubarche
testicualr enlargement
breast bud forms-thelarche

446
Q

Tanner stage 3

A

coarsening of pubic hair
penis lengeth increases
breast mounds form

447
Q

Tanner stage 4

A

coarse hair across pubis, penid gets bigger, breast gets bigger and aerola gets bigeer

448
Q

Tanner stage 5

A

coarse hair across the pubis and middle thigh penis and testis unloader. adult breast contours and aerola gets less fluffy

449
Q

testicular atrophy, long extremities, gynecomastia, female hair distribution, and intellectual disabiltiy- what in the condition and what are the hormonal level with it

A

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
Q

what if the testosterone is high and the LH is high

A

defective androgen receptor

451
Q

what if the T is high and the LH low

A

testosterone secreting tumor or exogenous steroids

452
Q

what is the T is low and the LH is high

A

primary hypogonadism

453
Q

what if the T and the LH are low

A

hypogonadotropic hypogonadism

454
Q

what is a 46 XX DSD present as

A

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
Q

what does a 46 XY DSD present as

A

testes are present but external lgenitalia are female or ambiguous. Most common is androgen insensitivity syndrome or testicular feminization

456
Q

what is placental aromatase deficiecny

A

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
Q

what is androgen insensitivity syndrome 46 XY

A

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
Q

5 alpha reductase deficiency

A

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
Q

Kallman syndrome

A

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
Q

what is the mutation in Kallman syndrome

A

KAL1 gene and FGF 1 receptor

461
Q

hydatidifrom mole (complete)

A

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
Q

what are the general symptoms of a molar pregnancy and what casuses this

A

pelvic pain, vaginal beleeding, early preeclampsia, theca leutial cysts, hyperemesis, hyperthyroid

463
Q

Partial Mole

A

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
Q

choriocarcinoma

A

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
Q

what kind of discharge might you see from choriocarcinoma

A

muddy brown discharge

466
Q

placental aburption

A

premature sepearation of the placenta from the uterine wall before delivery

467
Q

what are the risk factors for placental aburption

A

trauma like MVA, cocaine, HTN smoking preeclampsia

468
Q

what is the presentation of placental aburption

A

abrupt painful bleeding in third trimester wit hDIC, maternal shock, fetal distress

469
Q

what does DIC happen with placental abruption

A

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
Q

what are the risk factors for placenta acreta

A

prior C section, infalmmation, placenta previa

471
Q

placenta accreta

A

placenta attaches to the myometrium without penetrating it

472
Q

placenta increta

A

placenta goes into the myometrium

473
Q

placenta percreta

A

placenta perforrates into the uterien sourer or rectum or bladder

474
Q

what is the presentation of placenta accreta and what does it cause as complications

A

often detected on ultrasound and no separation of placenta after delivery leading to postpartum hemorrhagee and Sheehan syndrome

475
Q

placenta previa risk factors

A

multiparity prior c section

476
Q

placenta previa presentation

A

painless third trimester bleeding

477
Q

placenta previa what is it

A

placenta to lower uterine semgent over or next to the cervical os

478
Q

vasa previa presentaion

A

triad of membrane rupture, painless vaginal bleedign and fetal bradycardia

479
Q

what is vasa previa

A

it is where the fetal vessels run over or in close proximity to the cervical os leading to vessel rupture, exsanguinatio and death.

480
Q

what should be done about vasa previa

A

it is an emergency C section

481
Q

what is associated with vasa previa

A

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
Q

Postpartum hemorrhage what is it from

A

uterine atony, trauma, thrombin and tissue like retained products of conception

483
Q

if the uterus is large and boggy from the myometrium not clamping down, what can be ligated to stop a life threatening hemorrhage

A

internal iliac artery ligation

484
Q

ectopic pregnancy occurs where

A

ampulla of the fallopian tube

485
Q

what is the history normal for ectopic prengnacy

A

lower than expected HCG, appendicitis, amenorrhea, and sudden low abdominal pain

486
Q

what are the risk factors for ectopic pregnancy

A

prior ectopic, history of infertility, salpingitis from PID, ruptured appendix, prior tubal surgery

487
Q

polyhydramnios

A

oto much amniotic fluid associated with esophageal duodenal atresia, anencephaly and inability to swallow fluid maternal diabetes, fetal anemia , multiple gestations

488
Q

oligohydramnios

A

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
Q

gestational hypertension

A

BP>140/90 after the 20th week of gestation. No preexisting HTN

490
Q

treatment for gestation HTn

A

hydralazine, alpha methyldopa, labetalol, nifedipine try to deliver 37-39 weeks

491
Q

preeclampsia

A

new onset HTN with either proteinuria or end organ dysfunction after 20 weeks. May proceed to exlampsia or sieures

492
Q

what is the cause of preeclampsia

A

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
Q

what are the complications of preeclampsia

A

placental abruption, coagulopathy, renal failure ueroplacental insufficienct, eclampsia

494
Q

what increases the incidence of preeclampsia

A

pre-existing HTN, DM, CKD, autoimmune disorders

495
Q

treatment of preeclampsia

A

antihypertensives, IV mg sulfate, definitive is delivery

496
Q

eclampsia

A

preeclampsia and maternal seizures

497
Q

what is maternal death from in eclampsia

A

ARDS, sroke, intracranial hemorrhage

498
Q

treatment of eclampsia

A

IV MG sulfate, antihypertensives, immediate delivery

499
Q

HELLP

A

hemolysis, elevated LFTs, low platelets. manifestation of severe preeclampsia

500
Q

presentation of HELP

A

pre with nausea vomitting, absornmianl pain for 12 hours and high BP and RUQ

501
Q

what is seen on histology of HELLp

A

schostocytes

502
Q

what can the HELLLP lead to

A

hepatic subcapsular heamotmas leading to rupture and severe hypotension

503
Q

for gynecologic tumors what is the incidence by type

A

endometrial>ovarian>cervical

504
Q

what is the most common gynecologic tumors worldwide

A

cervical from lack of screening

505
Q

what is the worst for prognosis in gynecologic tumors

A

ovarian>endometrial cervical

506
Q

gestation diabetes

A

big headed big babdy from decreased insulin sensitivity. use diet and insulin. Baby can have beta cell hyperplasia leading to hypoglycemia neonatallay

507
Q

pre-gestation diabetes

A

DM prior to pre need to manage wit insulin and big baby with cardiac defects and sacral agenesis

508
Q

what is a high grade CIn

A

atypical cells are by on the lower 1.3 of the cervia lepthelum and to the epithelial surface and go to invasive

509
Q

what is low grade CIN

A

cells are not in the lower 1/3 of the vagina

510
Q

what is it called if the CIN invades the BM

A

it is invasive

511
Q

what is micro invasive CIN

A

it goes into the BM

512
Q

septic abortion

A

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
Q

what are the long term complications of septic abortion

A

it is adhesions secondary ammenorhea and infertility

514
Q

sqamous cell caricnoma

A

it is in the vagina and is rarely primary

515
Q

what is clear cell adenocarcinoma associated with and where is it

A

vagina and from DES exposure

516
Q

Sarcoma botryoides- embroyngal rhabdomyosarcoma

A

affects girls<4 years old- spindle shaped cells and design positive grape mass from the vagina

517
Q

dysplasia and carcinoma in situ for cervical cancer

A

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
Q

dysplasia and carcinoma in situ for cervical cancer- what causes it

A

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
Q

invasive cervical carcinoma

A

scc and pap smear of cervial dupsplasia lateral invasion can block the ureters and cause renal failure

520
Q

premature ovarian failure

A

premature atresia of the ovarina follicles in some of reproductive age and signs of puberty before 40

521
Q

causes of anovulation

A

eprgancny, PCOS, obestivy, HPO axis issues, premature ovarian failure, increased prolactin, thyroid issues, eating disorder, athletes, cushign, adrenal insufficiency

522
Q

follicular cyst

A

distention of enraptured gradian follicle asoscited wit hhyperesterogeism and endometrial hyperplasia most common in young women ncan lead to torsio

523
Q

theca-leutin cysts

A

often bilateral, multiple and due to gonadotropin stimulation associated with choriocarcinoma and hyatidiform moles- from increased HCG

524
Q

serous cystadenoam

A

ovarian neoplasm which his the most common- lined with fallopian tube like epithelium and often bilateral

525
Q

what is the most common person and presentation for ovarian neplsma

A

women>55 adnexal mass

526
Q

what increases the chance of malignancy in ovarian masses

A

advanced age, infertility, endometriosis, PCOS, genetic predispsotion like BRCA1 and 2, Lynch syndrome and strong family history

527
Q

what decreases the chance of malignancy in ovarian masses

A

previous pregnancy, history of breast feeding, OCPs, tubal ligation

528
Q

what do you measure for recurrence of ovarian mass

A

CA125

529
Q

mucinos cystadenoam

A

multiloculated large cells that have mucus secreting epithelim

530
Q

endometrioma

A

endometriosis with ovary cyst formation mass presents wit pelvic pain dysmenorrhea, dyspareniuna and chocolate cysts

531
Q

mature cystic teratoma

A

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
Q

what ovarian tumor can present with hyperthyroidism and why

A

mature cystic teratoma can present with ectopic thyroid tissue

533
Q

Brenner tumor

A

loos like the bladder solid tumor that is pale yellow tan and encapsulated and coffee bean nuclei

534
Q

fibrosmas

A

bundles of single shaped fibrolasts with Meigs syndrome of ovarian fibroma, acites, hydrothorax and pulling in the groin

535
Q

what is Meigs syndrome and what is it associated with

A

ovarian fibroma, ascites, hydrothorax and pulling sensation in the groin

536
Q

thecoma

A

like granolas cell tumors may produce estrogen presents with abnormal uterine bleeding in postmenopausal woman

537
Q

granulosa cell tumor

A

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
Q

serous cystadenoma

A

malignant ovarina neoplasm bilateral with psammoma bodies

539
Q

mucinous cystadenocarcinom

A

psydomyxoma periotinei intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor

540
Q

immature teratoma

A

aggerssive contains getal tissue neuroectodem and it is before 20 years old and represented by immature/embyonic like neural tissue

541
Q

dysgerminoma- W

A

adolescents wit hquiaalent to seminoma- it is increased HCG and LDH asa tumor markers wit fired egg cells

542
Q

yolk sac tumor or woman

A

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
Q

Krukenberg tumor

A

Gi malignancy that mets to the ovaries and mucin secreting signet ring celsl

544
Q

endometrial poly

A

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
Q

adenomyosis

A

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
Q

Leiomyoma

A

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
Q

endometrial hyperplasia

A

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
Q

risk factors for endometrial hyperplasia

A

anovualtroy cycles, HRT, pcos, and granulosa cell tumor

549
Q

endometritis

A

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
Q

endometriosis

A

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
Q

treatmetn for endometriosis

A

NSAIDs OCP, progestin GNRH, danazol, laproscoptic removal

552
Q

leiomyosarcoma

A

malignant from myometrium which is denovo not from leioma and it is a rapidly enlarging uterus

553
Q

fibroadenoma of the breast- typical patient

A

women under 35

554
Q

what is the typical presentation of fibroadenoma of the breast

A

increased size and tenderness with the estrogen and small well defined mobile pass

555
Q

what is the histology of the fibroadenoma

A

glands and cystic spaces with epitheliumn that atrophies and the storm is hyalinzied and benign myxoid stroma

556
Q

fibrocystic breast changes

A

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
Q

aclerosis adenossi

A

increased acini and stomal fibrosis associated wit calcifications and slight increased risk of cancer

558
Q

intraducatal pailloma

A

small papillary tumor within lactiferous ducts typically beneath areola most common cause of bloody discharge. papilalry cells with fibrovascualr core

559
Q

epithelial hyperplasia

A

increased cells in the terminal ductal or lobular epithelium and increased risk of carcinoma with atpyical cells

560
Q

phyllodes tumor

A

large mass of connective tissue wit cyst s that are lead like most common in 5th decade of life and can befcome malignan

561
Q

fat necrosis of the breast

A

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
Q

lactational mastitis

A

breastfeeding increased risk of staph aureus from cracks n the nipple. treat with antibiotics and keep breast feeding

563
Q

gynecomastia

A

breast enlargemetn in men due to increased estrogen compared to androgen- cirrhosis, hypogonadisn, testicualr tumors, spirlactone, cimetidine, ketoconazole

564
Q

after amstectomy with eaxillary LN dissection can cause what

A

chroninc lymphaenam and angiosarcoma with shot slit infiltration with abnormal vascular spaces

565
Q

what receptors have worse prognosis for breast cancer

A

triple negative

566
Q

what is the most important prognostic factor for early state disease

A

axillary LN involement

567
Q

what is the most often axillary LN involved

A

upper-outer quadrant of the breast

568
Q

what increases your risk for malignancy of the breast

A

increases estrogen, increased menstrual cycles, older age at first live brith, ocestiy, BRCA1, and BRCA2, and AA ethnicity for triple negative

569
Q

DCIS

A

fill ductal lyme and arises from ductal atypia

570
Q

what is seen on mammography of DCIS

A

microcalcifications

571
Q

what is seen on histology of DCIS

A

pleomorphic cells with central necrosis does not pass basement membrane and can lead to Pagget

572
Q

comedocarcinoma

A

ductal with central necrosis subtype of DCIS

573
Q

Paget disease

A

underlyins DCIS or underlying invasive breast cancer. edematous nipple patches

574
Q

invasive ductal carcinoma

A

firm fibrous rock hard mass with sharp margins and small glandular duct cells with stellate infiltration- most of the breast cancer

575
Q

invasive lobular carcinoma

A

orderly row of cells due to decrease e cad herein expression- bilateral with multiple lesions in the same locatio

576
Q

nmedulalry carcinoma

A

fleshy, cellualr ,lymphocytic infiltrate

577
Q

inflammatory breast cancer

A

dermal lymphatic invasion by breast carcinoma Peau d organdy neoclassic lymphatic drainage- itchy rash and obstruction of lymph drainage

578
Q

dimpling

A

signs of invoelment of suspensory ligaments leading to traction dab breast dimple

579
Q

peyronie diease

A

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
Q

ischemic priapism

A

painful sustained erection lasting more than 4 horus. sickle cells, dildenafil and trazadone, teat wit corporal aspiration, intravarenosal phenylephrine or surgical decompresion

581
Q

SCC of the dick

A

more common in Asia, africa, south America the precursor lesions are below can be from HPV

582
Q

bowen disease

A

penile shaft lesion with leukoplaskia

583
Q

erythropalsia of Queryrat

A

cancer of the glans that presents are erythroplakia

584
Q

Bowenoid papulosis

A

carcinoma incite of unclear malignant potential in young person as reddish papules

585
Q

cryptorchismim

A

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
Q

varicocelel

A

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
Q

what can compress the left renal vein

A

aorta and SMA

588
Q

congenital hydrocele

A

scotal swelling in infants due to incompelte obliteration fo processus vaginalis

589
Q

acquired hydrocele

A

scotal fluid collection from infection, trauma or tumor

590
Q

spermatocele

A

csyt due to dilated epidydimal duct or rete testes- paratesticualr fluculant nodule

591
Q

what are the risk factors for testicular germ cells tumors

A

cryptorchisdism, klineferlts, most are mixed germ cell tumros

592
Q

seminoma

A

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
Q

yolk sac tumors

A

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
Q

choriocarcinoma

A

malignant increased in HCG from disorder syncitiotrophoblastic and cytoptphiblastic tissue mets to the lungs and brain. gynecomastia ad hyperthryoid

595
Q

what does choriocaricnoma cause hyperthyroid

A

increased BHCg which has the same alpha unit at TSH

596
Q

teratoma

A

males may be malignant the later they are caught

597
Q

embroynal carcinoma

A

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
Q

Lydia cell tumors

A

golden brown color containing REinke crystals and eosinihilic cytoplasmic inclusions produce androgens or estrogens- gynecomastia, and prcosuous pebbly in boys

599
Q

Stroll cell tumors

A

androblastoma from sex cord stroma

600
Q

testicualr lymphoma

A

most common testicular cancer in older men- not a primary center arises from matastatic lymphoma to the testes and is aggressive

601
Q

BPH

A

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
Q

what is the treatment for BPH

A

alpha 1 antagonists lieke terazosin and tasulosin which hcuase realization of the smooth muscle. five alpha reductase inhibitors like finasteride, and tadalafil

603
Q

prostatitis

A

dysturia frquency regency low back pain, warm tender enalrged prostate

604
Q

what is the cause of acute protatitis

A

it is ecoli in older people and neisseria or clap in younger people

605
Q

what is the cause of conic prostatitis

A

tends to be a bacterial

606
Q

prostatic adenocarcinoam

A

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
Q

what type of bone mets does prostate cancer have

A

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

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