First Aid Pics II Flashcards by Caroline Motschwiller

What is SMA syndrome?

SMA syndrome = transverse (distal 1/3) portion of the duodenum is entrapped btwn the SMA and the aorta causing intestinal obstruction

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Location of Meissner vs. Auerbach plexus

Meissner = submucosal nerve plexus- located in the submucosa (first layer right under the mucosa)

Auerbach = in the muscularis propria

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Specific change seen in Barrett’s esophagus

Barrett’s esophagus = a type of metaplasia = change in stress on a cell type changes the type of cell

Stem cells change from making nonkeratinized stratified squamous cells to making intestinal epithelium (nonciliated columnar ep. w/ goblet cells) that is more adapted to deal w/ gastric acid

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What is this CT w/ oral contrast showing?

Narrowing of the distal duodenum- 2/2 circumferential ectopic pancreatic tissue = annular pancreas

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Differentiate the venous drainage above vs. below the pectinate line

Above pectinate line: enters IVC thru inferior mesenteric vein from the superior rectal vein

Below pectinate line: enters IVC thru the common iliac vein from the inferior rectal vein

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Using ‘SAD PUCKER’ mneumonic, name the GI retroperitoneal structures

Suprarenal (adrenal) gland

Aorta and IVC

Duodenum (parts 2,3,4)

Pancreas (except the tail)

Ureter

Colon (descending and ascending)

Kidneys

Esophagus

Rectum

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Which type of hernia is in each of the 3 X’ed areas

Lateral to inferior epigastric vessels = indirect inguinal hernia
Medial to inferior epigastric vessels (in Hasselbach’s triangle) = direct inguinal hernia
Inferior to inguinal ligament = Femoral hernia

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Explain how a gallstone can cause both cholangitis and pancreatitis

If gallstone sits at the ampulla of Vater it blocks both the common bile duct and the pancreatic duct (double duct sign)

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What happens to bilirubin after conjugation in the liver?

Gut bacteria converts it into urobilinogen

80% of urobilinogen is excrete in feces (gives feces its brown color)

20% of urobilinogen is reabsorbed, 10% of which is excreted in urine (gives urine its yellow color), other 90% re-enters the enterohepatic circulation

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Differentiate sliding vs. paraesophageal hiatal hernia

Hiatal hernia = diaphragmatic hernia where stomach protrudes upwards thru esophageal hiatus

sliding = GE jxn above esophageal hiatus
paraesophageal = GE jxn is normal, but fundus of stomach herniates

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Name the layers of the gut wall

‘MSMS’ from lumen outwards

mucosa = epithelium, lamina propria, muscularis propria
submucosa = secretes fluid, contains Meisner (submucosal) nerve plexus
muscularis externa = motility (muscle), myenteric (Auerbach) plexus
serosa when intraperitoneal (or adventitia when retroperitoneal)

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How to differentiate esophageal atresia w/ and w/o tracheo-esophageal fistula

Both first diagnosable by trying to pass NG tube and it doesn’t enter stomach

W/o TEF => gasless abdomen (on CXR)

W/ TEF = gass in the abdomen

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S/p episode of vomiting pt presents w/ this CT

(a) Dx
(b) Mgmt

(a) Dx = pneumomediastinum, given clinical scenario most likely 2/2 Boerrhave syndrome = transmural tear in esophagus from violent vomiting
(b) Mgmt = immediate surgery

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Explain the arrowed finding

Stomach has a ‘cerebriform’ appearance (look like brain gyrae) b/c the rugae are so hypertrophied = gastric mucosa hyperplasia = Menetrier disease

acquired premalignant condition of massive gastric folds
increased risk of gastric adenocarcinoma

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Name the organization of the femoral region

Lateral to medial: nerve, artery, vein, empty, lymphatics

‘venous to the penis’ = vein more medial

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Name the borders of the anatomic triangle that direct inguinal hernias protrude through

Hasselbach (inguinal) triangle borders:

medial border = lateral border of the rectus abdominis
lateral border = inferior epigastric vessels
inferior border = inguinal ligament

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What are Brunner’s glands?

Brunner’s glands = duodenal glands (mark transition from stomach to duodenum)

Secrete HCO3- to:

provide alkaline environment to activate intestinal enyzmes
protect against acidity of chyme

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Describe the mechanism of the two drugs used to decrease production of stomach acid

PPI that directly inhibits the ATPase that pumps out H+ in exchange for K+
H2 blocker = histamine receptor agonist to inhibit the main stimulatory signal of H+ production (histamine from ECL cells)

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Label the branches of the abdominal aorta

come out anteriorly if they supply the gut (celiac trunk, SMA, IMA)
come out laterally if they supply non-gut structures (adrenal, renal, gonadal)

Celiac trunk out at T12 level, IMA at L3

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What are portosystemic anastamoses

(a) Name the 3 major ones

Portosystemic anastamoses = connection btwn portal and systemic circulation

(a) 3 major:
- esophageal (left gastric and esophageal)
- caput medusae (paraumbilical recanalizes to small epigastric veins of anterior abd wall)
- anorectal varices (superior rectal to middle/inferior rectal a)

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Label the branches of the celiac artery

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Which are in the body of the stomach, antrum, duodenum?

(a) Parietal cells
(b) Mucus cells
(c) D cells
(d) K cells
(e) I cells
(f) Chief cells
(g) S cells
(h) G cells

(a) Parietal cells in the body of the stomach (secrete H+)
(b) Mucus cells (secrete bicarb/mucus) in antrum
(c) D cells in the antrum secrete somatostatin
(d) K cells in the duodenum secrete GIP (gastric inhibitory protein)
(e) I cells in the duodenum secrete CCK to stimulate pancreatic secretions
(f) Chief cells in the body of the stomach secrete pepsinogen
(g) S cells in the duodenum secrete secretin
(h) G cells in the antrum secrete gastrin (respond to vagus nerve)

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Explain the concept of the alkaline tide post-prandially

Food in stomach stimulates gastrin secretion and H+ secretion, which in exchange pushes a bicarb into the serum

-basically pushing H+ into GI lumen creates an extra HCO3- that gets shuttled into the bloodstream to keep even charge inside the cell

So alkaline tide refers to a transient rise in pH often postprandially

-also seen in more severe form w/ vomitting where parietal cells compenstae for lost gastric acid creating huge alkaline tide and causing metabolic alkalosis

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What are plicae circularis?

(a) Differentiate from gastric folds
(b) Differentiate from haustra
(c) Location
(d) Fxn

Plicae circularis = circular folds in the (c) jejunum and ileum of the small intestines

(a) Permanent, don’t disappear w/ distention like gastric folds
(b) Plicae circularis are circumferential (all the way around) while haustra are larger and don’t reach all the way around
(d) Increase surface area for absorption

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Locate the site of a femoral hernia

Femoral hernias go thru the femoral ring = space btwn femoral vein and lymphatics (just medial to femoral vein)

Which zone of the liver is affected first by (a) ischemia (b) viral hepatitis (c) Alcoholic hepatitis (d) Metabolic toxins vs. exogenous toxins

Zone I = closest to arterial supply (portal triad) Zone III = closest to ventral vein (most deoxygenated) (a) Zone III (b) Zone I (c) Zone III (d) Metabolic toxins first affect zone III, exogenous toxins (cocaine) first affect zone I

What are Peyer's patches? (a) Location- which layer? (b) Fxn

= organized lymphoid follicules in the gut (a) Distal SI (mostly ileum, some jejunum, few/rare duodenum). In submucosa layer and extend into mucosa layer (b) Immune surveillance- contain macrophages, dendritic cells, B and T cells, trap foreign particles and surveillance and destroy them

Describe the 3 receptors on parietal cells that stimulate H+ secretion

1. M3 (muscarinic) receptors that respond to ACh from vagus nerve 2. Gastrin-responsive receptors directly responsive to gastrin 3. H2 receptor stimulated by histamine from ECL cells (stimulated by gastrin) - H2 receptor: G coupled protein to activate ATPase that pumps out H+ in exchange for a K+

Differentiate apical and basolateral membrane of hepatocytes

Basolateral membrane faces sinusoids Apical membrane faces bile caliculi

Name the cutoffs of the embryologic (a) Forgut (b) Midgut (c) Hindgut

(a) Forgut: pharynx to proximal 1/3 duodenum - structures supplied by celiac artery (b) Midgut: Duodenum to first 2/3 of transverse colon - blood supply from SMA (c) Hindgut: Distal 1/3 of transverse colon to anal canal above the pectinate line - blood supply from IMA

Gastrochesis vs. omphalocele

Omplalocele- abdominal contents are covered by peritoneum, worse prognosis 2/2 associated cardiac defects Gastrochesis- abdominal contents not covered by peritoneum

Differentiate the histologic appearance of the classes of lymphocytes

- Neutrophils = multilobed nucleus (2-5) w/ azurophilic lysosome granules - monocytes (macrophage precursors) have large kidney-shaped nucleus w/ extensive "frosted glass cytoplasm" - Macrophage - Eosinophil = bilobate nucleus, eosinophilic granules of uniform size - Basophil: densely basophilic granules containing heparin and histamine

What are Langerhans cells?

Langerhans cells = dendritic cells in the skin -dendritic cells are highly phagocytic APCs, link the innate and adaptive immune system by expressing MHC class II and Fc receptors on surface

How to distinguish plasma cells on histology

"Clock face" chromatin distribution w/ abundant RER -basically see clock-face appearance of nuclei

Name components of vascular endothelial cells that are (a) Prothrombotic (b) Anti-thrombotic (c) Stabilize plt plug

Vascular endothelial cells have tons of stuff (a) Prothrombotic = vWF (in alpha granules) and factor VIII (b) Anti-thrombotic = PGI2 (prostacyclin = inhibits plt activation and vasodilates) and tPA (c) Vascular endothelial cell contains thromboplastin that converts plasmiogen to plasmin so plasmin can stabilize fibrin clot (plasmin coverts fibrinogen to fibrin)

If you see an oval-shaped enlarged RBC on peripheral smear, what other blood cell abnormality would you expect to see?

Oval-shaped enlarged RBC = Macro-ovalocyte- seen in folate and B12 deficiency (megaloblastic macrocytic anemia) or bone marrow failure -megaloblastic features involve enlargement of RBCs = macro-ovalocyte Also exepct hypersegmented neutrophils

Give the etiology of basophilic stipling in the absence of anemia

Basophilic stipling = visualized ribosomes in cell periphery 2/2 defect in rRNA breakdown - can occur b/c of regenerative anemias (both Fe deficiency and megaloblastic) - w/o anemia: think of lead poisoning

Dx suggested by presence of the following cells on peripheral smear

Acanthocytes = spur cells = presence of abnormally spiked RBC membrane -indicates dx of liver disease of abetalipoproteinemia (type of cholesterol dysregulation)

Name 4 conditions where the following cells are seen

Target cells = RBCs w/ excess membrane in the middle (interupting central pallor) 'HALT to the target' - HbC disease (glutamate --\> lysine) - Asplenia - liver disease - thalassemia

Type of RBC is most classically associated w/ what d/o?

Dacrocyte = 'teardrop' cell is classically indicative of myelofibrosis - myelofibrosis = BM infiltrated and replaced by CT - RBC is tugged to one end (creating tear drop shape) as it squeezes out of bone marrow or reticuloendothelial system w/ an increased amount of CT

Name 2 d/o w/ the following finding

Stimulation of hematopoesis outside the normal sites (usually confined to long bones) causes hyperplasia of skull and facial bone =\> crewcut appearance on Xray and chipmunk facies -2/2 extramedullary hematopoiesis Seen classically in: beta-thalassemia minor and sickle cell

Lab Values in iron deficiency anemia

Iron deficiency anemia: low serum Fe (duh), elevated TIBC/transferrin level (liver sees low iron so pumps out more transferrin) -ferritin (stoarge) reduced

Lab values seen in anemia of chronic disease

Anemia of chronic disease: chronic inflammatory state = elevated inflammatory makers = elevated hepcidin sequesters iron away inside cells so it's not accessible to RBCs for heme production - elevated ferritin (b/c stores are high b/c can't be accessed) - low serum iron - low transferrin saturation (none in blood) - TIBC is reduced (always goes opposite of ferritin)

Lab values seen in sideroblastic anemia

Sideroblastic anemia = defective heme synthesis - high ferritin (high stores b/c not being used) - high serum iron and high TIBC (again high b/c not getting used) - low TIBC (b/c always opposite ferritin)

Changes in TIBC and transferrin saturation seen in pregnancy and OCPs

- increaesd TIBC - low percent saturation

Explain the mechanism of opioids

Opioids agonize the mu, delta, and kappa opioid receptors to (1) decrease synaptic nt release from presynaptic neuron (2) hyperpolarize postsynaptic neuron -opioid binding to receptor =\> opens K+ and closes Ca2+ channels to reduce release of ACh, NE, 5-HT, glutamate, and substance P

Where do benzos and barbiturates work? (a) What else works here?

Both benzos and barbiturates bind the GABA-A receptor (ligand-gated Cl- channel) (a) Also bound by EtOH but barbiturates increase duration of Cl- channel opening to reduce neuronal firing, while benzos increased frequency of Cl- channel opening (so duration vs. frequency)

Name two Parkinsons drugs that centrally inhibit DA degradation

Both COMT inhibitors (specifically Tolcopone works both peripherally and centrally) and MAO-B inhibitor Selegiline work centrally in presynaptic neuron to decrease DA degradation into

Mechanism of amantadine in use of Parkinsons tx

Amantadine (also antiviral) increases dopamine availability by increasing presynaptic DA release and inhibiting DA reuptake

Differentiate mechanism of tolcapone and entacpone

Both are COMT inhibitors that reduce degradation of DA (so useful as adjunct tx in Parkinsons d/o where DA is reduced) But tolcapone works both centrally and peripherally, while Entacpone works only peripherally -both used in ADJUNCT to L-DOPA (NOT ALONE)

Name the 4 pathways of dopaminergic transmission and explain their role in schizophrenia

4 main dopamine pathways 1. Mesolimbic: VTA to nucleus accumbens, responsible for positive symptoms 2. Mesocortical- VTA to prefrontal cortex repsonsible for negative symptoms 3. Nigrostriatal- substantia nigra to striatum responsible for stimulation of purposeful movement 4. Tuberoinfundibular pathway- DA pathways in hypothalmus from arcuate and periventricular nucleus to the infundibular region, responsible for inhibiting prolactin release

Dx = horseshoe kidney stuck lower in abdomen under root of the IMA

Explain the location of a horseshoe kidney

During development kidneys move from pelvis up into the abdomen, w/ lower poles fused the horseshoe kidney gets stuck at the root of the inferior mesenteric artery =\> doesn't ascend fully so present in lower abdomen

Differentiate the three embryologic structures of the renal system

1. Pronephros first- don't do anything 2. Mesonephros that act as kidneys for the first trimester, then go away or in males contribute to the GU system 3. Metanephros are the permanent stuff that starts to form at the 5th week of gestation

Explain the etiology of a duplex collecting system

Duplex collecting system = two ureters for one kidney, increased risk VUR, ureteral obstruction, and UTI Etiology is embryological: bifurcation of ureteric bud before it enters the metanephric blastema, or have 2 ureteric buds that reach the metanpehric blastema

What letter senses and responds to NaCl concentration

Macula densea (A)- specialized cells that line the thick ascending loop and lay btwn the afferent and efferent arteriole are sensitive to the NaCl concentration of incoming blood -stimulate renin release if NaCl concentration drops

Relationship btwn ureter and vas deferens

"Water runs under the bridge" - ureter runs under both the uterine artery (females) and ductus deferens (males) Ex: manipulation of uterine artery in the cardinal ligament during surgery can damage ureter =\> obstruction or leak

Differentiate the two components of the metanephros

Metanephros comprised of the ureteric bud and the metanpehric mesenchyme Ureteric bud =\> ureter, pelvis, calyces, collecting ducts Metanephric mesenchyme =\> nephrons

Differentiate activity of prostaglandins and ATII at the afferent and efferent arteriole

PGE preferentially vasodilate afferent arteriole =\> increasing both RBF and GRF so FF stays constant ATII preferentially constricts the efferent arteriole which decreases RBF but increases GFR =\> increases FF

Percent of sodium reabsorbed in each part of the nephron

- Most (65-80%) reabsorbed in PCT - thin descending loop impermeable to Na+ - thick ascending loop: 10-20% Na - DCT: 5-10%

Where does Mg and Ca reabsorption get reabsorbed in the nephron?

Mg and Ca get reabsorbed in the thick ascending limb paracellularly (btwn the interstitial cells straight into blood) -driven by positive lumen potential from K+ backleak

Action of aldo on the collecting tubule

Aldo - upregulates ENac to increase Na reabsorption - stimulates K+ secretion out into filtrate - stimulates H+ ATPase =\> increase H+ secretion

Distinguish the two components of the JGA

Juxtaglomerular apparatus: 1. Macula densa = cells of the DCT that sense NaCl concentration and moderate renin secretion 2. JG cells = modified smooth muscle cells of the afferet arteriole that secrete renin 3. Also includes mesangial cells

What cells release EPO

Interstitial cells in the peritubular capillary bed (arises from the efferent arteriole) -renal peritubular interstitial cells

Function of Winter's formula

Winter's formula calculates the respiratory compensation expected for a simple metabolic acidosis If the pt PCO2 is markedly different than the PCO2 calculated by Winter's formula, then there is a second pH disturbance simultaneously occuring pCO2 = 1.5 (HCO3) + 8 +/- 2

Where in the kidney is vitamin D activated?

25-OH vit D --\> 1,25-OH vit D by 1 alpha hydroxylase in the PCT -proximal convoluted tubule cells have 1 alpha hydroxylase

Benign renal tumor associated w/ large eosinophilic cells w/ abundant mitochondria

Renal oncocytom = benign renal epithelial cell tumor Often surgically removed just to exclude RCC

Diuretic that (a) Increases urine calcium (b) Decreases urine calcium and mechanism

(a) Loop diuretics increase urinary calcium excretion by reducing paracellular calcium reabsorption in PCT (b) Thiazide diuretics increase calcium reabsorption by enhancing Ca reabsorption at the DCT

MC type of monozygotic twins

Most monozygotic twins cleave btwn 4-8 days, causing monochorionic, diamniotic twins -so in two sacs (diamniotic) but one placenta (monochorionic)

Explain functional structure of the placenta

Fetal: cytotrophoblasts and syncytiotrophoblast line chorionic villi that protrude into lacunae (spaces filled w/ maternal blood). Maternal artery from the decidua basalis (derived from endometrium) delivers blood into the decidua basalis

4 structures w/in the umbilical cord

Umbilical cord 1,2: two umbilical arteries returning de-O2 blood from fetal internal iliac arteries 3: single umbilical vein- delivers O2 blood to fetal IVC via ductus venosus or liver 4: allantoic duct = connects yolk sac and urogenital sinus, becomes the allantois that connects the fetal bladder and yolk sac

Differentiate urachal cyst from Meckel diverticulum

Both arise from failure of something connecting yolk sac to inside (either fetal bladder = urachus, or midgut lumen = vitelline duct) to obliterate fully Urachal cyst = partial failure of urachus to obliterate =\> fluid-filled cavity lined w/ uroepithelium btwn umbilicus and bladder Meckel diverticulum = partial closure of vitelline duct w/ open portion to instestinal lumen

Derivatives from the 6 aortic arches

1st arch- maxillary artery (end branch of external carotid artery) 2nd arch- Stapedial artery and hyoid artery 3rd (C is the 3rd letter)- common carotid artery, proximal part of internal carotid artery 4th- aortic arch on left, proximal R. subclavian on R 6th- proximal part of pulmonary arteries and ductus arteriosus

Structures derived from the 4 brachial pouches

Brachial pouches ('CAP') are from endoderm 1st pouch- middle ear cavity 2nd pouch- tonsillar lining 3rd pouch- thymus and inferior parathyroids (ironically 3rd pouch structures end up below 4th pouch structures) 4th pouch- superior parathyroids

Mesonephric vs. paramesonephric duct

Females: mesonpehric duct degenerates, paramesonpehric --\> internal female genitalia (fallopian tubes, uterus, upper vagina) Males: paramesonephric degenerates, mesonephric duct --\> seminiferous tubules, epididmyis, ejaculatory duct, ductus deferens

Function of SRY gene

SRY gene on male chromosome codes for testes-dermining factor for testes development Testes need to develop so there are sertoli and leydig cells present to produce mullerian inhibitory factor and testosterone respectively

Male equivalent of (a) Glans cliteris (b) Labia minora (c) Labia majora (d) Bartholin glands

Male equivalent (a) Clitoris = glans penis (from genital tubercle) (b) Labia minora = ventral shaft of penis (from urogenital folds) (c) Labia majora = scrotum (from labioscrotal swelling) (d) Bartholin glands = Bulbourethral glands of Cowper

Function of the infundibulopelvic (suspensatory) ligament of the ovary (a) Vessels contained

Suspensatory ligament attaches the ovary to the lateral pelvic wall (a) Contains ovarian vessles (artery and vein) that need to be ligated during oophorectomy

Functional of the cardinal ligament (a) BV contained

Cardinal ligament attaches the cervix to the side wall of the pelvis (a) Contains the uterine vessels

Round ligament of uterus (a) Fxn (b) Remnant

Round ligament of the uterus connects the fundus to the labia majora- goes down thru round inguinal canal to continue downwards

Function of broad ligament

Broad ligament attaches the fallopian tube, ovary, and uterus both to each other and to the pelvic wall

MC location of cervical cancer

Cervical transformation zone = transition btwn stratified squamous of ectocervix and simple columnar of endocervix - very distinct border, literally can be one cell thick - this transformation zone is the MC location of cancer, and is what we sample w/ pap smear

Pathway of sperm for ejaculation

SEVEN UP Seminiferous tubules Epididymis Vas deferens Ejaculatory duct nothing Urethra Penis

Describe the anatomy of the seminiferous tubule (a) Location of cells (b) Location of blood supply

So capillaries and Interstitial cells of Leydig (stimulated by LH to release testosterone) are in the intersitium Then spermagonia line the seminiferous tubueles and are surrounded by supporting Sertoli cells (stimulated by FSH to release inhibin)

Explain the interaction btwn the two supporting cells in the ovary that leads to estrogen production

LH stimulates theca cells to convert cholesterol to androgens, then androgens from theca cells are taken up by granulosa cells Granulosa cells stimualted by FSH to convert androgens to estrogens Estrogen formed in the ovary = estradiol which is the most potent (more potent than estrone from peripheral fat and estriol from placenta)

Explain when oocytes undergo each part of meiosis I and II

Primary oocyte starts meiosis I during fetal life -meiosis I arrested in prOphase I for years until Ovulation Then meiosis II is arrested in METalphase II until fertilization (sperm MET egg) = secondary oocyte If fertilization doesn't occur, secondary oocyte degenerates before finishing meiosis II a

Blood hormones that cause ovulation

Get peak in estrogen that causes LH surge from anterior pituitary, LH surge causes rupture of follicle (ovulation) After ovulation start to see progesterone rise b/c corpus luteum produced from leftover granulosa and theca cells in ovary

Spermatid vs. Spermatogonium vs. Speratozoon

Speratogonium: dipoid gamete cell before meiosis has even started "gonium is eventually going to be sperm" Spermatogonium --\> primary spermatocyte (diploid) --\> secondary spermatocyte (haplod) --\> haploid spermatid Spermiogenesis converts haploid spermatid to mature spermatozoon ("zoon is zooming to egg") by adding acrosome

Differentiate placenta accreta/increta/percreta

Defective decidual layer causes abnormal attachment of placenta to myometrium Placenta accreta = placenta attaches to the myometrium w/o penetrating it (MC type) Placenta increa = placenta penetrates into myometrium Placenta percreta (most severe)- placenta penetrates into myometrium and into uterine serosa- so invades entire uterine wall, can even cause placental attachment to rectum or bladder

What is vasa previa? (a) Association w/ velamentous umbilical cord insertion

Vasa previa = when the fetal vessels run over the cervical os - can cause painless vaginal bleeding w/ fetal bradycardia (under 110 bpm), usually indicates emergency C-sxn (a) Velamentous umbilical cord = cord inserts in chorioamniotic membrane rather than the placenta =\> the fetal vessels travel to the placenta unprotected by Wharton jelly

Name 2 benign tumors of breast stroma

Breast stroma tumors 1. Fibroadenoma = MC tumor in F under 35, size and tenderness fluctuates w/ estrogen exposure, not a precursor to breast cancer 2. Phylloides tumor = bulky mass of CT w/ 'leaf like' projection - may become malignant

Use of Leuprolide

Leuprolide = GnRH analog (synthetic GnRH) - can give in pulsatile fashion to stimulate anterior pituitary: used in infertility - can give continuously to inhibit anterior pituitary: used in prostate cancer, uterine fibroids, precocious puberty

3 feedbacks on NE release from presynaptic terminal

1. ATII increases NE release 2. Alpha-2 innervation inhibits NE release 3. NE itself exerts negative feedback, acts on presynaptic alpha 2 to decrease NE release

Explain effect of NE on (a) BP (b) HR

NE- think primarily alpha1 agonist (a) Increases MAP w/ no change in pulse pressure b/c increase is in both systolic and diastolic (from alpha1 mediated vasoconstriction) (b) Reflex bradycardia - alpha1 mediated increase in BP =\> reduced HR from reflexive beta tone from carotid body

Effect of isoproterenol on (a) BP (b) HR

Isoproterenol = equal beta 1 and beta 2 agonist, no alpha (a) Decrease in MAP w/ increase in pulse pressure - beta2 mediated vasodilation reduces MAP, diastolic reduced more then systolic (b) HR increased thru beta1 chronotropy

Change in BP when high Epi is on board and Phentolamine is administered

High dose epi is mostly alpha w/ some beta, alpha1 predominates. So see increase (net pressor effect) before alpha blockade (Phentolamine) given -then when phentolamine is given beta2 activity of Epi is uninhibited =\> see reversal in BP change, now net depressor effect of epi

Differentiate zero and first order kinetics

Zero-order elimination = constant rate of elimination, doesn't depend on concentration 1st order = constant fraction of the drug eliminated per unit time, so elimination directly correlates w/ drug concentraiton

Formula for therapeutic index

TI = TD50 / ED50 TD50 - median toxic dose ED50 = medium effective dose Wider the TI = easier drug is to dose and prevent side effects, more wiggle room

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